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首页> 外文期刊>Cell and Tissue Research >Role of Notch signaling in granulosa cell proliferation and polyovular follicle induction during folliculogenesis in mouse ovary
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Role of Notch signaling in granulosa cell proliferation and polyovular follicle induction during folliculogenesis in mouse ovary

机译：Notch信号在小鼠卵巢滤泡形成过程中对颗粒细胞增殖和多卵泡滤泡诱导的作用

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In the fetal mouse ovary, oocytes are connected by an intercellular bridge and form germ cell cysts. Folliculogenesis begins after birth. To study the role of Notch signaling in folliculogenesis, double-immunohistochemical localization of laminin and Ki-67 was performed in mouse ovaries from embryonic day 17.5 (E17.5) to postnatal day 4 (P4). Most cysts and follicles contained Ki-67-negative cells; however, a few Ki-67-positive cells were present in cysts from E17.5 through P4, indicating that a small number of pre-granulosa cells continue to proliferate during folliculogenesis. To examine the effects of an inhibitor of Notch signaling (DAPT) and a synthetic estrogen (diethylstilbestrol [DES]) on folliculogenesis, an organ-culture system was established. The numbers of cysts, primordial follicles (PrFs) and primary follicles were unchanged by DES, whereas the total number of PrFs and of PrFs with Ki-67-negative cells was reduced by DAPT. In organ-cultured neonatal ovaries, only DAPT treatment increased degenerating cells defined as oocytes. On the contrary, the number of polyovular follicles (PFs) and the PF incidence were significantly increased in ovaries organ-cultured with DES at day 20 post-grafting. In organ-cultured fetal and neonatal ovaries, DAPT reduced Notch 3 and Hey2 mRNAs, whereas DES increased Hey2 mRNA. These results suggest that Notch signaling in fetal ovaries is involved with PrF assembly by the regulation of oocyte survival rather than by cell proliferation. In PF induction, as a result of the disruption of interactions between oocytes and pre-granulosa cells, DES and Notch signaling act independently.
机译：在胎儿小鼠卵巢中，卵母细胞通过细胞间桥连接并形成生殖细胞囊肿。卵泡发生在出生后开始。为了研究Notch信号在卵泡形成中的作用，在小鼠卵巢中从胚胎第17.5天（E17.5）到出生后第4天（P4）进行了层粘连蛋白和Ki-67的双免疫组化定位。大多数囊肿和卵泡中都含有Ki-67阴性细胞。然而，从E17.5到P4的囊肿中存在一些Ki-67阳性细胞，这表明少数卵前颗粒细胞在卵泡形成过程中继续增殖。为了检查Notch信号抑制剂（DAPT）和合成雌激素（diethylstilbestrol [DES]）对卵泡形成的影响，建立了器官培养系统。 DES改变了囊肿，原始卵泡（PrFs）和初级卵泡的数目，而DAPT减少了PrFs和Ki-67阴性细胞的PrFs总数。在器官培养的新生儿卵巢中，只有DAPT处理才能增加退化为卵母细胞的细胞。相反，在移植后第20天用DES器官培养的卵巢中，多卵泡卵泡（PFs）的数量和PF发生率显着增加。在器官培养的胎儿和新生儿卵巢中，DAPT降低了Notch 3和Hey2 mRNA的表达，而DES则提高了Hey2 mRNA的表达。这些结果表明，胎儿卵巢中的Notch信号传导通过调节卵母细胞存活而不是细胞增殖而与PrF组装有关。在PF诱导中，由于卵母细胞和颗粒前细胞之间相互作用的破坏，DES和Notch信号独立发挥作用。

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