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Hypoxia-inducible factor 1α modulates adhesion, migration, and FAK phosphorylation in vascular smooth muscle cells by Katina M. Corley; Caroline J. Taylor; Brenda Lilly is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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## Abstract Hypoxia promotes angiogenesis by modulating the transcriptional regulator hypoxia‐inducible factor 1α (HIF‐1α). HIF‐1α is a master regulator of the hypoxic response, and its proangiogenic activities include, but are not limited to, regulation of vascular endothelial growth factor (VEGF). The remodeling of the vasculature during angiogenesis requires an initial destabilization step, which facilitates endothelial sprouting, followed by vessel growth, and restabilization through investment of smooth muscle cells. The complex dynamics of hypoxia‐induced angiogenesis prompted us to investigate what aspects of this multi‐step process are regulated by HIF‐1α. To do so, we analyzed the molecular properties of aortic and coronary artery smooth muscle cells in response to forced expression of HIF‐1α, and by treatment with cobalt chloride, which mimics hypoxia. Our results demonstrate that HIF‐1α causes a marked reduction in the ability of smooth muscle cells to migrate and adhere to extracellular matrices. Analysis of focal adhesion proteins showed no significant difference in expression or localization of vinculin or focal adhesion kinase (FAK). However, investigation of FAK pho

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Author

Katina M. Corley; Caroline J. Taylor; Brenda Lilly

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley (ISSN 0730-2312)

Published

2005

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)