title: Different migration of vascular smooth muscle cells from human coronary artery bypass vessels. Role of Rho/ROCK pathway.
abstract: BACKGROUND
  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).
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Cardiovascular Research, Physiology Institute, University of Zurich, Zurich, Switzerland.
authors.forename: Sabine
authors.initials: S
authors.lastname: Weiss
authors.forename: Karin
authors.initials: K
authors.lastname: Frischknecht
authors.forename: Helen
authors.initials: H
authors.lastname: Greutert
authors.forename: Sravan
authors.initials: S
authors.lastname: Payeli
authors.forename: Jan
authors.initials: J
authors.lastname: Steffel
authors.forename: Thomas F
authors.initials: TF
authors.lastname: Lüscher
authors.forename: Thierry P
authors.initials: TP
authors.lastname: Carrel
authors.forename: Felix C
authors.initials: FC
authors.lastname: Tanner
mesh_terms: D002465:Cell Movement / Q000502:physiology*; D002478:Cells, Cultured; D001026:Coronary Artery Bypass; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins / Q000378:metabolism; D008323:Mammary Arteries / Q000166:cytology* / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000166:cytology* / Q000378:metabolism; D032389:Myocytes, Smooth Muscle / Q000166:cytology* / Q000378:metabolism; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism; D020796:Receptor, Platelet-Derived Growth Factor alpha / Q000378:metabolism; D020797:Receptor, Platelet-Derived Growth Factor beta / Q000378:metabolism; D012501:Saphenous Vein / Q000166:cytology* / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology; D022502:Stress Fibers / Q000502:physiology; D020741:rho GTP-Binding Proteins / Q000378:metabolism; D054460:rho-Associated Kinases
chemical_list: D047908:Intracellular Signaling Peptides and Proteins; D020796:Receptor, Platelet-Derived Growth Factor alpha; D020797:Receptor, Platelet-Derived Growth Factor beta; D017346:Protein Serine-Threonine Kinases; D054460:rho-Associated Kinases; D020741:rho GTP-Binding Proteins