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Many studies have shown that cyclic adenosine-5'-monophosphate (cAMP)-dependent protein kinase A (PKA) and G-protein-coupled receptor 3 (GPR3) are crucial for controlling meiotic arrest in oocytes. However, it is unclear how gonadotropins modulate these factors to regulate oocyte maturation, especially by gap junctional communication (GJC). Using an in vitro meiosis-arrested mouse cumulus-oocyte complex (COC) culture model, we showed that there is a close relationship between follicle-stimulating hormone (FSH) and the PKA type I (PKAI) and GPR3. The effect of FSH on oocyte maturation was biphasic, initially inhibitory and then stimulatory. During FSH-induced maturation, rapid cAMP surges were observed in both cumulus cells and oocyte. Most GJC between cumulus cells and oocyte ceased immediately after FSH stimulation and recommenced after the cAMP surge. FSH-induced maturation was blocked by PKAI activator 8-AHA-cAMP. Levels of PKAI regulatory subunits and GPR3 decreased and increased, respectively, after FSH stimulation. In the presence of the GJC inhibitor carbenoxolone (CBX), FSH failed to induce the meiotic resumption and the changes in PKAI, GPR3 and cAMP surge in oocyte were no longer detected. Furthermore, GPR3 was upregulated by high cAMP levels, but not by PKAI activation. When applied after FSH stimulation, the specific phosphodiesterase 3A (PDE3A) inhibitor cilostamide immediately blocked meiotic induction, regardless of when it was administered. PKAI activation inhibited mitogen-activated protein kinase (MAPK) phosphorylation in the oocytes of COCs, which participated in the initiation of FSH-induced meiotic maturation in vitro. Just before FSH-induced meiotic maturation, cAMP, PKAI, and GPR3 returned to basal levels, and PDE3A activity and MAPK phosphorylation increased markedly. These experiments show that FSH induces a transient increase in cAMP levels and regulates GJC to control PKAI and GPR3 activities, thereby creating an inhibitory phase. After PDE3A and MAPK activities increase, meiosis resumes.

Titel:	FSH modulates PKAI and GPR3 activities in mouse oocyte of COC in a gap junctional communication (GJC)-dependent manner to initiate meiotic resumption.
Autor/in / Beteiligte Person:	Li, J ; Mao, G ; Xia, G
Link:	Volltext (PDF)
Zeitschrift:	PloS one, Jg. 7 (2012), Heft 9, S. e37835
Veröffentlichung:	San Francisco, CA : Public Library of Science, 2012
Medientyp:	academicJournal
ISSN:	1932-6203 (electronic)
DOI:	10.1371/journal.pone.0037835
Schlagwort:	Animals Cumulus Cells cytology Cumulus Cells drug effects Cyclic AMP analogs & derivatives Cyclic AMP metabolism Cyclic AMP pharmacology Cyclic Nucleotide Phosphodiesterases, Type 3 metabolism Enzyme Activation drug effects Female Mice Mitogen-Activated Protein Kinases metabolism Oocytes cytology Oocytes drug effects Phosphorylation drug effects Signal Transduction drug effects Time Factors Cell Communication drug effects Cumulus Cells metabolism Cyclic AMP-Dependent Protein Kinase Type I metabolism Follicle Stimulating Hormone pharmacology Gap Junctions metabolism Meiosis drug effects Oocytes metabolism Receptors, G-Protein-Coupled metabolism
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article; Research Support, Non-U.S. Gov't Language: English [PLoS One] 2012; Vol. 7 (9), pp. e37835. <i>Date of Electronic Publication: </i>2012 Sep 13. MeSH Terms: Cell Communication / drug effects ; Cumulus Cells / metabolism ; Cyclic AMP-Dependent Protein Kinase Type I / metabolism ; Follicle Stimulating Hormone / pharmacology ; Gap Junctions / metabolism ; Meiosis / drug effects ; Oocytes / metabolism ; Receptors, G-Protein-Coupled / metabolism ; Animals ; Cumulus Cells / cytology ; Cumulus Cells / drug effects ; Cyclic AMP / analogs & derivatives ; Cyclic AMP / metabolism ; Cyclic AMP / pharmacology ; Cyclic Nucleotide Phosphodiesterases, Type 3 / metabolism ; Enzyme Activation / drug effects ; Female ; Mice ; Mitogen-Activated Protein Kinases / metabolism ; Oocytes / cytology ; Oocytes / drug effects ; Phosphorylation / drug effects ; Signal Transduction / drug effects ; Time Factors References: Dev Biol. 2008 Apr 1;316(1):124-34. (PMID: 18280465) ; Endocrinology. 