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Cell Biochem Biophys. 2008;52(3):125-38. doi: 10.1007/s12013-008-9030-7. Epub 2008 Nov 4.

Lung ischemia: a model for endothelial mechanotransduction.

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1
Institute for Environmental Medicine, University of Pennsylvania Medical Center, 1 John Morgan Building, 3620 Hamilton Walk, Philadelphia, PA, 19104-6068, USA.

Abstract

Endothelial cells in vivo are constantly exposed to shear associated with blood flow and altered shear stress elicits cellular responses (mechanotransduction). This review describes the role of shear sensors and signal transducers in these events. The major focus is the response to removal of shear as occurs when blood flow is compromised (i.e., ischemia). Pulmonary ischemia studied with the isolated murine lung or flow adapted pulmonary microvascular endothelial cells in vitro results in endothelial generation of reactive oxygen species (ROS) and NO. The response requires caveolae and is initiated by endothelial cell depolarization via K(ATP) channel closure followed by activation of NADPH oxidase (NOX2) and NO synthase (eNOS), signaling through MAP kinases, and endothelial cell proliferation. These physiological mediators can promote vasodilation and angiogenesis as compensation for decreased tissue perfusion.

PMID:
18982455
PMCID:
PMC2667227
DOI:
10.1007/s12013-008-9030-7
[Indexed for MEDLINE]
Free PMC Article
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