Multiple pathways mediate luteinizing hormone regulation of cGMP signaling in the mouse ovarian follicle.

Autor:	Liu X; College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, People's Republic of China Department of Obstetrics, Gynecology and Reproductive Sciences, Center for Reproductive Sciences, The Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, University of California San Francisco (UCSF) Medical Center, UCSF, San Francisco, California., Xie F; Department of Obstetrics, Gynecology and Reproductive Sciences, Center for Reproductive Sciences, The Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, University of California San Francisco (UCSF) Medical Center, UCSF, San Francisco, California., Zamah AM; Department of Obstetrics, Gynecology and Reproductive Sciences, Center for Reproductive Sciences, The Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, University of California San Francisco (UCSF) Medical Center, UCSF, San Francisco, California., Cao B; College of Animal Science and Technology, Northwest A&F, Yangling, Shaanxi, People's Republic of China caobinyun@126.com., Conti M; Department of Obstetrics, Gynecology and Reproductive Sciences, Center for Reproductive Sciences, The Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, University of California San Francisco (UCSF) Medical Center, UCSF, San Francisco, California contim@obgyn.ucsf.edu.
Jazyk:	angličtina
Zdroj:	Biology of reproduction [Biol Reprod] 2014 Jul; Vol. 91 (1), pp. 9. Date of Electronic Publication: 2014 Apr 16.
DOI:	10.1095/biolreprod.113.116814
Abstrakt:	Luteinizing hormone (LH) regulation of the epidermal growth factor (EGF) network is critical for oocyte maturation and the ovulatory process. Recent studies have indicated that C-type natriuretic peptide (CNP) and its receptor natriuretic peptide receptor B (NPR2) play an important role in the control of meiotic arrest. Here, we investigated the involvement of the EGF network in the LH-dependent regulation of the CNP/NPR2 axis and cGMP accumulation. LH/hCG treatment causes a major decrease in both cGMP and the CNP precursor (natriuretic peptide precursor C [Nppc]) mRNA accumulation in vivo and in vitro. However, the cGMP downregulation precedes the decrease in Nppc mRNA by more than 1 h. Amphiregulin, an EGF-like factor, suppresses Nppc mRNA levels in cultured follicles to the same extent as LH, and this effect is completely prevented by the EGF receptor (EGFR) kinase inhibitor AG1478. However, the LH-dependent suppression of Nppc is insensitive to AG1478. Similarly, Nppc suppression by LH occurs in follicles from EGFR null mice. These findings document that EGFR signaling is sufficient to downregulate CNP, but is not necessary for LH action. When cGMP concentration in the follicle is measured, the short-term, but not long-term, LH effects on cGMP are prevented by AG1478, suggesting that ligand availability may be responsible for the late response. Human CG decreases the CNP-dependent cGMP synthesis in wild-type and EGFR knockdown cumulus-oocyte complexes. These findings demonstrate that redundant pathways are involved in the regulation of cGMP. EGFR-dependent events are involved in the short-term regulation of cGMP, whereas the long-term effects may involve regulation of the CNP. (© 2014 by the Society for the Study of Reproduction, Inc.)
Databáze:	MEDLINE
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