人冠状动脉搭桥血管中血管平滑肌细胞的不同迁移。Rho/ROCK信号通路的作用。
Different migration of vascular smooth muscle cells from human coronary artery bypass vessels. Role of Rho/ROCK pathway.
作者信息
Weiss Sabine, Frischknecht Karin, Greutert Helen, Payeli Sravan, Steffel Jan, Lüscher Thomas F, Carrel Thierry P, Tanner Felix C
机构信息
Cardiovascular Research, Physiology Institute, University of Zurich, Zurich, Switzerland.
出版信息
J Vasc Res. 2007;44(2):149-56. doi: 10.1159/000099141. Epub 2007 Jan 29.
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).
METHODS AND 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.
背景
我们研究了来自乳内动脉（MA）的血管平滑肌细胞（VSMC）或内皮细胞（EC）的迁移是否与来自大隐静脉（SV）的VSMC或EC的迁移不同。
方法与结果
MA来源的VSMC向血小板衍生生长因子-BB（PDGF-BB，1-10 ng/ml）的迁移低于SV来源的VSMC；然而，细胞黏附、无趋化因子时的移动以及化学增活作用是相同的。与VSMC不同，EC对几种介质的迁移反应相似。MA来源的VSMC中血小板衍生生长因子受体-β的表达低于SV来源的VSMC，而α受体的表达则较高。PDGF-BB诱导的RhoA活性在MA中低于SV，而基础活性相同。瑞舒伐他汀和羟基法舒地尔损害了PDGF-BB诱导的MA和SV来源的VSMC迁移。甲羟戊酸和香叶基香叶基焦磷酸可挽救瑞舒伐他汀的抑制作用。PDGF-BB在MA来源的VSMC中诱导形成的应力纤维比SV来源的少。显性负性RhoA突变体抑制了PDGF-BB诱导的应力纤维形成，而组成型活性突变体则导致MA和SV中应力纤维形成最大化。瑞舒伐他汀和羟基法舒地尔损害了PDGF-BB诱导的MA和SV中的应力纤维形成。
结论
MA来源的VSMC向PDGF-BB的迁移低于SV来源的VSMC，这至少部分与Rho/ROCK途径活性较低有关。
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