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目的研究组蛋白乙酰化修饰对血管平滑肌细胞(VSMC)增殖及表型转换的影响。方法原代培养自发性高血压大鼠(SHR)VSMCs。免疫印迹检测胰岛素、PD98059、丁酸钠对VSMCs组蛋白去乙酰化酶1(HDAC1)、丝裂原活化蛋白激酶(MAPK)、组蛋白乙酰化、血小板衍生生长因子(PDGF)和α平滑肌肌动蛋白(-αSM actin)的影响。RT-PCR检测其对MAPK、PDGF和-αSM actin基因转录的作用。结果(1)胰岛素促进HDAC1的表达,丁酸钠明显抑制HDAC1的表达,PD98059对HDAC1的表达无明显影响;(2)免疫印迹显示胰岛素促进组蛋白H3乙酰化,而PD98059抑制胰岛素的这种作用;(3)胰岛素上调PDGF的表达,同时下调-αSM actin的表达。该作用可被PD98059和丁酸钠阻断。结论组蛋白乙酰化的改变参与了胰岛素介导SHR VSMCs增殖的过程,且这种过程通过MAPK信号传导途径。
Objective To investigate the effect of histone acetylation on the proliferation and phenotype change of vascular smooth muscle cells (VSMCs). Methods Primary cultured spontaneously hypertensive rats (SHR) VSMCs. Immunoblotting was used to detect the effects of insulin, PD98059 and sodium butyrate on HDAC1, MAPK, histone acetylation, platelet-derived growth factor (PDGF) and α-smooth muscle actin in VSMCs Protein (-αSM actin). RT-PCR detection of MAPK, PDGF and-αSM actin gene transcription. Results (1) Insulin promoted the expression of HDAC1, sodium butyrate significantly inhibited the expression of HDAC1, PD98059 had no significant effect on the expression of HDAC1; (2) Immunoblotting showed that insulin promoted histone H3 acetylation, while PD98059 inhibited this effect of insulin ; (3) Insulin up-regulated the expression of PDGF and down-regulated the expression of αSM actin. This effect can be blocked by PD98059 and sodium butyrate. Conclusion The change of histone acetylation is involved in the process of insulin-mediated proliferation of SHR VSMCs, and this process is through the MAPK signaling pathway.