Involvement of 17 beta estradiol and its membrane bound g protein coupled estrogen receptor gper in the regulation of oocyte maturation in a common carp cyprinus carpio

Abstract

The development and maturation of oocyte in fish is accomplished by complex and coordinated actions of gonadotropins ovary-derived growth factors, and sex steroids in concert to ensure the ovulation and spawning the huge number of viable oocyte form ovary. It is now well established that steroid hormone mainly estrogen (17and#946;-estradiol; E2) and progestins namely 17and#945;, 20and#946;-dihydroxy-4-pregnen-3-one (17,20and#946;-P), or 17and#945;, 20and#946;,21-trihydroxy-4-pregnen-3-one (20and#946;-S) are involved in oocyte growth and resumption of meiosis respectively. During oocyte growth fish ovarian follicle produce large amount of E2 to support the synthesis of yolk protein vitellogenin by the liver. Vitellogenin from plasma sequestered into growing oocyte, and during this period oocytes are arrested in the first meiotic prophase by high intracellular cAMP. cAMP levels decline when synthesis of maturation inducingsteroid (MIS) from the granulose cells of ovarian follicles increased during preovulatory period by the induction of luteinizing hormone (LH). MIS via non-genomic action by involving a membrane progestin receptor induces final oocyte maturation. It has long been unknown how the growing oocytes at first meiotic prophase get arrested. Over thirty years ago it was shown that estrogen can inhibit hormone induced oocyte maturation in salmonid, but until 2008, there was no convincing reports of follow up studies to further explore this finding. In the year 2008, Pang and his group first advocated that estrogen is involved in maintaining oocyte meiotic arrest in Atlantic croaker via membrane estrogen receptor, G protein-coupled membrane estrogen receptor (GPER) previously known as GPR30. newline