Estrogen caused a calcium rise via activation of the G protein-coupled estrogen receptor in SH-SY5Y cells
作者单位：Department of PhysiologyShanghai Jiaotong University School of Medicine
会议名称：《中国生理学会第24届全国会员代表大会暨生理学学术大会》
会议日期：2014年
学科分类：1001[医学-基础医学(可授医学、理学学位)] 10[医学]
基 金：supported by National Natural Science Foundation of China(#31171066)
关 键 词：Estrogen G protein-coupled estrogen receptor intracellular calcium SH-SY5Y cells
摘 要：The G protein-coupled estrogen receptor 1(GPER1,also known as GPR30),is a Gs or Gi/o coupled GPCR and has been reported to bind 17β-estradiol(E2)to mediate the non-genomic estrogenic ***1 has been detected in several brain regions,including the hypothalamus,the brainstem and the spinal ***,the signaling mechanisms of this receptor in neuronal cells are yet to be *** present study was aimed to test the hypothesis that activation of GPER1 might induce a change in intracellular calcium level in SH-SY5Y cells,a human neuroblastoma cell *** presence of GPER1 was confirmed by western blot and immunofluorescence ***,the receptor appeared to be enriched on the Golgi apparatus,rather than the plasma *** then performed calcium imaging and tested the effects of E2 and G-1,a synthetic GPER1 *** E2and G-1 evoked rapid(within seconds)and robust calcium rises in concentration-dependent manners(0.01μM for E2 and 0.1μM for G-1).The effects were blocked by the GPER1 antagonist G-15(3μM).In the absence of extracellular calcium,both E2 and G-1 only gave rise to minimal calcium ***,Cd Cl2(200μM),a non-selective inhibitor of the voltage-gated calcium channels,failed to block the increase of intracellular calcium induced by E2 or *** contrast,thapsigargin(10μM),which supposedly caused store depletion,prevented the calcium response to E2 and *** IP3R inhibitor,2-APB(100μM),also partially blocked the effects of E2 or *** results demonstrate that activation of GPER1 may induce a rapid calcium rise that appears to be dependent on both calcium entry and calcium *** channels mediating the calcium influx remain to be *** rise of intracellular calcium following activation of GPER1 may underlie some of the rapid effects of estrogen in the central nervous system.