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Publisher: Springer-Verlag (Total: 2352 journals)
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[SJR: 2.212] [H-I: 69] [3 followers] Follow
Hybrid journal (It can contain Open Access articles)
ISSN (Print) 1573-7209 - ISSN (Online) 0969-6970
Published by Springer-Verlag [2352 journals]
- Tumor angiogenesis and vascular normalization: alternative therapeutic
- Authors: Claire Viallard; Bruno Larrivée
Pages: 409 - 426
Abstract: Tumor blood vessels are a key target for cancer therapeutic management. Tumor cells secrete high levels of pro-angiogenic factors which contribute to the creation of an abnormal vascular network characterized by disorganized, immature and permeable blood vessels, resulting in poorly perfused tumors. The hypoxic microenvironment created by impaired tumor perfusion can promote the selection of more invasive and aggressive tumor cells and can also impede the tumor-killing action of immune cells. Furthermore, abnormal tumor perfusion also reduces the diffusion of chemotherapeutic drugs and radiotherapy efficiency. To fight against this defective phenotype, the normalization of the tumor vasculature has emerged as a new therapeutic strategy. Vascular normalization, by restoring proper tumor perfusion and oxygenation, could limit tumor cell invasiveness and improve the effectiveness of anticancer treatments. In this review, we investigate the mechanisms involved in tumor angiogenesis and describe strategies used to achieve vascular normalization.
PubDate: 2017-11-01
DOI: 10.1007/s10456-017-9562-9
Issue No: Vol. 20, No. 4 (2017)
- Authors: Claire Viallard; Bruno Larrivée
- History and conceptual developments in vascular biology and angiogenesis
research: a personal view
- Authors: Andreas Bikfalvi
Pages: 463 - 478
Abstract: Vascular biology is an important scientific domain that has gradually penetrated many medical and scientific fields. Scientists are most often focused on present problems in their daily scientific work and lack awareness regarding the evolution of their domain throughout history and of how philosophical issues are related to their research field. In this article, I provide a personal view with an attempt to conceptualize vascular development research that articulates lessons taken from history, philosophy, biology and medicine. I discuss selected aspects related to the history and the philosophy of sciences that can be extracted from the study of vascular development and how conceptual progress in this research field has been made. I will analyze paradigm shifts, cross-fertilization of different fields, technological advances and its impact on angiogenesis and discuss issues related to evolutionary biology, proximity of different molecular systems and scientific methodologies. Finally, I discuss briefly my views where the field is heading in the future.
PubDate: 2017-11-01
DOI: 10.1007/s10456-017-9569-2
Issue No: Vol. 20, No. 4 (2017)
- Authors: Andreas Bikfalvi
- Pathogenic role and therapeutic potential of pleiotrophin in mouse models
of ocular vascular disease
- Authors: Weiwen Wang; Michelle E. LeBlanc; Xiuping Chen; Ping Chen; Yanli Ji; Megan Brewer; Hong Tian; Samantha R. Spring; Keith A. Webster; Wei Li
Pages: 479 - 492
Abstract: Angiogenic factors play an important role in the pathogenesis of diabetic retinopathy (DR), neovascular age-related macular degeneration (nAMD) and retinopathy of prematurity (ROP). Pleiotrophin, a well-known angiogenic factor, was recently reported to be upregulated in the vitreous fluid of patients with proliferative DR (PDR). However, its pathogenic role and therapeutic potential in ocular vascular diseases have not been defined in vivo. Here using corneal pocket assays, we demonstrated that pleiotrophin induced angiogenesis in vivo. To investigate the pathological role of pleiotrophin we used neutralizing antibody to block its function in multiple in vivo models of ocular vascular diseases. In a mouse model of DR, intravitreal injection of pleiotrophin-neutralizing antibody alleviated diabetic retinal vascular leakage. In a mouse model of oxygen-induced retinopathy (OIR), which is a surrogate model of ROP and PDR, we demonstrated that intravitreal injection of anti-pleiotrophin antibody prevented OIR-induced pathological retinal neovascularization and aberrant vessel tufts. Finally, pleiotrophin-neutralizing antibody ameliorated laser-induced choroidal neovascularization, a mouse model of nAMD, suggesting that pleiotrophin is involved in choroidal vascular disease. These findings suggest that pleiotrophin plays an important role in the pathogenesis of DR with retinal vascular leakage, ROP with retinal neovascularization and nAMD with choroidal neovascularization. The results also support pleiotrophin as a promising target for anti-angiogenic therapy.
PubDate: 2017-11-01
DOI: 10.1007/s10456-017-9557-6
Issue No: Vol. 20, No. 4 (2017)
- Authors: Weiwen Wang; Michelle E. LeBlanc; Xiuping Chen; Ping Chen; Yanli Ji; Megan Brewer; Hong Tian; Samantha R. Spring; Keith A. Webster; Wei Li
- Low levels of physiological interstitial flow eliminate morphogen
gradients and guide angiogenesis
- Authors: Venktesh S. Shirure; Andrew Lezia; Arnold Tao; Luis F. Alonzo; Steven C. George
Pages: 493 - 504
Abstract: Convective transport can significantly distort spatial concentration gradients. Interstitial flow is ubiquitous throughout living tissue, but our understanding of how interstitial flow affects concentration gradients in biological processes is limited. Interstitial flow is of particular interest for angiogenesis because pathological and physiological angiogenesis is associated with altered interstitial flow, and both interstitial flow and morphogen gradients (e.g., vascular endothelial growth factor, VEGF) can potentially stimulate and guide new blood vessel growth. We designed an in vitro microfluidic platform to simulate 3D angiogenesis in a tissue microenvironment that precisely controls interstitial flow and spatial morphogen gradients. The microvascular tissue was developed from endothelial colony forming cell-derived endothelial cells extracted from cord blood and stromal fibroblasts in a fibrin extracellular matrix. Pressure in the microfluidic lines was manipulated to control the interstitial flow. A mathematical model of mass and momentum transport, and experimental studies with fluorescently labeled dextran were performed to validate the platform. Our data demonstrate that at physiological interstitial flow (0.1–10 μm/s), morphogen gradients were eliminated within hours, and angiogenesis demonstrated a striking bias in the opposite direction of interstitial flow. The interstitial flow-directed angiogenesis was dependent on the presence of VEGF, and the effect was mediated by αvβ3 integrin. We conclude that under physiological conditions, growth factors such as VEGF and fluid forces work together to initiate and spatially guide angiogenesis.
