PRKAR2B Expression at Different Times After HCG-Induced Ovulation in NMRI Mice
Publish place: 20th congress on reproductive biomedicine and 15th congress on stem cell biology & technology
Publish Year: 1398
نوع سند: مقاله کنفرانسی
زبان: English
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شناسه ملی سند علمی:
RROYAN20_281
تاریخ نمایه سازی: 29 مهر 1398
Abstract:
Background: Oocyte maturation and resumption of meiotic oc-cur by induction of hCG (Human chorionic gonadotropin) that hormone functions instead of the LH (Luteinizing Hormone). Diminishing The cAMP (Cyclic Adenosine Monophosphate) level will control the phosphorylation/dephosphorylation of cAMP-PKA effective for the activation of MPF (Matura-tion Promoting Factor) and the activation of MPF causes re-sumption of meiotic in immature oocytes. So the mechanisms cAMP-PKA regulate the meiotic status of oocytes. PRKAR2B (cAMP-dependent type 2 regulatory subunit beta) is expressed in ovarian follicles as well as other tissues such as white and brown adipose and brain. This gene produces PRKAR2B, one of the PKA members. Since hCG plays an important role in ovulation induction and according to the possible role of PRKAR2B gene in ovulation, the effect of hCG injection on the expression of PRKAR2B gene in MII oocytes was investigated. The real function of in the resumption of meiotic is unclear still. Materials and Methods: In this study, female mice were ran-domly assigned to four treatment and control groups. In each group, all mice were under ovarian stimulation by 10 IU PMSG (Pregnant Mare s Serum Gonadotropin). After 48 hours, they were inducted by hCG 10 IU due to ovulation. Mice were sac-rificed by spinal dislocation at the hours 16, 20, 24 and 28 for the released oocytes and gene expression of PRKAR2B after ovulation induction.Results: The lower number of MII oocytes at hour 28 in com-parison with those of other hours and PRKAR2B expression in the hour 24 group was significantly higher than those of other groups were seen while the expression was significantly lowest at hour 28.Conclusion: We could conclude this relation between PRKAR2B and the rate of cell proliferation. In respect to the re-sults of this study seems that the lower expression of PRKAR2B will result in the less yielded MII oocytes.
Authors
ar anvari
Department of Anatomical Sciences, Medical Cellular and Molecular Research Center, Gorgan, Iran