Yang Lei, Wei Qiang, Li Wei, Xi Qihui, Zhao Xiaoe, Ma Baohua
Key Laboratory of Animal Biotechnology of the Ministry of Agriculture, Northwest A&F University, Yangling, Shaanxi, 712100, China.
College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, 712100, People's Republic of China.
J Ovarian Res. 2016 Feb 16;9:6. doi: 10.1186/s13048-016-0218-y.
Previous studies have reported that follicle-stimulating hormone (FSH) is often added to culture media to induce oocyte meiotic resumption and maturation and to improve subsequent embryonic development during in vitro maturation (IVM). However, the underlying mechanisms remain unclear.
Cumulus-oocyte complexes (COCs) were collected from ovaries 46-48 h after the female mice were intraperitoneally injected with 8 IU equine chorionic gonadotropin (eCG) and then the COCs were cultured in different medium. qRT-PCR analysis was used to assess mRNA expression of EGF-like factors and natriuretic peptide receptor 2 (NPR2). Western Blot analysis was used to assess phosphorylation of mitogen-activated protein kinase 3/1 (MAPK3/1). The oocytes were morphologically assessed for meiotic resumption.
FSH stimulated the expression of EGF-like factors, the activation of MAPK3/1, a decrease in NPR2 mRNA and oocyte meiotic resumption. Moreover, the FSH-induced decrease in NPR2 and oocyte meiotic resumption occurred via the MAPK3/1 singling pathway, which was activated by the epidermal growth factor receptor (EGFR) pathway.
NPR2 is involved in FSH-mediated oocyte meiotic resumption, and this process is associated with the EGFR and MAPK3/1 signaling pathways.
先前的研究报道,在体外成熟(IVM)过程中,常常在培养基中添加促卵泡激素(FSH)以诱导卵母细胞减数分裂恢复和成熟,并改善随后的胚胎发育。然而,其潜在机制仍不清楚。
在雌性小鼠腹腔注射8 IU马绒毛膜促性腺激素(eCG)后46 - 48小时,从卵巢中收集卵丘-卵母细胞复合体(COCs),然后将COCs在不同培养基中培养。采用qRT-PCR分析评估表皮生长因子样因子和利钠肽受体2(NPR2)的mRNA表达。采用蛋白质免疫印迹分析评估丝裂原活化蛋白激酶3/1(MAPK3/1)的磷酸化。对卵母细胞的减数分裂恢复进行形态学评估。
FSH刺激表皮生长因子样因子的表达、MAPK3/1的激活、NPR2 mRNA的减少以及卵母细胞减数分裂恢复。此外,FSH诱导的NPR2减少和卵母细胞减数分裂恢复是通过由表皮生长因子受体(EGFR)途径激活的MAPK3/1信号通路发生的。
NPR2参与FSH介导的卵母细胞减数分裂恢复,并且该过程与EGFR和MAPK3/1信号通路相关。