PubDate: 2017-11-01
DOI: 10.1007/s10456-017-9559-4
Issue No: Vol. 20, No. 4 (2017)
- Authors: Venktesh S. Shirure; Andrew Lezia; Arnold Tao; Luis F. Alonzo; Steven C. George
- CXCL10 suppression of hem- and lymph-angiogenesis in inflamed corneas
through MMP13
- Authors: Nan Gao; Xiaowei Liu; Jiayin Wu; Juan Li; Chen Dong; Xinyi Wu; Xiao Xiao; Fu-Shin X. Yu
Pages: 505 - 518
Abstract: Though not present in the normal adult cornea, both hem- and lymph-angiogenesis can be induced in this tissue after an inflammatory, infectious, or traumatic insult. We previously showed that the chemokine CXCL10 plays a key role in eradicating invading Candida (C.) albicans in C57BL6 mouse corneas. However, even after the clearance of pathogens, infection-induced inflammation and angiogenesis continue to progress in the cornea. The aim of this study is define the role of CXCL10 as a major angiostatic factor in modulating cornea angiogenesis in B6 mouse corneas under pathogenic conditions. We showed that epithelial expression of CXCL10, driven by AAV9 vector, suppressed both infection- and inflammation-induced hem and lymph angiogenesis, whereas the neutralization of CXCL10 as well as its receptor CXCR3 greatly promoted these processes. The inhibitory effect of CXCL10 was unrelated to its antimicrobial activity, but through the suppression of the expression of many angiogenic factors, including VEGFa and c, and MMP-13 in vivo. Inhibition of MMP13 but not TIMPs, attenuated suture-induced neovascularization but had no effects on CXCL10 expression. Strikingly, topical application of CXCL10 post-C. albicans infection effectively blocked both hem- and lymph-angiogenesis and preserved the integrity of sensory nerves in the cornea. Taken together, CXCL10 has strong inhibitory effects on neovascularization, whereas MMP13 is required for neovascularization in C. albicans-infected corneas and the local application of CXCL10 or MMP13 inhibitors, alone or as adjuvant therapy, may target hem- and lymph-angiogenesis in the inflamed corneas.
PubDate: 2017-11-01
DOI: 10.1007/s10456-017-9561-x
Issue No: Vol. 20, No. 4 (2017)
- Authors: Nan Gao; Xiaowei Liu; Jiayin Wu; Juan Li; Chen Dong; Xinyi Wu; Xiao Xiao; Fu-Shin X. Yu
- Endothelium-derived fibronectin regulates neonatal vascular morphogenesis
in an autocrine fashion
- Authors: Christopher J. Turner; Kwabena Badu-Nkansah; Richard O. Hynes
Pages: 519 - 531
Abstract: Fibronectin containing alternatively spliced EIIIA and EIIIB domains is largely absent from mature quiescent vessels in adults, but is highly expressed around blood vessels during developmental and pathological angiogenesis. The precise functions of fibronectin and its splice variants during developmental angiogenesis however remain unclear due to the presence of cardiac, somitic, mesodermal and neural defects in existing global fibronectin KO mouse models. Using a rare family of surviving EIIIA EIIIB double KO mice, as well as inducible endothelial-specific fibronectin-deficient mutant mice, we show that vascular development in the neonatal retina is regulated in an autocrine manner by endothelium-derived fibronectin, and requires both EIIIA and EIIIB domains and the RGD-binding α5 and αv integrins for its function. Exogenous sources of fibronectin do not fully substitute for the autocrine function of endothelial fibronectin, demonstrating that fibronectins from different sources contribute differentially to specific aspects of angiogenesis.
PubDate: 2017-11-01
DOI: 10.1007/s10456-017-9563-8
Issue No: Vol. 20, No. 4 (2017)
- Authors: Christopher J. Turner; Kwabena Badu-Nkansah; Richard O. Hynes
- Optical clearing and fluorescence deep-tissue imaging for 3D quantitative
analysis of the brain tumor microenvironment
- Authors: Tonny Lagerweij; Sophie A. Dusoswa; Adrian Negrean; Esther M. L. Hendrikx; Helga E. de Vries; Jeroen Kole; Juan J. Garcia-Vallejo; Huibert D. Mansvelder; W. Peter Vandertop; David P. Noske; Bakhos A. Tannous; René J. P. Musters; Yvette van Kooyk; Pieter Wesseling; Xi Wen Zhao; Thomas Wurdinger
Pages: 533 - 546
Abstract: Background Three-dimensional visualization of the brain vasculature and its interactions with surrounding cells may shed light on diseases where aberrant microvascular organization is involved, including glioblastoma (GBM). Intravital confocal imaging allows 3D visualization of microvascular structures and migration of cells in the brain of mice, however, with limited imaging depth. To enable comprehensive analysis of GBM and the brain microenvironment, in-depth 3D imaging methods are needed. Here, we employed methods for optical tissue clearing prior to 3D microscopy to visualize the brain microvasculature and routes of invasion of GBM cells. Methods We present a workflow for ex vivo imaging of optically cleared brain tumor tissues and subsequent computational modeling. This workflow was used for quantification of the microvasculature in relation to nuclear or cellular density in healthy mouse brain tissues and in human orthotopic, infiltrative GBM8 and E98 glioblastoma models. Results Ex vivo cleared mouse brain tissues had a >10-fold imaging depth as compared to intravital imaging of mouse brain in vivo. Imaging of optically cleared brain tissue allowed quantification of the 3D microvascular characteristics in healthy mouse brains and in tissues with diffuse, infiltrative growing GBM8 brain tumors. Detailed 3D visualization revealed the organization of tumor cells relative to the vasculature, in both gray matter and white matter regions, and patterns of multicellular GBM networks collectively invading the brain parenchyma. Conclusions Optical tissue clearing opens new avenues for combined quantitative and 3D microscopic analysis of the topographical relationship between GBM cells and their microenvironment.
