| Tai CJ, Cheng KW, Nathwani PS, Leung PCK |
------>authors3_c=None ------>paper_class1=2 ------>Impact_Factor=None ------>paper_class3=0 ------>paper_class2=0 ------>vol=60 ------>confirm_bywho=tzengcr ------>insert_bywho=chenjtai ------>Jurnal_Rank=None ------>authors4_c=None ------>comm_author= ------>patent_EDate=None ------>authors5_c=None ------>publish_day=None ------>paper_class2Letter=None ------>page2= ------>medlineContent= ------>unit=E0111 ------>insert_date=20021207 ------>iam=1 ------>update_date= ------>author=??? ------>change_event=5 ------>ISSN=None ------>authors_c=None ------>score=273 ------>journal_name=32nd Annual meeting of the Society for the Study of Reproduction. Pullman, Washington ------>paper_name=The role of protein kinase C in regulating ATP-evoked intracellular calcium oscillations in cultured human granulosa-luteal cells ------>confirm_date=20021208 ------>tch_id=090048 ------>pmid=11158045 ------>page1=131 ------>fullAbstract=ATP has been shown to modulate progesterone production in human granulosa-luteal cells (hGLCs) in vitro. After binding to a G protein-coupled P2 purinergic receptor, ATP stimulates phospholipase C. The resultant production of diacylglycerol and inositol triphosphate activates protein kinase C (PKC) and intracellular calcium [Ca(2+)](i) mobilization, respectively. In the present study, we examined the potential cross-talk between the PKC and Ca(2+) pathway in ATP signal transduction. Specifically, the effect of PKC on regulating ATP-evoked [Ca(2+)](i) oscillations were examined in hGLCs. Using microspectrofluorimetry, [Ca(2+)](i) oscillations were detected in Fura-2 loaded hGLCs in primary culture. The amplitudes of the ATP-triggered [Ca(2+)](i) oscillations were reduced in a dose-dependent manner by pretreating the cells with various concentrations (1 nM to 10 microM) of the PKC activator, phorbol-12-myristate-13-acetate (PMA). A 10 microM concentration of PMA completely suppressed 10 microM ATP-induced oscillations. The inhibitory effect occurred even when PMA was given during the plateau phase of ATP evoked [Ca(2+)](i) oscillations, suggesting that extracellular calcium influx was inhibited. The role of PKC was further substantiated by the observation that, in the presence of a PKC inhibitor, bisindolylmaleimide I, ATP-induced [Ca(2+)](i) oscillations were not completely suppressed by PMA. Furthermore, homologous desensitization of ATP-induced calcium oscillations was partially reversed by bisindolylmaleimide I, suggesting that activated PKC may be involved in the mechanism of desensitization. These results demonstrate that PKC negatively regulates the ATP-evoked [Ca(2+)](i) mobilization from both intracellular stores and extracellular influx in hGLCs and further support a modulatory role of ATP and P2 purinoceptor in ovarian steroidogenesis. ------>tmu_sno=None ------>sno=6125 ------>authors2=None ------>authors3=None ------>authors4=None ------>authors5=None ------>authors6=None ------>authors6_c=None ------>authors=Tai CJ, Cheng KW, Nathwani PS, Leung PCK ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c=None ------>publish_area=None ------>updateTitle=Adenosine triphosphate-evoked cytosolic calcium oscillations in human granulosa-luteal cells: role of protein kinase C. ------>language=2 ------>check_flag= ------>submit_date= ------>country=None ------>no=1 ------>patent_SDate=None ------>update_bywho= ------>publish_year=1999 ------>submit_flag= ------>publish_month=None |