Abstract
Our recent data suggest that hypoxic induced increases in NO biosynthesis result in increases in intracellular free zinc that in turn contribute to vasoconstriction of small, non‐muscularized intra‐acinar arteries (<50 um). In order to understand the cellular changes behind this contractile behavior, we examined actin‐myosin dynamics and focal adhesion changes in isolated rat pulmonary microvascular endothelial cells (RPMVEC) in response to 30 minutes of hypoxia or exogenously applied zinc. Immunocytochemistry and confocal analysis showed that contraction in response to either 2% oxygen or zinc, were accompanied by increases in actin‐myosin interactions; stress fiber formation; and recruitment of focal adhesion proteins to cell‐matrix contacts. Live cell imaging of GFP tagged proteins provided real‐time information about the strengthening and alignment of actin stress fibers while total internal reflection (TIRF) imaging showed recruitment of paxillin, talin and zyxin to focal adhesions. These data suggest that the reorganization of cytoskeletal and focal adhesion proteins in response to hypoxia or zinc may be responsible for the force induction and cell stability necessary to elicit an active contractile response in pulmonary endothelium.Funded by NIH HL 081421 (CMS)
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