YIA 4 Wnt5a signalling promotes VSMC survival via WISP-1: consequences for VSMC viability in atherosclerotic plaques

CEJ Mill, JY Jeremy, SJ George

Research output: Contribution to journalArticle (Academic Journal)peer-review

Abstract

Apoptosis of vascular smooth muscle cells (VSMCs) within the fibrous cap of atherosclerotic plaques causes cap thinning and thereby plaque rupture and myocardial infarction. Identification of novel mechanisms that regulate VSMC survival may be useful for designing treatments to increase plaque stability. In this study we show that Wnt5a, a member of the Wnt family, induces β-catenin signalling in mouse primary VSMCs and retards oxidative stress (H(2)O(2))-induced VSMC apoptosis. Therefore we aimed to determine the mechanism underlying Wnt5a-induced VSMC survival. We observed that Wnt5a modulates the mRNA expression of the Wnt/β-catenin responsive gene Wnt1 inducible secreted protein (WISP)-1 (4.17±1.5 fold (n=8, p
Translated title of the contributionYIA 4 Wnt5a signalling promotes VSMC survival via WISP-1: consequences for VSMC viability in atherosclerotic plaques
Original languageEnglish
Pages (from-to)e7 - e7
Number of pages1
JournalHeart
Volume97(20)
DOIs
Publication statusPublished - Oct 2011

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