乏氧条件下miR-29a通过AMPK调控胰岛β细胞功能的研究

Study on the Function of AMPK Regulation in Pancreatic β Cells under Hypoxic Conditions Via miR-29a

目的:观察乏氧条件下miRNA调节AMPK对胰腺β细胞发挥的作用。方法:经细胞培养及Real-time PCR,观察在乏氧条件下miR-29a通过AMPK调控胰岛β细胞功能的发挥。结果:INS-1细胞,主要表达AMPKα2,其磷酸化AMPK活性在乏氧条件下增加。用Real time PCR检测AMPK的表达,发现乏氧说明在胰腺β细胞,主要表达AMPKα2亚基。乏氧能促进HIF-1α表达,促进AMPK的活化。同时AMPK可能受miR-29a的调节。结论:乏氧条件下胰岛β细胞主要表达为AMPKa2,说明AMPK能促进胰岛β细胞细胞增殖。

To explore the mechanism by which miRNA plays roles in pancreatic β cells through regulating AMPK under hypoxic condition. Method：Under the condition of lack of oxygen miR-29 a by AMPK regulation islet beta cell function were observed by cell culture and Real-time PCR.Result：The INS-1 cell primarily expressed AMPKα2,which the phosphorylation activity of AMPK was increased under hypoxic condition. the expression of AMPK was detected by Real time PCR,which suggested that pancreaticβcells primarily expressed AMPKα2 under hypoxic condition. Hypoxia could accelerate the expression of HIF-1αand the activation of AMPK. Meanwhile,AMPK might be regulated by miR-29a.Conclusion：Under the condition of lack of oxygen islet beta cells mainly expressed as AMPKa2, AMPK can promote cell proliferation islet beta cells.