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AvB3 integrin and airway angiogenesis

AvB3 integrin mediates adhesion and migration of many cell types and is highly expressed on activated and proliferating endothelial cells. Importantly, it has been shown to be an early maker of tumor angiogenesis. We questioned whether this glycoprotein is expressed in bronchial vessels, the site of neovascularization after chronic pulmonary ischemia. Additionally, we asked whether CINC‐3, a CXC chemokine growth factor important in this model (Sukkar, 2008), stimulates AvB3 expression in systemic endothelial cells. After left pulmonary artery ligation (LPAL) in rats, we measured the early time course (0–24h) of CINC‐3 protein (ELISA) in bronchoalveolar lavage fluid (BAL). We found a 8.7‐fold increase 6h after LPAL only in the left lung (not in sham operated rats; n=6). Using a labeled antibody, we targeted AvB3 by in situ perfusion of bronchial arteries. Examination of left airway after tissue degradation and by microscopy showed increased levels of AvB3 by 24h, which persisted for 3 days, compared to controls. To determine whether CINC‐3 induced AvB3 directly, we performed an in vitro study on rat systemic endothelial cells exposed to increasing concentrations of CINC‐3. CINC‐3 (100ng/ml) demonstrated a 2.3‐fold increase in AvB3 expression at 6h (flow cytometry). We speculate that AvB3 is an early marker of systemic neovascularization in this rat model of chronic pulmonary ischemia.