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 Vol 6: RGS5 promotes arterial growth during arteriogenesis.

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This article is from EMBO Molecular Medicine, volume 6.AbstractArteriogenesis—the growth of collateral arterioles—partially compensates for the progressive occlusion of large conductance arteries as it may occur as a consequence of coronary, cerebral or peripheral artery disease. Despite being clinically highly relevant, mechanisms driving this process remain elusive. In this context, our study revealed that abundance of regulator of G-protein signalling 5 RGS5 is increased in vascular smooth muscle cells SMCs of remodelling collateral arterioles. RGS5 terminates G-protein-coupled signalling cascades which control contractile responses of SMCs. Consequently, overexpression of RGS5 blunted Gαq-11-mediated mobilization of intracellular calcium, thereby facilitating Gα12-13-mediated RhoA signalling which is crucial for arteriogenesis. Knockdown of RGS5 evoked opposite effects and thus strongly impaired collateral growth as evidenced by a blockade of RhoA activation, SMC proliferation and the inability of these cells to acquire an activated phenotype in RGS5-deficient mice after the onset of arteriogenesis. Collectively, these findings establish RGS5 as a novel determinant of arteriogenesis which shifts G-protein signalling from Gαq-11-mediated calcium-dependent contraction towards Gα12-13-mediated Rho kinase-dependent SMC activation.Subject Categories Vascular Biology & Angiogenesis

Autor: Arnold, Caroline; Feldner, Anja; Pfisterer, Larissa; Hodebeck, Maren; Troidl, Kerstin; Genove, Guillem; Wieland, Thomas; Hecker, Markus; Korff, Thomas

Fuente: https://archive.org/

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