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Glucose-Induced Mesothelial Cell Senescence and Peritoneal Neoangiogenesis and Fibrosis

Correspondence to: A. Jörres, Department of Nephrology and Medical Intensive Care, Charité-Universitätsmedizin Berlin, Campus Virchow-Klinikum, Augustenburger Platz 1, D-13353 Berlin, Germany. achim.joerres@charite.de Recent years have changed our understanding of cellular senescence. It is now clear that cells senesce not only as a result of chronological or replicative ageing, but also in response to environmental stimuli that may put the integrity of DNA in danger (1). In this respect, cellular senescence may be viewed as a stress reaction. The phenomena associated with cellular senescence have been primarily studied in vitro; consequences of cellular senescence in vivo are not yet entirely clear. In normal tissues, senescent cells have been identified only sporadically. Their presence was found to be more abundant in benign and pre-neoplastic lesions but not in malignant tumors. This is consistent with the concept of senescence being a cancer-suppressing mechanism (1,2). On the other hand, however, accumulation of senescent cells with age is thought to compromise normal tissue functions. In this respect, senescent cells have been found at sites of age-related pathology, such as atherosclerosis and osteoarthritis (3,4). Little is known about senescence of mesothelial cells. We have recently detected cells bearing a senescence marker in freshly isolated specimens of normal human omentum (5). Gotloib et al. were the first to report on the presence of senescent mesothelial cells in rodents treated with peritoneal dialysis (PD) solutions (6,7). Peritoneal dialysis fluids may impose considerable stress on mesothelial cells, as visualized by increased expression of heat-shock proteins (8). Given that senescence may occur also in response to stress, we examined the expression of senescence-associated beta-galactosidase (SA-β-Gal) in human peritoneal mesothelial cells (HPMCs) treated with a PD solution. Senescence-associated β-Gal is a fairly specific and commonly used marker of senescence (9,10). We found that exposure of HPMCs to a conventional PD solution resulted in an almost twofold increase in SA-β-Gal activity (Figure 1). It remains to be determined which components of PD fluid were responsible for that effect. The consequences of HPMC senescence remain hypothetical. Senescent phenotype includes several features with potential relevance to clinical PD (Table 1). Importantly, some of these features seem to be exacerbated as a response to high glucose. Increased expression of transforming growth factorbeta (TGF-β) during senescence is particularly interesting since TGF-β has long been implicated in PD-induced peritoneal sclerosis (16–18). Profibrotic activity of TGF-β is due not only to its ability to induce synthesis of extra-