PubDate: 2017-11-01
DOI: 10.1007/s10456-017-9565-6
Issue No: Vol. 20, No. 4 (2017)
- Authors: Tonny Lagerweij; Sophie A. Dusoswa; Adrian Negrean; Esther M. L. Hendrikx; Helga E. de Vries; Jeroen Kole; Juan J. Garcia-Vallejo; Huibert D. Mansvelder; W. Peter Vandertop; David P. Noske; Bakhos A. Tannous; René J. P. Musters; Yvette van Kooyk; Pieter Wesseling; Xi Wen Zhao; Thomas Wurdinger
- Early prediction of tumor response to bevacizumab treatment in murine
colon cancer models using three-dimensional dynamic contrast-enhanced
ultrasound imaging
- Authors: Jianhua Zhou; Huiping Zhang; Huaijun Wang; Amelie M. Lutz; Ahmed El Kaffas; Lu Tian; Dimitre Hristov; Jürgen K. Willmann
Pages: 547 - 555
Abstract: Due to spatial tumor heterogeneity and consecutive sampling errors, it is critically important to assess treatment response following antiangiogenic therapy in three dimensions as two-dimensional assessment has been shown to substantially over- and underestimate treatment response. In this study, we evaluated whether three-dimensional (3D) dynamic contrast-enhanced ultrasound (DCE-US) imaging allows assessing early changes in tumor perfusion following antiangiogenic treatment (bevacizumab administered at a dose of 10 mg/kg b.w.), and whether these changes could predict treatment response in colon cancer tumors that either are responsive (LS174T tumors) or none responsive (CT26) to the proposed treatment. Our results showed that the perfusion parameters of 3D DCE-US including peak enhancement (PE) and area under curve (AUC) significantly decreased by up to 69 and 77%, respectively, in LS174T tumors within 1 day after antiangiogenic treatment (P = 0.005), but not in CT26 tumors (P > 0.05). Similarly, the percentage area of neovasculature significantly decreased in treated versus control LS174T tumors (P < 0.001), but not in treated versus control CT26 tumors (P = 0.796). Early decrease in both PE and AUC by 45–50% was predictive of treatment response in 100% (95% CI 69.2, 100%) of responding tumors, and in 100% (95% CI 88.4, 100%) and 86.7% (95% CI 69.3, 96.2%), respectively, of nonresponding tumors. In conclusion, 3D DCE-US provides clinically relevant information on the variability of tumor response to antiangiogenic therapy and may be further developed as biomarker for predicting treatment outcomes.
PubDate: 2017-11-01
DOI: 10.1007/s10456-017-9566-5
Issue No: Vol. 20, No. 4 (2017)
- Authors: Jianhua Zhou; Huiping Zhang; Huaijun Wang; Amelie M. Lutz; Ahmed El Kaffas; Lu Tian; Dimitre Hristov; Jürgen K. Willmann
- A new key player in VEGF-dependent angiogenesis in human hepatocellular
carcinoma: dimethylarginine dimethylaminohydrolase 1
- Authors: Nikki Buijs; J. Efraim Oosterink; Morgan Jessup; Henk Schierbeek; Donna B. Stolz; Alexander P. Houdijk; David A. Geller; Paul A. van Leeuwen
Pages: 557 - 565
Abstract: Background Anti-angiogenic therapies, targeting VEGF, are a promising treatment for hepatocellular carcinoma (HCC). To enhance this potential therapy, identification of novel targets in this pathway is of major interest. Nitric oxide (NO) plays a crucial role in VEGF-dependent angiogenesis. NO production depends on arginine as substrate and asymmetric dimethylarginine (ADMA) as inhibitor. Dimethylarginine dimethylaminohydrolase 1 (DDAH-1) catabolizes ADMA and therefore regulates NO and VEGF expression. This study unravels additional mechanisms to improve VEGF targeting therapies. Methods The expression of DDAH-1 was examined in HCC specimen and non-tumorous background liver of 20 patients undergoing liver resection. Subsequently, arginine/ADMA balance, NO production, and VEGF expression were analyzed. The influence of hypoxia on DDAH-1 and angiogenesis promoting factors was evaluated in HepG2 cells and primary human hepatocytes. Results DDAH-1 expression was significantly induced in primary HCC tumors compared to non-tumorous background liver. This was associated with an increased arginine/ADMA ratio, higher NO formation, and higher VEGF expression in human HCC compared to non-tumorous liver. Hypoxia induced DDAH-1, iNOS, and VEGF expression in a time-dependent manner in HepG2 cells. Conclusions Our results indicate that DDAH-1 expression is increased in human HCC, which is associated with an increase in the arginine/ADMA ratio and enhanced NO formation. Hypoxia may be an initiating factor for the increase in DDAH-1 expression. DDAH-1 expression is associated with promotion of angiogenesis stimulating factor VEGF. Together, our findings for the first time identified DDAH-1 as a key player in the regulation of angiogenesis in human HCC, and by understanding this mechanism, future therapeutic strategies targeting VEGF can be improved.
PubDate: 2017-11-01
DOI: 10.1007/s10456-017-9567-4
Issue No: Vol. 20, No. 4 (2017)
- Authors: Nikki Buijs; J. Efraim Oosterink; Morgan Jessup; Henk Schierbeek; Donna B. Stolz; Alexander P. Houdijk; David A. Geller; Paul A. van Leeuwen
- Microvascular ultrastructural changes precede cognitive impairment in the
murine APPswe/PS1dE9 model of Alzheimer's disease
- Authors: Patricia Kelly; Paul Denver; Simon C. Satchell; Maximilian Ackermann; Moritz A. Konerding; Christopher A. Mitchell
Pages: 567 - 580
Abstract: Cerebral and systemic organ microvascular pathologies coexist with human Alzheimer's disease (AD) neuropathology. In this study, we hypothesised that both cerebral and systemic microvascular pathologies exist in 4- to 5-month-old male APPswe/PS1dE9 (APP/PS1) transgenic mice prior to the onset of cognitive impairment. To assess this we examined recognition memory in both wild-type and APP/PS1 mice using the object recognition task (ORT; n = 11 per group) and counted thioflavin-S-positive plaques in brain (n = 6 per group). Vascular casts of brain, liver, spleen and kidneys were examined using scanning electron microscopy (n = 6 per group), and the urinary albumin-to-creatinine ratio (uACR; n = 5 per group) was measured as an index of glomerular permeability. Murine recognition memory was intact, as demonstrated by a significant preference for the novel object in the ORT paradigm. Brain sections of wild-type mice were devoid of thioflavin-S positivity, whereas age-matched APP/PS1 mice had an average of 0.88 ± 0.22 thioflavin-S-positive plaques in the cortex, 0.42 ± 0.17 plaques in the dentate gyrus and 0.30 ± 0.07 plaques in the cornus ammonis 1 region. The profiles of casted cerebral capillaries of wild-type mice were smooth and regular in contrast to those of APP/PS1 mice which demonstrate characteristic (0.5–4.6 μm) 'tags'. APP/PS1 mice also had a significantly reduced hepatic vessel number (p = 0.0002) and an increase in the number of splenic microvascular pillars (p = 0.0231), in the absence of changes in either splenic microvascular density (p = 0.3746) or glomerular ultrastructure. The highly significant reduction in uACR in APP/PS1 mice compared to wild-type (p = 0.0079) is consistent with glomerular microvascular dysfunction. These findings highlight early microvascular pathologies in 4- to 5-month-old APP/PS1 transgenic mice and may indicate an amenable target for pharmacological intervention in AD.
