Apelin-13促大鼠血管平滑肌细胞增殖的PKC-ERK1/2信号通路研究

目的研究G蛋白偶联受体APJ(血管紧张素受体样受体或称血管紧张素受体AT1相关的受体蛋白,putativere-ceptor protein related to the angiotensin receptor AT1)的内源性配体apelin-13通过PKC-ERK1/2-Cyclins信号通路促进大鼠血管平滑肌细胞(vascular smooth muscle cells,VSMCs)增殖的影响。方法培养SD大鼠胸主动脉VSMCs,Western blot检测p-ERK1/2、ERK1/2、细胞周期蛋白CyclinD1和CyclinE的表达,四噻唑蓝比色法观察PKC阻断剂GF109203X对apelin-13促大鼠VSMCs增殖的影响。结果Apelin-13剂量依赖性和时间依赖性地促进大鼠VSMCsp-ERK1/2表达增加,对ERK1/2表达没有明显影响,GF109203X可明显抑制apelin-13诱导的细胞增殖及p-ERK1/2、CyclinD1和CyclinE的表达。结论Apelin-13促进大鼠VSMCs增殖可能与ape-lin-APJ-PKC-ERK1/2-Cyclins信号通路有关。

The research of PKC-ERK1/2 signaling transduction pathway of rat VSMCs proliferation induced by apelin-13

Aim To investigate the effects of cell proliferation induced by apelin-13 via PKC-ERK1/2-Cyclins signaling pathway in rat vascular smooth muscle cells(VSMCs).Further to find new signaling pathway of apelin-APJ.Methods VSMCs were prepared from male Sprague-Dawley rats'thoracic aortas by the primary-explant method.Expression of p-ERK1/2,ERK1/2,CyclinD1 and CyclinE was detected by Western blot.The blockade effects of GF109203X were measured by MTT assay.Results Apelin-13 promoted the concentration-dependent and time-dependent expression of p-ERK1/2 during 2 μmol·L-1 and 4 h.The potent PKC inhibitor GF109203X decreased the expression of p-ERK1/2、CyclinD1 and CyclinE.MTT assay showed that GF109203X significantly inhibited the VSMCs proliferation stimulated by apelin-13.Conclusions The effects of apelin-13 promoted cell proliferation maybe involved in apelin-APJ-PKC-ERK1/2-Cyclins signal cascades in rat VSMCs.