血管紧张素Ⅱ在胚胎干细胞向心肌细胞分化中的作用

为检测血管紧张素Ⅱ（angiotensin Ⅱ，AⅡ）对小鼠胚胎干细胞（embryonic stem cells，ESCs）向心肌细胞方向分化的作用，采用10-4 mol/L维生素C诱导小鼠R1胚胎干细胞分化为心肌细胞. Western印记检测胚胎干细胞诱导分化的心肌细胞中表达血管紧张素Ⅱ1 型受体(angiotensin Ⅱ type 1 receptor,AT1R).诱导分化期间用1 μmol/L AⅡ刺激胚胎干细胞，计数搏动拟胚体的比例；诱导分化第14 d用real-time RT-PCR 和Western 印记检测心肌标志物的表达确定其作用. 结果显示，与对照组相比，1 μmol/L AⅡ处理组可显著增加搏动拟胚体的比例，上调心肌标志物mRNA的表达. 预先用1 μmol/L洛沙坦处理1 h后可显著阻碍这种上调作用. 本实验结果表明,AⅡ通过AT1R可促进小鼠R1胚胎干细胞向心肌细胞分化.

The Effect of Angiotensin Ⅱ on the Cardiac Differentiation in Embryonic Stem Cells

To investigate the effect of angiotensin Ⅱ(AⅡ) on the cardiac differentiation in embryonic stem cells (ESCs), R1 mouse ES cells were induced by 10-4 mol/L vitamin C to differentiate into cardiomyocytes. Western blotting revealed that angiotensin type 1 receptor (AT1R) expressed in cardiomyocytes derived from mouse embryonic stem cells. By administering 1μmol/L AⅡwith or without 1μmol/L Losartan (AT1R antagonist) pretreatment, we demonstrated that AⅡ significantly enhanced cardiac differentiation as determined by increased percentage of beating embryoid bodies and a higher expression level of cardiac markers. On the contrary, AⅡ stimulated differentiation was inhibited by the presence of AT1R antagonist. These findings suggested that AⅡ promoted differentiation of cardiomyo-cytes from embryonic stem cells via AT1R.