Department of Cardiology, The First Affiliated Hospital, University of South China, Hengyang, China.
Acta Biochim Biophys Sin (Shanghai). 2010 Jun 15;42(6):396-402. doi: 10.1093/abbs/gmq035.
Vascular smooth muscle cells (VSMCs) were prepared from thoracic aortas of male Sprague-Dawley rats by the explant method to observe VSMC proliferation via phosphoinositide 3 kinase (PI3K)/Akt signaling transduction pathway induced by apelin-13. Expression of PI3K, phospho-PI3K, phospho-Akt, ERK1/2, phospho-ERK1/2 and cyclin D1 was detected by western blot analysis. Results showed that apelin-13 promoted the expression of phospho-PI3K and phospho-Akt in dose- and timedependent manner. PI3K inhibitor LY294002 significantly decreased the expression of phospho-PI3K, phospho-Akt, phospho-ERK1/2, and cyclin D1 induced by apelin-13. The Akt inhibitor 1701-1 significantly diminished the expression of phospho-Akt, phospho-ERK1/2, and cyclin D1 stimulated by apelin-13. MTT assay results showed that PI3K inhibitor LY294002 and Akt inhibitor 1701-1 significantly inhibited the VSMC proliferation induced by apelin-13. Apelin-13 promoted VSMC proliferation through PI3K/Akt signaling transduction pathway.
血管平滑肌细胞(VSMCs)采用组织块贴壁法从雄性 Sprague-Dawley 大鼠胸主动脉中分离培养，观察阿肽素-13 通过磷酸肌醇 3 激酶(PI3K)/Akt 信号转导通路诱导的 VSMC 增殖。采用 Western blot 分析检测 PI3K、磷酸化 PI3K、磷酸化 Akt、ERK1/2、磷酸化 ERK1/2 和细胞周期蛋白 D1 的表达。结果表明，阿肽素-13 呈剂量和时间依赖性促进磷酸化 PI3K 和磷酸化 Akt 的表达。PI3K 抑制剂 LY294002 显著降低阿肽素-13 诱导的磷酸化 PI3K、磷酸化 Akt、磷酸化 ERK1/2 和细胞周期蛋白 D1 的表达。Akt 抑制剂 1701-1 显著降低阿肽素-13 诱导的磷酸化 Akt、磷酸化 ERK1/2 和细胞周期蛋白 D1 的表达。MTT 检测结果表明，PI3K 抑制剂 LY294002 和 Akt 抑制剂 1701-1 显著抑制阿肽素-13 诱导的 VSMC 增殖。阿肽素-13 通过 PI3K/Akt 信号转导通路促进 VSMC 增殖。
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