S1PR2和S1PR3通路激活Rac1参与HGF诱导的血管内皮屏障保护作用  

S1PR2 and S1PR3 pathway contributes to HGF-induced endothelial barrier enhancement by activating Rac1

作　　者：黄海涛 李星[2] 王亮[3] 倪秀芹[3] 

机构地区：[1]大庆市油田总医院普外科 [2]大庆市人民医院肾内科 [3]哈尔滨医科大学大庆校区解剖学教研室,黑龙江大庆163319

出　　处：《解剖科学进展》2015年第4期383-385,共3页Progress of Anatomical Sciences

基　　金：中国博士后基金(No.2013M531067)

摘　　要：目的观察肝细胞生长因子(hepatocyte growth factor,HGF)介导的1-磷酸鞘氨醇受体2(S1PR2)和1-磷酸鞘氨醇受体3(S1PR3)通路是否通过激活Ras相关C3肉毒素底物1(Rac1)增加血管内皮屏障保护功能。方法培养人肺动脉内皮细胞,应用小RNA干扰技术静默S1PR2/3后,给与HGF处理并应用GTP酶沉降及Western blot检测技术检测人肺血管内皮细胞GTP-Rac1活性变化。结果静默S1PR2或S1PR3后,给与HGF处理,GTP-Rac1活性较S1PR2或S1PR3未静默组明显减弱。结论 HGF介导的S1PR2和S1PR3通路通过激活Rac1增加血管内皮屏障保护功能。Objective To observe whether hepatocyte growth factor（HGF） mediated S1PR2 （ sphingosine-1- phosphate receptor 2 ） and S1PR3 （ sphingosine-l-phosphate receptor 3 ） pathways could increase vascular endothelial barrier function by activating Racl （ ras-related C3 botulinum toxin substrate 1 ） . Methods The human pulmonary arterial endothelial cells were cultivated and disposed with HGF（25 ng/ml, 5 min） after S1PR2 or S1PR3 was silenced by mRNA silencing technique. The activity and expression of GTP-Racl were determined by GTP enzyme sedimentation and Western blot respectively. Results Silencing S1PR2 or S1PR3 downregulated sign/ficantly the activity and expression level of HGF-indueed GTP-Rael protein. Conclusion S1PR2 and S1PR3 pathway contributes to HGF-indueed endothelial barrier enhancement by activating Rael.

关 键 词：S1P受体 人肺动脉内皮细胞 RAC1 肝细胞生长因子 

分 类 号：R331.3[医药卫生—人体生理学]