Journal
JOURNAL OF LIPID RESEARCH
Volume 50, Issue 11, Pages 2164-2172Publisher
ELSEVIER
DOI: 10.1194/jlr.M800533-JLR200
Keywords
RNA interference; meiotic resumption; oocyte
Categories
Funding
- National Natural Science Foundation [30701021]
- China Postdoctoral Science Foundation [20070410099]
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Meiosis activating sterol, produced directly by lanosterol 14-alpha-demethylase (CYP51) during cholesterol biosynthesis, has been shown to promote the initiation of oocyte meiosis. However, the physiological significance of CYP51 action on oocyte meiosis in response to gonadotrophins' induction remained to be further explored. Herein, we analyzed the role of CYP51 in gonadotrophin-induced in vitro oocyte maturation via RNA interference (RNAi). We showed that although both luteinizing hormone (LH) and follicle-stimulating hormone (FSH) significantly induced meiotic resumption in follicle-enclosed oocytes (FEOs), the effect of LH on oocyte meiosis resumption in FEOs was weaker than FSH. Moreover, both FSH and LH were able to upregulate CYP51 expression in cultured follicular granulosa cells when examined at 8 h or 12 h posttreatments, respectively. Interestingly, whereas knockdown of CYP51 expression via small interference RNA (siRNA) moderately blocked (23% reduction at 24 h) FSH-induced oocyte maturation [43% germinal vesicle breakdown (GVBD) rate in RNAi vs. 66% in control, P < 0.05] in FEOs, similar treatments showed no apparent effects on LH-induced FEO meiotic maturation (58% GVBD rate in RNAi vs. 63% in control, P > 0.05). Moreover, the results in a cumulus-enclosed oocytes (CEOs) model showed that approximately 30% of FSH-induced CEOs' meiotic resumption was blocked upon CYP51 knockdown by siRNAs. These findings suggest that FSH, partially at least, employs CYP51, and therefore the MAS pathway, to initiate oocyte meiosis.-Wang, C., B. Xu, B. Zhou, C. Zhang, J. Yang, H. Ouyang, G. Ning, M. Zhang, J. Shen, and G. Xia. Reducing CYP51 inhibits follicle-stimulating hormone-induced resumption of mouse oocyte meiosis in vitro. J. Lipid Res. 2009. 50: 2164-2172.
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