PUBLICATION

The dual role of cGMP in oocyte maturation of zebrafish

Authors
Li, J., Zhou, W., Wang, Y., Niu, C.
ID
ZDB-PUB-180409-2
Date
2018
Source
Biochemical and Biophysical Research Communications   499(4): 998-1003 (Journal)
Registered Authors
Keywords
Luteinizing hormone, Nitric oxide, Oocyte maturation, Ovary, Zebrafish, cGMP
MeSH Terms
  • Animals
  • Cell Differentiation*/drug effects
  • Chorionic Gonadotropin/pharmacology
  • Cyclic GMP/metabolism*
  • Female
  • Luteinizing Hormone/pharmacology
  • Nitric Oxide/metabolism
  • Oocytes/cytology*
  • Oocytes/metabolism*
  • Ovarian Follicle/cytology
  • Signal Transduction/drug effects
  • Soluble Guanylyl Cyclase/metabolism
  • Zebrafish/metabolism*
PubMed
29627575 Full text @ Biochem. Biophys. Res. Commun.
Abstract
The roles of cyclic guanosine monophosphate (cGMP) signaling in oocyte maturation attracts much attention in mammals, but its roles in fish are still largely unknown. Using zebrafish as a model, we demonstrated for the first time in fish that cGMP is involved in oocyte maturation, and its functional model in oocyte maturation is different from that of mammals. The intracellular cGMP could be regulated by nitric oxide (NO), we found that all three NO synthase enzymes and four soluble guanylyl cyclases (sGC) are expressed in the zebrafish ovary. Intriguingly, either the activation or inhibition of the NO/sGC/cGMP pathway in fully grown follicles could lead to oocyte maturation. During oocyte maturation, cGMP levels increased in the follicular cell layer but decreased in oocytes, while NO levels increased in follicular cells but remained constant in oocytes. Based on these findings in zebrafish, we propose a hypothetical model on the dual role of cGMP in oocyte maturation: in follicular cells the LH signal could increase the level of NO and cGMP which induces oocyte maturation, while in the oocyte the decreased cGMP level can also induce oocyte maturation. These findings help us to understand the molecular mechanism of fish oocyte maturation.
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Human Disease / Model
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