PubDate: 2017-11-01
DOI: 10.1007/s10456-017-9568-3
Issue No: Vol. 20, No. 4 (2017)
- Authors: Patricia Kelly; Paul Denver; Simon C. Satchell; Maximilian Ackermann; Moritz A. Konerding; Christopher A. Mitchell
- PDGFRβ-P2A-CreER T2 mice: a genetic tool to target pericytes in
- Authors: Henar Cuervo; Brianna Pereira; Taliha Nadeem; Mika Lin; Frances Lee; Jan Kitajewski; Chyuan-Sheng Lin
Pages: 655 - 662
Abstract: Pericytes are essential mural cells distinguished by their association with small caliber blood vessels and the presence of a basement membrane shared with endothelial cells. Pericyte interaction with the endothelium plays an important role in angiogenesis; however, very few tools are currently available that allow for the targeting of pericytes in mouse models, limiting our ability to understand their biology. We have generated a novel mouse line expressing tamoxifen-inducible Cre-recombinase under the control of the platelet-derived growth factor receptor β promoter: PDGFRβ-P2A-CreER T2 . We evaluated the expression of the PDGFRβ-P2A-CreER T2 line by crossing it with fluorescent reporter lines and analyzed reporter signal in the angiogenic retina and brain at different time points after tamoxifen administration. Reporter lines showed labeling of NG2+, desmin+, PDGFRβ+ perivascular cells in the retina and the brain, indicating successful targeting of pericytes; however, signal from reporter lines was also observed in a small subset of glial cells both in the retina and the brain. We also evaluated recombination in tumors and found efficient recombination in perivascular cells associated with tumor vasculature. As a proof of principle, we used our newly generated driver to delete Notch signaling in perivascular cells and observed a loss of smooth muscle cells in retinal arteries, consistent with previously published studies evaluating Notch3 null mice. We conclude that the PDGFRβ-P2A-CreER T2 line is a powerful new tool to target pericytes and will aid the field in gaining a deeper understanding of the role of these cells in physiological and pathological settings.
PubDate: 2017-11-01
DOI: 10.1007/s10456-017-9570-9
Issue No: Vol. 20, No. 4 (2017)
- Authors: Henar Cuervo; Brianna Pereira; Taliha Nadeem; Mika Lin; Frances Lee; Jan Kitajewski; Chyuan-Sheng Lin
- Pharmacological intervention of MKL/SRF signaling by CCG-1423 impedes
endothelial cell migration and angiogenesis
- Authors: David Gau; William Veon; Teresa L. Capasso; Ralph Bottcher; Sanjeev Shroff; Beth L. Roman; Partha Roy
Pages: 663 - 672
Abstract: De novo synthesis of cytoskeleton-regulatory proteins triggered by the megakaryoblastic leukemia (MKL)/serum response factor (SRF) transcriptional system in response to pro-angiogenic growth factors lies at the heart of endothelial cell (EC) migration (a critical element of angiogenesis) and neovascularization. This study explores whether pharmacological intervention of MKL/SRF signaling axis by CCG-1423 is able to suppress angiogenesis. Our studies show that CCG-1423 inhibits migration and cord morphogenesis of EC in vitro and sprouting angiogenesis ex vivo and in vivo, suggesting CCG-1423 could be a novel anti-angiogenic agent. Kymography analyses of membrane dynamics of EC revealed that CCG-1423 treatment causes a major defect in membrane protrusion. CCG-1423 treatment led to attenuated expression of several actin-binding proteins that are important for driving membrane protrusion including ArpC2, VASP, and profilin1 (Pfn1) with the most drastic effect seen on the expression of Pfn1. Finally, depletion of Pfn1 alone is also sufficient for a dramatic decrease in sprouting angiogenesis of EC in vitro and ex vivo, further suggesting that Pfn1 depletion may be one of the mechanisms of the anti-angiogenic action of CCG-1423.
PubDate: 2017-11-01
DOI: 10.1007/s10456-017-9560-y
Issue No: Vol. 20, No. 4 (2017)
- Authors: David Gau; William Veon; Teresa L. Capasso; Ralph Bottcher; Sanjeev Shroff; Beth L. Roman; Partha Roy
- Erratum to: miRNAs: micro-managers of anticancer combination therapies
- Authors: Judy R. van Beijnum; Elisa Giovannetti; Dennis Poel; Patrycja Nowak-Sliwinska; Arjan W. Griffioen
Pages: 673 - 673
PubDate: 2017-11-01
DOI: 10.1007/s10456-017-9564-7
Issue No: Vol. 20, No. 4 (2017)
- Authors: Judy R. van Beijnum; Elisa Giovannetti; Dennis Poel; Patrycja Nowak-Sliwinska; Arjan W. Griffioen
- Mechanisms of angiogenesis in microbe-regulated inflammatory and
neoplastic conditions
- Authors: Sanaullah Sajib; Fatema Tuz Zahra; Michail S. Lionakis; Nadezhda A. German; Constantinos M. Mikelis
Abstract: Commensal microbiota inhabit all the mucosal surfaces of the human body. It plays significant roles during homeostatic conditions, and perturbations in numbers and/or products are associated with several pathological disorders. Angiogenesis, the process of new vessel formation, promotes embryonic development and critically modulates several biological processes during adulthood. Indeed, deregulated angiogenesis can induce or augment several pathological conditions. Accumulating evidence has implicated the angiogenic process in various microbiota-associated human diseases. Herein, we critically review diseases that are regulated by microbiota and are affected by angiogenesis, aiming to provide a broad understanding of how angiogenesis is involved and how microbiota regulate angiogenesis in microbiota-associated human conditions.
