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1 Institute of Molecular and Cellular Biology, School of Life Sciences, National Taiwan University, Taipei 106, Taiwan
2 Institute of Physiology, School of Medicine, National Yang-Ming University, Taipei 112, Taiwan
3 Institute of Biological Chemistry, Academia Sinica, Taipei 115, Taiwan
4 Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, Texas 79430, USA
(Requests for offprints should be addressed to J-J Hwang, Institute of Physiology, School of Medicine, National Yang-Ming University, 155 Linong Street, Section 2, Taipei 112, Taiwan; Email: jiuanh{at}ym.edu.tw)
The present study was designed to explore the role of gap junctions in follicle-stimulating hormone (FSH) and transforming growth factor ß1 (TGFß1)-stimulated steroidogenesis in ovarian granulosa cells of gonadotropin-primed immature rats. There were three specific aims. First, we investigated the effect of FSH and TGFß1 as well as lindane (a general gap junction blocker) on the level of connexin43 (Cx43), the major gap junction constituent in granulosa cells, and on gap junction function. The second aim was to determine the effect of lindane on FSH and TGFß1-stimulated progesterone production and the levels of two critical players, cytochrome P450 side-chain cleavage (P450scc) enzyme and steroidogenic acute regulatory (StAR) protein. The third aim was to further investigate the specific involvement of Cx43 gap junctions in FSH and TGFß1-stimulated steroidogenesis using a Cx43 mimetic peptide blocker. Immunoblotting analysis showed that FSH plus TGFß1 dramatically increased the levels of phosphorylated Cx43 without significantly influencing the level of nonphosphorylated Cx43, and this stimulatory effect was completely suppressed by lindane. Also, immunofluorescence analysis showed that Cx43 immuno-reactivity increased in the FSH plus TGFß1-treated group and predominantly appeared in a punctate pattern at cell–cell contact sites, and lindane reduced such cell periphery immunostaining. Furthermore, TGFß1 enhanced the FSH-induced gap junction intercellular communication and lindane completely suppressed this effect. In addition, lindane suppressed the FSH and TGFß1-stimulated increases in progesterone production and the levels of P450scc enzyme and StAR protein. This study demonstrates a clear temporal association between the Cx43 protein level/gap junction communication and progesterone production in rat ovarian granulosa cells in response to FSH and TGFß1 as well as lindane. Furthermore, a specific Cx43 gap junction blocker suppressed FSH plus TGFß1-stimulated progesterone production. In conclusion, this study suggests that Cx43 gap junctions may play a critical role in FSH plus TGFß1-stimulated progesterone production in rat ovarian granulosa cells.
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