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Title:: Phenotypic modulation of vascular smooth muscle cells and change of mitogenactivated protein kinase phosphatase1(MKP1) after intimal injury

作者:: 张新平¹; 庞月华²; 冯义伯¹; 谷翔¹; 黎明¹ ; 付作林¹; 史春志¹; 1.华中科技大学同济医学院附属协和医院心内科, 湖北武汉 430022; 2.乌鲁木齐市友谊医院, 新疆乌鲁木齐 830049

Author(s):: ZHANG Xinping; PANG Yuehua; FENG Yibai; GU Xiang; LI Ming; FU Zuolin; SHI Chunzhi; 1. Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, China; 2. Friendship Hospital of Urumchi, Urumchi, Xinjiang 830049, China

关键词:: 内膜损伤; 血管平滑肌细胞; 表型转化; 丝裂原激活蛋白激酶磷酸酶1

Keywords:: intimal injury; vascular smooth muscle cells; phenotypic modulation; MKP1

分类号:: R543.5

DOI:: -

文献标识码:: A

摘要:: 目的观察动脉内膜损伤后血管平滑肌细胞(vascular smooth muscle cells,VSMC)表型转化和丝裂原激活蛋白激酶磷酸酶-1(mitogenactivated protein kinase phosphatase1,MKP1)表达的动态变化。方法分别用HE染色、免疫组化和逆转录聚合酶链(RTPCR)方法检测假损伤组(S组)和损伤后不同时间点血管形态学改变及血管壁中增殖细胞核抗原(PCNA)、平滑肌α肌动蛋白(SMαactin)和MKP1 mRNA及蛋白表达的变化。结果 ①损伤后1 d中膜腔侧、3 d管腔内表面可见增殖的VSMC,5~7 d新生内膜(neointima, NI)形成并逐渐增厚,14~35 d NI进行性增厚;各组中膜均有增殖的VSMC向腔面集聚。②S组中膜VSMC及内皮细胞PCNA为阴性;中膜于损伤后1~14 d, NI于5~14 d PCNA阳性细胞率逐渐增多,14 d达高峰,28 d后开始逐渐减少,但NI阳性率多于中膜。③S组中膜SMαactin表达为阳性,内皮为阴性;中膜阳性面积于损伤后1 d开始减少,3 d最为明显,5 d后开始逐渐增加,NI阳性表达弱于中膜。④S组中膜MKP1呈弱阳性或阳性表达,损伤后1d即开始下降,5~7 d达最低, 14 d 稍有回升,至35 d仍未回到假损伤组水平; NI阳性表达弱于中膜。MKP1表达变化与PCNA表达变化呈负相关。结论 VSMC增殖能力与其表型转化密切相关, MKP1参与了损伤后VSMC表型转化的调节。

Abstract:: AIM To explore phenotypic modulation of vascular smooth muscle cells (VSMC) and change of MKP1 expression after intimal injury of rabbit carotid arteries. METHODS The model of vascular restenosis established by balloon injury of rabbit carotid arteries was used. HE staining, immunohistochemistry and reverse transcriptasepolymerase chain reaction (RTPCR) were used to detect the change of proliferation cell nuclear antigen (PCNA),smooth muscle αactin (SMαactin), MKP1 mRNA and protein expression, and morphology of shaminjured group and injury groups at different time. RESULTS The proliferation of VSMC was observed on the side of the medium lumen at 1 d and on the surface of vascular lumen at 3 d after injury. The neointima was formed and gradually getting thickening at 5-7 d, and thickening was more obvious and rapid at 14-35 d. The expression of PCNA was negative in the medium and endothelium in shaminjured group. Positive cell rate of PCNA was gradually increased at 1-14 d in the medium and at 5-14 d in the neointima, reaching maximum at 14 d and declining gradually at 28 d. Positive cell rate of PCNA in the neointima was higher than that in the medium. Expression of SMαactin was positive in the medium, negative in the endothelium in shaminjured group. Positive cell area of SMαactin began to decrease at 1 d in the medium, getting to the minimum at 3 d and started to increase at 5 d. Expression of SMαactin in the neointima was lower than in the medium. Expression of MKP1 was feeble positive or positive in shaminjured group. Expression of MKP1 initially decreased at 1 d, reaching lowest value at 5-7 d, increased gradually from 14 d. MKP1 was negatively correlated with PCNA in the vascular wall after injury. CONCLUSION There is a close relationship between phenotypic modulation and proliferation ability of VSMC. MKP1 participates in regulation of phenotypic modulation of VSMC after intimal injury.

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动脉内膜损伤后血管平滑肌细胞表型转化及MKP1表达的变化(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

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