PubDate: 2017-11-06
DOI: 10.1007/s10456-017-9583-4
- Authors: Sanaullah Sajib; Fatema Tuz Zahra; Michail S. Lionakis; Nadezhda A. German; Constantinos M. Mikelis
- A genomic screen for angiosuppressor genes in the tumor endothelium
identifies a multifaceted angiostatic role for bromodomain containing 7
- Authors: Judy R. van Beijnum; Patrycja Nowak-Sliwinska; Maaike van Berkel; Tse J. Wong; Arjan W. Griffioen
Abstract: Tumor angiogenesis is characterized by deregulated gene expression in endothelial cells (EC). While studies until now have mainly focused on overexpressed genes in tumor endothelium, we here describe the identification of transcripts that are repressed in tumor endothelium and thus have potential suppressive effects on angiogenesis. We identified nineteen putative angiosuppressor genes, one of them being bromodomain containing 7 (BRD7), a gene that has been assigned tumor suppressor properties. BRD7 was studied in more detail, and we demonstrate that BRD7 expression is inversely related to EC activation. Ectopic expression of BRD7 resulted in a dramatic reduction of EC proliferation and viability. Furthermore, overexpression of BRD7 resulted in a bromodomain-dependent induction of NFκB-activity and NFκB-dependent gene expression, including ICAM1, enabling leukocyte–endothelial interactions. In silico functional annotation analysis of genome-wide expression data on BRD7 knockdown and overexpression revealed that the transcriptional signature of low BRD7 expressing cells is associated with increased angiogenesis (a.o. upregulation of angiopoietin-2, VEGF receptor-1 and neuropilin-1), cytokine activity (a.o. upregulation of CXCL1 and CXCL6), and a reduction of immune surveillance (TNF-α, NFκB, ICAM1). Thus, combining in silico and in vitro data reveals multiple pathways of angiosuppressor and anti-tumor activities of BRD7.
PubDate: 2017-09-26
DOI: 10.1007/s10456-017-9576-3
- Authors: Judy R. van Beijnum; Patrycja Nowak-Sliwinska; Maaike van Berkel; Tse J. Wong; Arjan W. Griffioen
- 3D endothelial cell spheroid/human vitreous humor assay for the
characterization of anti-angiogenic inhibitors for the treatment of
proliferative diabetic retinopathy
- Authors: Sara Rezzola; Imtiaz M. Nawaz; Anna Cancarini; Cosetta Ravelli; Stefano Calza; Francesco Semeraro; Marco Presta
Abstract: Proliferative diabetic retinopathy (PDR) represents a main cause of acquired blindness. Despite the recognition of the key role exerted by vascular endothelial growth factor (VEGF) in the pathogenesis of PDR, limitations to anti-VEGF therapies do exist. Thus, rapid and cost-effective angiogenesis assays are crucial for the screening of anti-angiogenic drug candidates for PDR therapy. In this context, evaluation of the angiogenic potential of PDR vitreous fluid may represent a valuable tool for preclinical assessment of angiostatic molecules. Here, vitreous fluid obtained from PDR patients after pars plana vitrectomy was used as a pro-angiogenic stimulus in a 3D endothelial cell spheroid/human vitreous assay. The results show that PDR vitreous is able to stimulate the sprouting of fibrin-embedded HUVEC spheroids in a time- and dose-dependent manner. A remarkable variability was observed among 40 individual vitreous fluid samples in terms of sprouting-inducing activity that was related, at least in part, to defined clinical features of the PDR patient. This activity was hampered by various extracellular and intracellular signaling pathway inhibitors, including the VEGF antagonist ranibizumab. When tested on 20 individual vitreous fluid samples, the inhibitory activity of ranibizumab ranged between 0 and 100% of the activity measured in the absence of the drug, reflecting a variable contribution of angiogenic mediators distinct from VEGF. In conclusion, the 3D endothelial cell spheroid/human vitreous assay represents a rapid and cost-effective experimental procedure suitable for the evaluation of the anti-angiogenic activity of novel extracellular and intracellular drug candidates, with possible implications for the therapy of PDR.
PubDate: 2017-09-13
DOI: 10.1007/s10456-017-9575-4
- Authors: Sara Rezzola; Imtiaz M. Nawaz; Anna Cancarini; Cosetta Ravelli; Stefano Calza; Francesco Semeraro; Marco Presta
- Tumor vessel disintegration by maximum tolerable PFKFB3 blockade
- Authors: Lena-Christin Conradi; Aleksandra Brajic; Anna Rita Cantelmo; Ann Bouché; Joanna Kalucka; Andreas Pircher; Ulrike Brüning; Laure-Anne Teuwen; Stefan Vinckier; Bart Ghesquière; Mieke Dewerchin; Peter Carmeliet
Abstract: Blockade of the glycolytic activator PFKFB3 in cancer cells (using a maximum tolerable dose of 70 mg/kg of the PFKFB3 blocker 3PO) inhibits tumor growth in preclinical models and is currently being tested as a novel anticancer treatment in phase I clinical trials. However, a detailed preclinical analysis of the effects of such maximum tolerable dose of a PFKFB3 blocker on the tumor vasculature is lacking, even though tumor endothelial cells are hyper-glycolytic. We report here that a high dose of 3PO (70 mg/kg), which inhibits cancer cell proliferation and reduces primary tumor growth, causes tumor vessel disintegration, suppresses endothelial cell growth for protracted periods, (model-dependently) aggravates tumor hypoxia, and compromises vascular barrier integrity, thereby rendering tumor vessels more leaky and facilitating cancer cell intravasation and dissemination. These findings contrast to the effects of a low dose of 3PO (25 mg/kg), which induces tumor vessel normalization, characterized by vascular barrier tightening and maturation, but reduces cancer cell intravasation and metastasis. Our findings highlight the importance of adequately dosing a glycolytic inhibitor for anticancer treatment.
