| Lai TH |
------>authors3_c=??? ------>paper_class1=1 ------>Impact_Factor=5.236 ------>paper_class3=2 ------>paper_class2=1 ------>vol= ------>confirm_bywho=wslee ------>insert_bywho=cmbyht18 ------>Jurnal_Rank=14.0 ------>authors4_c=??? ------>comm_author=1 ------>patent_EDate=None ------>authors5_c= ------>publish_day=1 ------>paper_class2Letter=None ------>page2= ------>medlineContent= ------>unit=E1300 ------>insert_date=20071220 ------>iam=4 ------>update_date=None ------>author=??? ------>change_event=6 ------>ISSN= ------>authors_c=??? ------>score=-1000 ------>journal_name=Endocrinology (in press) ------>paper_name=Follicle-Stimulating Hormone-Induced Galphah/Phospholipase C-delta1 Signaling Mediating a Noncapacitative Ca2 Influx through T-Type Ca2Channels in Rat Sertoli Cells ------>confirm_date=20091118 ------>tch_id=083002 ------>pmid=18063675 ------>page1= ------>fullAbstract=Our previous study demonstrated that FSH-induced immediate Ca(2+) influx in rat Sertoli cells (SCs) is mediated by the Galphah/phospholipase C-delta1 (PLC-delta1) signaling pathway. As to which Ca(2+) channel is responsible for such Ca(2+) influx was not understood. In this study, thapsigargin triggered an in-store calcium release and evoked a 1.5-fold elevation of intracellular Ca(2+) in Ca(2+)-free media, whereas FSH exhibited no effect. The readdition of CaCl(2) (2.5 mm) to FSH-pretreated or thapsigargin-sensitized SCs in Ca(2+)-free media immediately elicited a rapid Ca(2+) influx or a 2-fold increase of second intracellular Ca(2+) elevation, respectively. The addition of Ca(2+) chelator EGTA (0.2 mm) reduced the FSH-induced elevation of intracellular Ca(2+) in SCs incubated with CaCl(2). However, pretreatment with dantrolene (25 microM), which inhibits in-store calcium release, did not affect the FSH-induced elevation of intracellular Ca(2+). NiCl(2) (10 microM), a T-type calcium channel blocker, abolished the FSH-induced SC Ca(2+) influx. Furthermore, mibefradil (10 and 100 microm), another specific blocker for T-type Ca(2+) channels, dose-dependently suppressed the FSH-induced Ca(2+) influx. In contrast, nifedipine (10 and 50 microm) or omega-conotoxin GVIA (100 and 500 nm), blocker of L- or N-type Ca(2+) channels, respectively, did not affect the FSH-induced SC Ca(2+) influx. On the other hand, FSH-induced Ca(2+) influx was significantly reduced by pretreatment of SCs with myristoylated synthetic peptide (0.1 and 1 microm) of PLC-delta1 fragment TIPWNSLKQGYRHVHLL but not affected by 2~,5~-dideoxyadenosine (3 and 15 microm), a selective inhibitor of adenylate cyclase. In conclusion, the FSH-induced Galphah/PLC-delta1 pathway-dependent Ca(2+) influx of rat SCs is mediated by T-type Ca(2+) channels and independent of in-store calcium release. ------>tmu_sno=None ------>sno=16563 ------>authors2=Lin YF ------>authors3=Wu FC ------>authors4=Tsai YH ------>authors5= ------>authors6= ------>authors6_c= ------>authors=Lai TH ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c=??? ------>publish_area=0 ------>updateTitle=Follicle-stimulating hormone-induced Galphah/phospholipase C-delta1 signaling mediating a noncapacitative Ca2+ influx through T-type Ca2+ channels in rat sertoli cells. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2007 ------>submit_flag=None ------>publish_month=12 |