Different migration of vascular smooth muscle cells from human coronary artery bypass vessels. Role of Rho/ROCK pathway
Autor: | Sabine, Weiss, Karin, Frischknecht, Helen, Greutert, Sravan, Payeli, Jan, Steffel, Thomas F, Lüscher, Thierry P, Carrel, Felix C, Tanner |
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Rok vydání: | 2006 |
Předmět: |
rho GTP-Binding Proteins
rho-Associated Kinases Receptor Platelet-Derived Growth Factor alpha Myocytes Smooth Muscle Intracellular Signaling Peptides and Proteins Protein Serine-Threonine Kinases Muscle Smooth Vascular Receptor Platelet-Derived Growth Factor beta Cell Movement Stress Fibers Humans Saphenous Vein Coronary Artery Bypass Mammary Arteries Cells Cultured Signal Transduction |
Zdroj: | Journal of vascular research. 44(2) |
ISSN: | 1018-1172 |
Popis: | We examined whether vascular smooth muscle (VSMC) or endothelial cell (EC) migration from internal mammary artery (MA) differed from VSMC or EC migration from saphenous vein (SV).Migration to PDGF-BB (1-10 ng/ml) was lower in VSMC from MA than SV; however, attachment, movement without chemokine, and chemokinesis were identical. Unlike VSMC, migration of EC was similar in response to several mediators. Expression of PDGF receptor-beta was lower in VSMC from MA than SV, while alpha-receptor expression was higher. PDGF-BB-induced RhoA activity was lower in MA than SV, while basal activity was identical. Rosuvastatin and hydroxyfasudil impaired PDGF-BB-induced migration of VSMC from MA and SV. Mevalonate and geranylgeranylpyrophosphate rescued inhibition by rosuvastatin. PDGF-BB induced less stress fiber formation in VSMC from MA than SV. A dominant negative RhoA mutant inhibited stress fiber formation to PDGF-BB, while a constitutively active mutant resulted in maximal stress fiber formation in MA and SV. Rosuvastatin and hydroxyfasudil impaired PDGF-BB-induced stress fiber formation in MA and SV.VSMC migration to PDGF-BB is lower in MA than SV, which is at least in part related to lower activity of the Rho/ROCK pathway. |
Databáze: | OpenAIRE |
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