PI3K/Akt signaling transduction pathway is involved in rat vascular smooth muscle cell proliferation induced by apelin-13

PI3K/Akt signaling transduction pathway is involved in rat vascular smooth muscle cell proliferation induced by apelin-13
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PI3K/Akt信号转导通路参与apelin-13诱导大鼠血管平滑肌细胞增殖

DOI:
10.1093/abbs/gmq035
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发表时间:
2010-06-01
影响因子:
3.7
通讯作者:
Chen, Linxi
Chen, Linxi
中科院分区:
生物学3区
文献类型:
--
作者:
Liu, Changhui;Su, Tao;Chen, Linxi

文献摘要

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采用贴块法从雄性SD大鼠的胸主动脉分离血管平滑肌细胞(VSMCs),观察apelin-13通过PI3K/Akt信号转导通路诱导的VSMC增殖。免疫印迹法检测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,apelin-13以剂量和时间依赖的方式促进磷酸化PI3K和磷酸化Akt的表达。PI3K抑制剂LY294002显著降低Apelin-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显著抑制Apelin-13刺激的磷酸化Akt、磷酸化ERK1/2和细胞周期蛋白D1的表达。四甲基偶氮唑盐比色试验结果显示,PI3K抑制剂LY294002和Akt抑制剂1701-1可明显抑制Apelin-13诱导的VSMC增殖。Apelin-13通过PI3K/Akt信号转导途径促进VSMC增殖。
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 time-dependent 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.