KNOCKOUT OF CALCIUM-INDEPENDENT PHOSPHOLIPASE A2BETA ATTENUATES ENDOTHELIUM

$7,565P41FY2009RRNIH

Washington University, Saint Louis MO

Investigators

Linked publications & trials

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Abstract

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The mechanisms regulating constriction and relaxation of vascular smooth muscle in healthy and diseased blood vessels are incompletely understood, but the activation of one or more phospholipases leading to the initial release of arachidonic acid and lysophospholipids play prominent roles. To identify the role of specific phospholipases in the constriction of mesenteric arterioles induced by phenylephrine (PE) and endothelium-dependent vasodilation induced by acetylcholine (ACh), we measured changes in the diameter of second- and third-order mesenteric arterioles isolated from mice lacking the [unreadable] isoform of calcium-independent phospholipase A2 (iPLA2[unreadable]-/-) as well as inhibition of iPLA2b in wild-type vessels using mechanism based inhibition.

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