安普克
化学
磷酸化
AMP活化蛋白激酶
蛋白激酶A
卵母细胞
二甲双胍
内分泌学
内科学
一磷酸腺苷
腺苷
激酶
细胞生物学
生物
生物化学
医学
胰岛素
胚胎
作者
Sylvie Bilodeau‐Goeseels,Paul L. Panich,John P. Kastelic
出处
期刊:Zygote
[Cambridge University Press]
日期:2010-06-23
卷期号:19 (2): 97-106
被引量:13
标识
DOI:10.1017/s0967199410000195
摘要
Summary The adenosine monophosphate-activated protein kinase (AMPK) activators, 5′-aminoimidazole-4-carboxamide 1-β- d -ribofuranoside (AICAR) and metformin (MET), inhibit resumption of meiosis in bovine cumulus-enclosed oocytes (CEO) and denuded oocytes (DO). The objectives of this study were to: (1) examine the effects of AMPK inhibitors on bovine oocyte meiosis in vitro ; and (2) determine if AICAR or MET activates oocyte and/or cumulus cell AMPK. The AMPK inhibitor compound C (CC; 0.5, 1, 5, and 10 μM) did not reverse the inhibitory effects of AICAR (1 mM) and MET (2 mM) on bovine oocyte meiosis. Additionally, CC (5 and 10 μM) inhibited meiosis ( p < 0.05) in CEO and DO cultured for 7 h. Okadaic acid (1 μM) reversed the inhibitory effect of MET (2 mM) and CC (5 μM; p < 0.05) but not of AICAR (1 mM). Phosphorylation of the alpha subunit of AMPK on Thr172 is required for activation. Based on western blot analysis, AICAR, MET and CC did not affect Thr172 phosphorylation levels in DO and oocytes from complexes ( p > 0.05). In cumulus cells, Thr172 phosphorylation decreased after 3 h of culture ( p < 0.05), regardless of the presence of AMPK modulators in the culture medium. Higher concentrations of AICAR (2 mM) and MET (10 mM) did not affect Thr172 phosphorylation, but phosphorylation on Ser79 of ACC, a substrate of AMPK, was increased in response to MET ( p < 0.05). In conclusion, we inferred that the inhibitory effect of AICAR and MET on bovine oocyte meiosis was probably not mediated through activation of AMPK. Moreover, these compounds probably inhibited meiosis through different pathways.
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