Sato Eimei, Kimura Naoko, Yokoo Masaki, Miyake Yuko, Ikeda Joh-E
Laboratory of Animal Reproduction, Graduate School of Agricultural Science, Tohoku University, Sendai 981-8555, Japan.
Microsc Res Tech. 2006 Jun;69(6):427-35. doi: 10.1002/jemt.20302.
In the mouse, oogonia enter the prophase of the first meiotic division and differentiate into oocyte while developing in the fetal ovary. Shortly after birth, all oocytes are arrested in the dictyate stage of late prophase in the developing follicles; a small number of follicles reach the ovulatory stage; the rest are lost by apoptosis. The resumption of meiotic division and nuclear progression to metaphase II (oocyte maturation) occur in the ovulatory follicles. In this article we review recent morphological data that have clarified how cytokines and glycosaminoglycans (GAGs) are involved in mouse follicular development, atresia, and maturation during oogenesis, as exogenous/endogenous factors. (1) Microvascular networks and angiogenic factors (epidermal growth factor; GAGs) are deeply involved in selective mouse oocyte growth beyond approximately 20-30 microm in diameter. (2) Gonadotropin-inducible neuronal apoptosis inhibitory protein may indirectly affect oocyte survival as a result of the inhibition of apoptotic granulosa-cell death during folliculogenesis. (3) The pattern of oocyte degeneration depends on follicle and oocyte developmental stages, and follicle stimulating hormone accelerates the process of degeneration of oocytes. (4) The process of degeneration of mouse oocytes/eggs is modulated by tumor necrosis factor-alpha that is accumulated in the expanded cumulus during oocyte maturation. (5) A colloidal iron-positive substance was detected in the intercellular spaces of follicular tissue, especially in the cumulus mass. Cells located where the cumulus mass and granulosa cell layer interwound became enlarged during the resumption of oocyte meiosis. Colloidal iron-positive substances accumulated extensively within the intercellular spaces of the enlarged cells.
在小鼠中,卵原细胞在胎儿卵巢发育过程中进入第一次减数分裂前期并分化为卵母细胞。出生后不久,所有卵母细胞在发育中的卵泡中停滞于减数分裂前期晚期的双线期;少数卵泡达到排卵阶段;其余的则通过凋亡而丢失。减数分裂的恢复以及细胞核向中期II的进展(卵母细胞成熟)发生在排卵卵泡中。在本文中,我们综述了最近的形态学数据,这些数据阐明了细胞因子和糖胺聚糖(GAGs)作为外源性/内源性因素如何参与小鼠卵泡发育、闭锁和卵母细胞发生过程中的成熟。(1)微血管网络和血管生成因子(表皮生长因子;GAGs)深度参与了直径约20 - 30微米以上的小鼠卵母细胞的选择性生长。(2)促性腺激素诱导的神经元凋亡抑制蛋白可能由于在卵泡发生过程中抑制颗粒细胞凋亡而间接影响卵母细胞存活。(3)卵母细胞退化的模式取决于卵泡和卵母细胞的发育阶段,促卵泡激素加速卵母细胞的退化过程。(4)小鼠卵母细胞/卵子的退化过程受到肿瘤坏死因子-α的调节,该因子在卵母细胞成熟过程中积聚在扩张的卵丘中。(5)在卵泡组织的细胞间隙中检测到一种胶体铁阳性物质,尤其是在卵丘团块中。在卵母细胞减数分裂恢复期间,位于卵丘团块和颗粒细胞层缠绕处的细胞会变大。胶体铁阳性物质在这些变大细胞的细胞间隙中大量积聚。