PubDate: 2017-09-05
DOI: 10.1007/s10456-017-9573-6
- Authors: Lena-Christin Conradi; Aleksandra Brajic; Anna Rita Cantelmo; Ann Bouché; Joanna Kalucka; Andreas Pircher; Ulrike Brüning; Laure-Anne Teuwen; Stefan Vinckier; Bart Ghesquière; Mieke Dewerchin; Peter Carmeliet
- Endothelial progenitor cells in multiple myeloma neovascularization: a
brick to the wall
- Authors: Maria Margarida Tenreiro; Maria Leonor Correia; Maria Alexandra Brito
Abstract: Multiple myeloma (MM) is characterized by the clonal expansion of plasma cells in the bone marrow that leads to events such as bone destruction, anaemia and renal failure. Despite the several therapeutic options available, there is still no effective cure, and the standard survival is up to 4 years. The evolution from the asymptomatic stage of monoclonal gammopathy of undetermined significance to MM and the progression of the disease itself are related to cellular and molecular alterations in the bone marrow microenvironment, including the development of the vasculature. Post-natal vasculogenesis is characterized by the recruitment to the tumour vasculature of bone marrow progenitors, known as endothelial progenitor cells (EPCs), which incorporate newly forming blood vessels and differentiate into endothelial cells. Several processes related to EPCs, such as recruitment, mobilization, adhesion and differentiation, are tightly controlled by cells and molecules in the bone marrow microenvironment. In this review, the bone marrow microenvironment and the mechanisms associated to the development of the neovasculature promoted by EPCs are discussed in detail in both a non-pathological scenario and in MM. The latest developments in therapy targeting the vasculature and EPCs in MM are also highlighted. The identification and characterization of the pathways relevant to the complex setting of MM are of utter importance to identify not only biomarkers for an early diagnosis and disease progression monitoring, but also to reveal intervention targets for more effective therapy directed to cancer cells and the endothelial mediators relevant to neovasculature development.
PubDate: 2017-08-24
DOI: 10.1007/s10456-017-9571-8
- Authors: Maria Margarida Tenreiro; Maria Leonor Correia; Maria Alexandra Brito
- Frizzled-5: a high affinity receptor for secreted frizzled-related
protein-2 activation of nuclear factor of activated T-cells c3 signaling
to promote angiogenesis
- Authors: Yuri K. Peterson; Patrick Nasarre; Ingrid V. Bonilla; Eleanor Hilliard; Jennifer Samples; Thomas A. Morinelli; Elizabeth G. Hill; Nancy Klauber-DeMore
Abstract: Secreted frizzled-related protein 2 (SFRP2) is a pro-angiogenic factor expressed in the vasculature of a wide variety of human tumors, and modulates angiogenesis via the calcineurin-dependent nuclear factor of activated T-cells cytoplasmic 3 (NFATc3) pathway in endothelial cells. However, until now, SFRP2 receptor for this pathway was unknown. In the present study, we first used amino acid alignments and molecular modeling to demonstrate that SFRP2 interaction with frizzled-5 (FZD5) is typical of Wnt/FZD family members. To confirm this interaction, we performed co-immunofluorescence, co-immunoprecipitation, and ELISA binding assays, which demonstrated SFRP2/FZD5 binding. Functional knock-down studies further revealed that FZD5 is necessary for SFRP2-induced tube formation and intracellular calcium flux in endothelial cells. Using protein analysis on endothelial cell nuclear extracts, we also discovered that FZD5 is required for SFRP2-induced activation of NFATc3. Our novel findings reveal that FZD5 is a receptor for SFRP2 and mediates SFRP2-induced angiogenesis via calcineurin/NFATc3 pathway in endothelial cells.
PubDate: 2017-08-24
DOI: 10.1007/s10456-017-9574-5
- Authors: Yuri K. Peterson; Patrick Nasarre; Ingrid V. Bonilla; Eleanor Hilliard; Jennifer Samples; Thomas A. Morinelli; Elizabeth G. Hill; Nancy Klauber-DeMore
- Prox1-GFP/Flt1-DsRed transgenic mice: an animal model for simultaneous
live imaging of angiogenesis and lymphangiogenesis
- Authors: Wei Zhong; Xinbo Gao; Shuangyong Wang; Kyuyeon Han; Masatsugu Ema; Susanne Adams; Ralf H. Adams; Mark I. Rosenblatt; Jin-Hong Chang; Dimitri T. Azar
Abstract: The roles of angiogenesis in development, health, and disease have been studied extensively; however, the studies related to lymphatic system are limited due to the difficulty in observing colorless lymphatic vessels. But recently, with the improved technique, the relative importance of the lymphatic system is just being revealed. We bred transgenic mice in which lymphatic endothelial cells express GFP (Prox1-GFP) with mice in which vascular endothelial cells express DsRed (Flt1-DsRed) to generate Prox1-GFP/Flt1-DsRed (PGFD) mice. The inherent fluorescence of blood and lymphatic vessels allows for direct visualization of blood and lymphatic vessels in various organs via confocal and two-photon microscopy and the formation, branching, and regression of both vessel types in the same live mouse cornea throughout an experimental time course. PGFD mice were bred with CDh5CreERT2 and VEGFR2lox knockout mice to examine specific knockouts. These studies showed a novel role for vascular endothelial cell VEGFR2 in regulating VEGFC-induced corneal lymphangiogenesis. Conditional deletion of vascular endothelial VEGFR2 abolished VEGFA- and VEGFC-induced corneal lymphangiogenesis. These results demonstrate the potential use of the PGFD mouse as a powerful animal model for studying angiogenesis and lymphangiogenesis.
PubDate: 2017-08-09
DOI: 10.1007/s10456-017-9572-7
- Authors: Wei Zhong; Xinbo Gao; Shuangyong Wang; Kyuyeon Han; Masatsugu Ema; Susanne Adams; Ralf H. Adams; Mark I. Rosenblatt; Jin-Hong Chang; Dimitri T. Azar


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Rachel Zoe Confirms That Bump Was Not a Food Belly — It's a Baby!
Who wants to place bets on what kind of fur it's wearing when it comes out of the womb?By Amy Odell
Who wants to place bets on what kind of fur it's wearing when it comes out of the womb?By Amy Odell
Well. This has never happened before.By Amy Odell
A source says she's more than four months along — and having a boy!By Amy Odell
She's not drinking OR traveling, sources have noted. SUSPICIOUS.By Amy Odell
Or maybe she's pregnant.By Amy Odell
A source tells 'OK!' she's three months along.By Amy Odell
Lena Dunham Defends Girls Writer Murray Miller From Sexual Assault Allegation
Polls Show Roy Moore Crashing in Alabama
Meryl Streep Went After an Abuser With Cher, and Won
What the Hell Is Going On With Henry Cavill's Mustache in Justice League?
