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目的:观察动脉内膜损伤后血管平滑肌细胞(VSMC)表型转化和p38MAPK及丝裂原激活蛋白激酶磷酸酶-1(MKP-1)表达的动态变化。方法:分别用免疫组化、免疫印迹(Westernblot)和逆转录-聚合酶链反应方法检测假损伤组(S组)和损伤组损伤后不同时间点血管壁中增殖细胞核抗原(PCNA)、平滑肌α肌动蛋白(SMα-actin)、p38蛋白和MKP-1mRNA及蛋白表达的变化。结果:①S组中膜VSMC及内皮细胞PCNA为阴性表达;中膜于损伤后1~14d,新生内膜(NI)于5~14d阳性细胞率逐渐增加,28d后开始逐渐减少,NI阳性率高于中膜。②S组中膜SMα-actin表达为阳性,内皮为阴性;中膜阳性表达于损伤后1d开始减少,3d最为明显,5d后开始逐渐增加,NI阳性表达弱于中膜。③S组中膜p38呈阴性或弱阳性;损伤后1~35d呈持续高表达,NI阳性表达强于中膜。p38与PCNA表达变化呈正相关。④S组中膜MKP-1呈弱阳性或阳性表达;损伤后1d即开始下降,14~28d稍有回升,至35d仍未回到S组水平,NI阳性表达稍弱于中膜。MKP-1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,p38MAPK和MKP-1参与了损伤后VSMC表型转化的信号转导及其调节。
Objective: To observe the phenotypic changes of vascular smooth muscle cells (VSMCs) and the expression of p38MAPK and mitogen-activated protein kinase phosphatase-1 (MKP-1) after arterial intimal injury. Methods: The expressions of proliferating cell nuclear antigen (PCNA), smooth muscle α (TGFβ1), interleukin-6 Changes of SMα-actin, p38 protein and MKP-1 mRNA and protein expression. Results: (1) The expression of VSMC and endothelial cell PCNA were negative in group S, while in neointima between 1 and 14 days after injury, the positive rate of neointimal hyperplasia (NI) increased gradually from 5 to 14 days and gradually decreased after 28 days, the positive rate of NI was high In the membrane. ② The expression of SMα-actin was positive in S group and the endothelium was negative. The expression of neutrophil in the middle membrane decreased from 1 day after injury. The most obvious was 3d and gradually increased after 5 days. The positive expression of NI was weaker than that in the middle membrane. (3) In group S, the expression of p38 was negative or weakly positive. The expression of p38 was continuously high from 1 to 35 days after injury, and the positive expression of NI was stronger than that of the media. p38 and PCNA expression was positively correlated. ④ The expression of MKP-1 in S group was weakly positive or positive. The level of MKP-1 began to decline on the 1st day after injury and rose slightly after 14-28 days. The level of MKP-1 in S group was still lower than that of S group at 35 days. MKP-1 and PCNA expression was negatively correlated. CONCLUSION: VSMC proliferative ability is closely related to its phenotypic transformation, and p38MAPK and MKP-1 are involved in signal transduction and regulation of VSMC phenotype after injury.