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Follicle-Stimulating Hormone-Induced Gh/Phospholipase C-1 Signaling Mediating a Noncapacitative Ca²⁺ Influx through T-Type Ca²⁺ Channels in Rat Sertoli Cells

Division of Reproduction Medicine (T.-H.L.), Department of Obstetrics and Gynecology, Cathay General Hospital, Taipei, Taiwan 106, Republic of China; Fu Jen Catholic University School of Medicine (T.-H.L.), Taipei, Taiwan, 242, Republic of China; and Graduate Institute of Cell and Molecular Biology (Y.-F.L., F.-C.W., Y.-H.T.), Graduate Institute of Medical Sciences, Taipei Medical University, (Y.-F.L., F.-C.W., Y.-H.T.), Center for Reproduction Medicine & Sciences, Taipei Medical University Hospital (Y.-H.T.), Taipei, Taiwan 110, Republic of China

Address all correspondence and requests for reprints to: Yuan-Feng Lin or Yu-Hui Tsai, Ph.D., Graduate Institute of Medical Sciences, Taipei Medical University, 250, Wu-Hsing Street, Taipei, Taiwan 110, Republic of China. E-mail: cmbyht18{at}tmu.edu.tw.

Our previous study demonstrated that FSH-induced immediate Ca²⁺ influx in rat Sertoli cells (SCs) is mediated by the Gh/phospholipase C-1 (PLC-1) signaling pathway. As to which Ca²⁺ channel is responsible for such Ca²⁺ influx was not understood. In this study, thapsigargin triggered an in-store calcium release and evoked a 1.5-fold elevation of intracellular Ca²⁺ in Ca²⁺-free media, whereas FSH exhibited no effect. The readdition of CaCl₂ (2.5 mM) to FSH-pretreated or thapsigargin-sensitized SCs in Ca²⁺-free media immediately elicited a rapid Ca²⁺ influx or a 2-fold increase of second intracellular Ca²⁺ elevation, respectively. The addition of Ca²⁺ chelator EGTA (0.2 mM) reduced the FSH-induced elevation of intracellular Ca²⁺ in SCs incubated with CaCl₂. However, pretreatment with dantrolene (25 µM), which inhibits in-store calcium release, did not affect the FSH-induced elevation of intracellular Ca²⁺. NiCl₂ (10 µM), a T-type calcium channel blocker, abolished the FSH-induced SC Ca²⁺ influx. Furthermore, mibefradil (10 and 100 µM), another specific blocker for T-type Ca²⁺ channels, dose-dependently suppressed the FSH-induced Ca²⁺ influx. In contrast, nifedipine (10 and 50 µM) or -conotoxin GVIA (100 and 500 nM), blocker of L- or N-type Ca²⁺ channels, respectively, did not affect the FSH-induced SC Ca²⁺ influx. On the other hand, FSH-induced Ca²⁺ influx was significantly reduced by pretreatment of SCs with myristoylated synthetic peptide (0.1 and 1 µM) of PLC-1 fragment TIPWNSLKQGYRHVHLL but not affected by 2',5'-dideoxyadenosine (3 and 15 µM), a selective inhibitor of adenylate cyclase. In conclusion, the FSH-induced Gh/PLC-1 pathway-dependent Ca²⁺ influx of rat SCs is mediated by T-type Ca²⁺ channels and independent of in-store calcium release.