Montana Congressman Who Assaulted Reporter Lied to Police About It
Gymnast Gabby Douglas Apologizes After Backlash to Modesty Comment to Fellow Olympian Aly Raisman
The Danger of Knowing You're on the 'Right Side of History'
We Are All Implicated in the Post-Weinstein Reckoning
What's New on Netflix: November 2017
Explaining That Justice League Post-Credits Scene — and Its Confusing Cameo

subset: commoncrawl


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Couples Counselor
Alice Locke-Chezar, MFT, ATR
Marriage & Family Therapist, Registered Art Therapist
Being part of a loving couple is hard work. My clients often come to me when they feel their lives and their relationship spiraling out of control. I help my clients to look back at what brought them together, to see what is currently tearing them apart, and to explore past family patterns and make certain they are not being blinldy repeated. As the elements of the current situation become clearer, I help my clients learn important tools to foster clear communication, understanding and empathy. Armed with greater understanding and important tools, they can heal their wounds and find joy comfort and support being together.
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Sean Faulkner, MFTi
Marriage and Family Therapist Intern
Couples typically do not seek counseling until there is a major break down in their relationship and hope to find a counselor to "fix" their problems. Resolving your issues is not my goal as a counselor--my goal is to help you and your partner learn and develop new ways to communicate which will allow you two to resolve your own issues together as a couple, both during and after therapy. I aim to help you and your partner develop long-term skills which you can use for years to come.
Couples Counselor
Matthew Lindgren, MFT
Licensed Marriage and Family Therapist
Your relationship used to be full of love and laughter. Maybe now you're at a point of crisis where you're considering moving out & call it all off. You've been trying to work things out. Maybe you saw a therapist who didn't seem to know how to help, or you've had bad experiences with therapists in the past. Therapy does cost money, but it's far less expensive than a divorce, new living arrangement & the considerable pain & suffering of ending a relationship. You owe it to yourself & your partner to to make an appt. with me today. http://matt-lindgren-oakland-marriage-therapist.com/
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Jonathan Eli Herrick, jonathan herrick
Licensed Clinical Social Worker
Jonathan Herrick, LCSW and his wife Barbara Carroll, MA work together and are both passionate about helping couples work through the struggles that we have worked through to be able to enjoy a deeply rich relationship. Having counseled many hundreds of couples we have a wide range of skills. We are highly pragmatic and pro-active, and adjust our approach to match the particular couple. We help couples improve communication, improve intimacy, reduce conflict, handle an affair, adjust to raising children and enrich their relationship, To learn about our work, visit embraceCouples.com and read my book The Heart of Relationship
Couples Counselor
Robert Nemerovski, Psy.D.
Licensed Psychologist
Couples often come to counseling when they have difficulty talking with each other or resolving an issue. Some find that a familiar struggle or behavioral pattern "dynamic" comes up over and over again. Commonly, tensions and emotions can run high, and each person may feel some combination of distant, resentful, sad, hurt, worried, or angry. Couples counseling is a special opportunity to understand these patterns and explore new communication, behaviors, and connection. I help facilitate a more productive conversation in a safe environment and offer exercises and other resources to practice from home. I welcome and provide couples counseling to people from all backgrounds.
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Sandra Amat, MFT
Licensed Marriage Family Therapist
I view relationship as a vehicle to support greater deepening and healing. It is in relationship that we see our deepest vulnerability, insecurity and unprocessed wounding. Where do we get more triggered than in our primary relationship? I believe that sharing the attitude of using the relationship as a vehicle to heal, allows couples to get on the same page as they work through their issues. It becomes less about who will win this argument and more about how the couple can support each other in healing. Together we can explore relationship dynamics and work toward creating a supportive environment for growth, transformation and healing.
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Zak Forrest, Zachary Forrest, LMFT
Licensed Psychotherapist
Issues that can be worked on in couples counseling often stem from conscious and unconscious assumptions and expectations that each person has about the other. The individual sees the other through the lens of their upbringing and relationship history. I help couples unpack the complex and often tangled web of how each person is understood and misunderstood in the eyes of the other. In doing so, each partner can have a deeper understanding of themselves and their partner, generating compassion, clearer communication, and emotional space from pressing issues.
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Peter Bernhardt, MFT
Marriage Family Therapist
Are you trapped in destructive cycles of anger and blame? Have you lost trust because of an affair? Are you avoiding your partner or feeling disengaged? Is it hard for you to have real conversations or solve problems together? I will help you untangle your painful negative cycles of communication and build new stronger connections. You can learn to have power over that cycle by learning your triggers and undoing them. You will learn about the roots of the cycle learned in early relationships. Call, text or email me to set an appointment.
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Dietmar Brinkmann, MA, LMFT
Licensed Marriage and Family Therapist
Most couples come to therapy because they find it hard to communicate with each other. They want to resolve endless fights and avoid getting caught in fruitless arguments. When feelings are raw it can be so hard to feel close and end the negative cycle of blame and defensive withdrawal. In couple therapy, I help you feel safe to express yourself. You and your partner will learn to listen to each other with compassion and grow a shared understanding of what makes your relationship work. I use Emotionally Focused Therapy, an approach proven by extensive research to strengthen the emotional bond that is the heart of every relationship.
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Jeff Cohen, MA, MFT
Licensed Marriage & Family Therapist
I work with a lot of couples, and have helped them learn to relate with more empathy, effective communication and positive regard. I'll help you to better understand each other, and to manage conflict in a more productive and supportive way. Though we are by nature drawn to be in relationship, there are now well understood reasons—rooted in our neurobiology and our attachment patterns (which I'll explain)—that often make functioning in relationships difficult. In addition to helping you understand the source of these difficulties, I'll guide you in using that knowledge to create a more intimate, enriching and secure partnership, one based on the principle that you are in each other's care.
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Megan Goodwin, Psy.D.
Dr. Goodwin finds working with couples to be very rewarding. She uses an eclectic, research-based approach which focuses on increasing insight and compassion to both the self and the other partner, (re)building friendship, and teaching behaviors that improve communication and connection. She believes in building on couples and individual strengths. Her approach is active, warm, and non-judgmental. Dr. Goodwin also has experience working with couples around sexual issues, an important aspect of many relationships. Dr. Goodwin also enjoys working with LGTBQ couples and individuals.
