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• W2130791602 startingPage "L1117" @default.
• W2130791602 abstract "The systemic vasculature in and surrounding the lung is proangiogenic, whereas the pulmonary vasculature rarely participates in neovascularization. We studied the effects of the proangiogenic ELR+ CXC chemokine MIP-2 (macrophage inflammatory protein-2) on endothelial cell proliferation and chemotaxis. Mouse aortic, pulmonary arterial, and lung microvascular endothelial cells were isolated and subcultured. Proliferation ([ 3 H]thymidine uptake) and migration (Transwell chemotaxis) were evaluated in each cell type at baseline and upon exposure to MIP-2 (1–100 ng/ml) without and with exposure to hypoxia (24 h)-reoxygenation. Baseline proliferation did not vary among cell types, and all cells showed increased proliferation after MIP-2. Aortic cell chemotaxis increased markedly upon exposure to MIP-2; however, neither pulmonary artery nor lung microvascular endothelial cells responded to this chemokine. Assessment of CXCR 2 , the G protein-coupled receptor through which MIP-2 signals, displayed no baseline difference in mRNA, protein, or cell surface expression among cell types. Exposure to hypoxia increased expression of CXCR 2 of aortic endothelial cells only. Additionally, aortic cells, compared with pulmonary cells, showed significantly greater protein and activity of cathepsin S, a proteolytic enzyme important for cell motility. Thus the combined effects of increased cathepsin S activity, providing increased motility and enhanced CXCR 2 expression after hypoxia, both contribute to the proangiogenic phenotype of systemic arterial endothelial cells." @default.
• W2130791602 created "2016-06-24" @default.
• W2130791602 creator A5010419940 @default.
• W2130791602 creator A5028535687 @default.
• W2130791602 date "2005-06-01" @default.
• W2130791602 modified "2023-09-23" @default.
• W2130791602 title "Difference in proangiogenic potential of systemic and pulmonary endothelium: role of CXCR₂" @default.
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• W2130791602 doi "https://doi.org/10.1152/ajplung.00370.2004" @default.
• W2130791602 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15722378" @default.
• W2130791602 hasPublicationYear "2005" @default.
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