视黄酸诱导H9c2细胞p38 MAPK转位的研究

目的了解H9c2心肌细胞中p38MAPK的分布及其在全反式视黄酸(atRA)诱导下的转位。方法对H9c2细胞进行饥饿加药,应用激光扫描共聚焦显微镜对细胞内的p38进行定位扫描。通过对p38荧光强度的核浆比进行分析,得出atRA与SB202190对H9c2细胞内p38核转位的影响。结果在未受刺激细胞内,p38较多分布在胞浆;经atRA分别刺激细胞5min,30min后,胞浆中p38的荧光强度均变弱,核浆比显示实验组与对照组间有显著性差异。SB202190能明显抑制atRA诱导的p38核转位(P<0.01),并且,由SB202190抑制组与对照组的p38核浆比能看出,SB202190降低了26.1%的p38核转位。结论atRA能诱导心肌细胞中p38的核转位,p38信号转导通路可能参与心脏的发育调控。

Translocation of p38 MAPK induced by retinoic acid in H9c2 cells

OBJECTIVE: To study the distribution of p38 MAPK and translocation of p38 induced by all-trans retinoic acid (atRA) in cardiomyocytes. METHODS: H9c2 cells were cultured in the normal growth medium containing 10% fetal bovine serum. Cells were serum-starved overnight followed by atRA (0.05 micromol/L) treatment or SB202190 (10 micromol/L) pretreatment. The localization of p38 under different conditions was detected by Confocal Laser Scanning Microscopy. Then the ratio of p38 localized in nuclei to cytoplasm was analyzed by a Leica Microsystem. Thus, the statistical analysis of these data showed the effects of atRA or SB202 190 on p38 translocation. RESULTS: p38 was located more in the cytoplasm without stimulation, while in the cells with atRA treatment for 5 min and 30 min, p38 labeled with green fluorescence in the cytoplasm decreased. The p38 ratio of nuclei to cytoplasm showed that there was a significant difference between atRA groups and control. As the specific inhibitor of p38, SB202190 could obviously inhibited the nuclear translocation of p38 induced by atRA (P < 0.01). And compared with control, SB202190 could make the nuclear translocation of p38 decrease by 26.1%. CONCLUSION: atRA could induce the nuclear translocation of p38 in cardiomyocytes. And p38 pathway might participate in the regulation of heart development.