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Rawna Romero, LMFT
Licensed Marriage Family Therapist
If you are having difficulties as a couple, psychotherapy can help you: (1) Understand one another better (2) Identify more satisfying, fulfilling and compassionate ways of relating (3) Understand the correlation between your early family lives and the ways you view or experience your partnership or marriage (4) Learn to community more from your heart (5) Develop a more collaborative approach to conflicts (6) Acknowledge and draw upon your strengths (7) Become more intimate (8) Cope with life's hardships and challenges IF YOU THINK PSYCHOTHERAPY CAN HELP, PLEASE CALL ME: Rawna Cheri Romero, LMFT 415-533-9724
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Amelia Katkov, MA, MFTI
We don't always have examples of how to have a successful or healthy relationship, and sometimes find ourselves without the tools to navigate challenges within our own relationships. In working with me you can expect to build tools for truly and actively listening to your partner while also learning how to provide your partner with the same support. These tools can be safely mastered in my office, and then taken with you for continued use in your relationship.
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Thank you for visiting our California search of licensed therapists for couples in San Bruno who specialize in helping relationships and marriages heal and overcome division and hurt. Relationships are hard. Unless you are actively working towards coming together, by default you are drifting apart. It takes work. A licensed therapist is an expert at helping to untangle the mess that can develop when things go wrong. Find honest and effective couples Counseling in San Bruno and renew your relationship.
San Bruno is located in San Mateo County, California. It has a land area of 5.46 square miles and a water area of 0.00 square miles.  The population of San Bruno is 43,185 people with 14,899 households and a median annual income of $83,888. .
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Mostly Affordable
Establishing weekly sessions with a professional therapist is considered affordable in San Bruno for the average family. While sustaining a commitment to therapy is usually not an issue, if mental health treatment feels like a burden please ask your counselor about accepted insurance plans or sliding scale fees


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TIAA CREF Investment Management LLC maintained its stake in shares of Home Bancorp, Inc. (NASDAQ:HBCP) during the second quarter, according to the company in its most recent filing with the Securities & Exchange Commission. The fund owned 16,504 shares of the bank's stock at the close of the second quarter. TIAA CREF Investment Management LLC owned approximately 0.22% of Home Bancorp worth $702,000 as of its most recent SEC filing.
A number of other institutional investors and hedge funds also recently made changes to their positions in HBCP. Bank of New York Mellon Corp lifted its holdings in Home Bancorp by 3.2% during the 1st quarter. Bank of New York Mellon Corp now owns 29,101 shares of the bank's stock worth $982,000 after buying an additional 889 shares during the period. American International Group Inc. lifted its stake in shares of Home Bancorp by 6.7% in the 1st quarter. American International Group Inc. now owns 3,527 shares of the bank's stock valued at $119,000 after purchasing an additional 220 shares during the period. Geode Capital Management LLC lifted its stake in shares of Home Bancorp by 5.7% in the 1st quarter. Geode Capital Management LLC now owns 33,284 shares of the bank's stock valued at $1,123,000 after purchasing an additional 1,782 shares during the period. Renaissance Technologies LLC lifted its stake in shares of Home Bancorp by 9.2% in the 1st quarter. Renaissance Technologies LLC now owns 150,100 shares of the bank's stock valued at $5,066,000 after purchasing an additional 12,600 shares during the period. Finally, First Quadrant L P CA acquired a new position in shares of Home Bancorp in the 2nd quarter valued at about $365,000. 42.96% of the stock is currently owned by hedge funds and other institutional investors.
HBCP has been the topic of a number of recent analyst reports. BidaskClub downgraded Home Bancorp from a "buy" rating to a "hold" rating in a research note on Wednesday, July 19th. UBS AG downgraded Home Bancorp from an "outperform" rating to a "market perform" rating in a research note on Wednesday, July 26th. Raymond James Financial, Inc. downgraded Home Bancorp from an "outperform" rating to a "market perform" rating in a research note on Wednesday, July 26th. Zacks Investment Research raised Home Bancorp from a "hold" rating to a "buy" rating and set a $46.00 price objective on the stock in a research note on Thursday, July 27th. Finally, Sandler O'Neill reissued a "hold" rating and issued a $46.00 price objective on shares of Home Bancorp in a research note on Wednesday, October 18th. One research analyst has rated the stock with a sell rating and four have assigned a hold rating to the stock. The company has a consensus rating of "Hold" and an average target price of $47.00.
Home Bancorp, Inc. (NASDAQ HBCP) opened at $40.48 on Wednesday. The stock has a market capitalization of $300.66, a PE ratio of 16.09 and a beta of 0.14. The company has a debt-to-equity ratio of 0.34, a current ratio of 0.99 and a quick ratio of 0.98. Home Bancorp, Inc. has a 52 week low of $32.17 and a 52 week high of $47.20.
Home Bancorp (NASDAQ:HBCP) last issued its earnings results on Tuesday, October 24th. The bank reported $0.59 EPS for the quarter, missing analysts' consensus estimates of $0.63 by ($0.04). Home Bancorp had a net margin of 22.54% and a return on equity of 9.72%. The firm had revenue of $18.25 million during the quarter, compared to the consensus estimate of $18.54 million. sell-side analysts predict that Home Bancorp, Inc. will post 2.56 earnings per share for the current fiscal year.
The company also recently announced a quarterly dividend, which will be paid on Friday, November 17th. Investors of record on Monday, November 6th will be given a $0.14 dividend. This represents a $0.56 dividend on an annualized basis and a yield of 1.38%. The ex-dividend date of this dividend is Friday, November 3rd. Home Bancorp's payout ratio is 22.67%.
In related news, CEO John W. Bordelon sold 15,578 shares of the business's stock in a transaction dated Friday, October 27th. The stock was sold at an average price of $43.59, for a total value of $679,045.02. The sale was disclosed in a document filed with the Securities & Exchange Commission, which is available through this hyperlink. Insiders own 15.50% of the company's stock.
Home Bancorp Profile
Home Bancorp, Inc is a bank holding company for Home Bank, N.A. (the Bank). The Bank conducts business through banking offices in the Greater Lafayette, Baton Rouge, Greater New Orleans and Northshore (of Lake Pontchartrain) regions of south Louisiana and the Natchez and Vicksburg regions of west Mississippi.
Want to see what other hedge funds are holding HBCP? Visit HoldingsChannel.com to get the latest 13F filings and insider trades for Home Bancorp, Inc. (NASDAQ:HBCP).
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