1984 Feb;114(2):418-27. (PMID: 6197295) ; J Cell Sci. 2007 Apr 15;120(Pt 8):1330-40. (PMID: 17389684) ; Mol Cell Endocrinol. 1988 Mar;56(1-2):115-21. (PMID: 2453385) ; Endocrinology. 2011 Nov;152(11):4377-85. (PMID: 21914782) ; Science. 2004 Dec 10;306(5703):1947-50. (PMID: 15591206) ; Mol Cell Biol. 1993 Aug;13(8):4852-9. (PMID: 8336722) ; Dev Biol. 2002 Jun 15;246(2):441-54. (PMID: 12051828) ; Cell Cycle. 2009 Feb 15;8(4):665-70. (PMID: 19223768) ; Dev Biol. 1995 Nov;172(1):72-85. (PMID: 7589815) ; Nat Genet. 2002 Apr;30(4):446-9. (PMID: 11912493) ; Curr Biol. 2000 Oct 19;10(20):1303-6. (PMID: 11069114) ; Dev Biol. 1982 Mar;90(1):144-53. (PMID: 7199496) ; Mol Biol Rep. 2012 May;39(5):5831-9. (PMID: 22207171) ; Proc Natl Acad Sci U S A. 1996 May 14;93(10):4730-5. (PMID: 8643471) ; J Biol Chem. 2002 May 24;277(21):18810-6. (PMID: 11886856) ; Science. 2010 Oct 15;330(6002):366-9. (PMID: 20947764) ; Biol Reprod. 1997 Apr;56(4):976-84. (PMID: 9096881) ; Dev Biol. 2003 Nov 1;263(1):126-38. (PMID: 14568551) ; J Cell Biol. 2005 Oct 24;171(2):255-65. (PMID: 16247026) ; Physiol Rev. 2004 Jan;84(1):137-67. (PMID: 14715913) ; Science. 2002 Aug 23;297(5585):1343-5. (PMID: 12193786) ; Dev Biol. 2002 May 1;245(1):200-12. (PMID: 11969266) ; Hum Reprod. 1988 Aug;3(6):761-6. (PMID: 2464614) ; Mol Endocrinol. 2008 Jul;22(7):1682-94. (PMID: 18467523) ; Mol Cell Biol. 2000 Mar;20(5):1596-603. (PMID: 10669737) ; Mol Reprod Dev. 2008 Jan;75(1):105-14. (PMID: 17549700) ; Dev Biol. 2003 Jun 15;258(2):385-96. (PMID: 12798295) ; Biol Reprod. 2001 Nov;65(5):1444-51. (PMID: 11673261) ; Proc Natl Acad Sci U S A. 2005 Jun 21;102(25):8922-6. (PMID: 15956199) ; J Exp Zool. 1988 Jan;245(1):86-96. (PMID: 2832512) ; Reproduction. 2001 Oct;122(4):619-28. (PMID: 11570969) ; Dev Biol. 1995 Feb;167(2):502-12. (PMID: 7875374) ; J Clin Invest. 2004 Jul;114(2):196-205. (PMID: 15254586) ; Reproduction. 2001 May;121(5):647-53. (PMID: 11427152) ; Proc Natl Acad Sci U S A. 2002 Dec 24;99(26):16794-9. (PMID: 12477927) ; Dev Dyn. 2008 Dec;237(12):3777-86. (PMID: 19035343) ; Dev Biol. 1986 Apr;114(2):453-62. (PMID: 2420661) ; Biol Reprod. 2002 Sep;67(3):981-7. (PMID: 12193411) ; Biochem Biophys Res Commun. 1992 Apr 15;184(1):454-60. (PMID: 1314594) ; Mol Cell. 2003 Apr;11(4):1101-8. (PMID: 12718894) ; Biol Reprod. 1996 Dec;55(6):1315-24. (PMID: 8949889) ; Adv Cyclic Nucleotide Res. 1979;10:69-92. (PMID: 222125) ; Cell Cycle. 2006 Feb;5(3):227-31. (PMID: 16418576) ; Gamete Res. 1989 Jul;23(3):323-34. (PMID: 2476369) ; Dev Dyn. 2006 Nov;235(11):2961-8. (PMID: 16937372) ; Dev Biol. 2005 Dec 15;288(2):397-404. (PMID: 16289135) ; Biol Reprod. 2004 Mar;70(3):548-56. (PMID: 14568915) ; J Biol Chem. 2004 Oct 8;279(41):43321-9. (PMID: 15299023) ; Nat Immunol. 2009 Apr;10(4):420-6. (PMID: 19234474) ; Dev Biol. 2005 Nov 15;287(2):249-61. (PMID: 16229830) ; Dev Biol. 2000 Oct 15;226(2):167-79. (PMID: 11023678) Substance Nomenclature: 0 (GPR3 protein, mouse) ; 0 (Receptors, G-Protein-Coupled) ; 39824-30-1 (8-aminohexylamino cAMP) ; 9002-68-0 (Follicle Stimulating Hormone) ; E0399OZS9N (Cyclic AMP) ; EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinase Type I) ; EC 2.7.11.24 (Mitogen-Activated Protein Kinases) ; EC 3.1.4.17 (Cyclic Nucleotide Phosphodiesterases, Type 3) ; EC 3.1.4.17 (Pde3a protein, mouse) Entry Date(s): Date Created: 20121003 Date Completed: 20130319 Latest Revision: 20211021 Update Code: 20231215 PubMed Central ID: PMC3441574

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FSH modulates PKAI and GPR3 activities in mouse oocyte of COC in a gap junctional communication (GJC)-dependent manner to initiate meiotic resumption.