INHIBITION OF OOCYTE MATURATION IN THE MOUSE - PARTICIPATION OF CAMP, STEROID-HORMONES, AND A PUTATIVE MATURATION-INHIBITORY FACTOR

INHIBITION OF OOCYTE MATURATION IN THE MOUSE - PARTICIPATION OF CAMP, STEROID-HORMONES, AND A PUTATIVE MATURATION-INHIBITORY FACTOR
复制标题

DOI:
10.1016/0012-1606(83)90198-7
复制
发表时间:
1983-01-01
影响因子:
2.7
通讯作者:
SCHULTZ, RM
SCHULTZ, RM
中科院分区:
生物学3区
文献类型:
--
作者:
EPPIG, JJ;FRETER, RR;SCHULTZ, RM

文献摘要

被引文献

相似文献

对卵丘细胞通过cAMP依赖性过程抑制卵母细胞成熟的假设进行了验证(R。M.舒尔茨河,巴西-地蒙哥马利,P.F. Ward-Bailey和J.J. Eppig [1983])。用卵泡刺激素(FSH)处理分离的卵丘细胞-卵母细胞复合体,导致卵丘细胞cAMP水平和卵母细胞成熟的第一种形态学表现--生发泡破裂(GVBD)的抑制程度呈剂量依赖性增加。低于完全减数分裂抑制所需浓度的cAMP膜渗透类似物二丁酰cAMP(dbcAMP)对卵丘细胞包裹的卵母细胞的抑制作用比对裸露的卵母细胞的抑制作用更大。卵丘细胞封闭和裸露的卵母细胞成熟在同一时间在dbcAMP的情况下。消融耦合卵丘细胞的卵母细胞的差距连接废除了卵丘细胞的成熟抑制作用,促进FSH或低浓度的dbcAMP。显然,卵母细胞成熟的抑制是由颗粒/卵丘细胞来源的因子介导的,而不是cAMP,其需要cAMP用于其活性和/或产生,以及卵丘细胞和卵母细胞之间的完整细胞间偶联途径。多种类固醇激素增强FSH诱导的卵丘细胞封闭卵母细胞成熟抑制。类固醇激素抑制成熟裸露的卵母细胞,但只有当卵母细胞cAMP水平升高cAMP类似物或毛喉素。单独使用类固醇并不能抑制卵丘细胞封闭或裸露卵母细胞的成熟。类固醇单独或与FSH组合不影响卵丘细胞和卵母细胞之间的代谢偶联,睾酮也不影响毛喉素诱导的剥脱卵母细胞中cAMP水平。显然,卵母细胞是类固醇激素与cAMP依赖性过程在抑制成熟中的协同活性的位点。这些研究的结果进行了讨论的作用,细胞间通讯,cAMP,一个假定的成熟抑制因子和类固醇激素在小鼠卵母细胞成熟的抑制。
The hypothesis that cumulus cells inhibit oocyte maturation by a cAMP-dependent process was tested (R. M. Schultz, R. Montgomery, P. F. Ward-Bailey and J. J. Eppig [1983]). Treatment of isolated cumulus cell-oocyte complexes with follicle-stimulating hormone (FSH) resulted in a dose-dependent increase in both cumulus cell cAMP levels and in the extent of inhibition of germinal vesicle breakdown (GVBD), the 1st morphological manifestation of oocyte maturation. Concentrations of a membrane-permeable analog of cAMP, dibutyryl cAMP (dbcAMP), that were below those required for complete meiotic inhibition had a greater inhibitory effect on cumulus cell-enclosed oocytes than on denuded oocytes. Cumulus cell-enclosed and denuded oocytes matured at the same time in the absence of dbcAMP. Ablation of the gap junctions that couple cumulus cells to the oocyte abolished the maturation-inhibitory action of cumulus cells that was promoted either by FSH or low concentrations of dbcAMP. Apparently, inhibition of oocyte maturation is mediated by a factor of granulosa/cumulus cell origin, other than cAMP, which requires cAMP for its activity and/or generation, and an intact intercellular coupling pathway between cumulus cells and the oocyte. A variety of steroid hormones potentiated the FSH-induced inhibition of maturation in cumulus cell-enclosed oocytes. Sterid hormones inhibited maturation in denuded oocytes, but only when oocyte cAMP levels were elevated by cAMP analogs or forskolin. Steroids alone did not inhibit maturation of either cumulus cell-enclosed or denuded oocytes. The steroids alone or in combination with FSH did not affect metabolic coupling between the cumulus cells and oocytes, nor did testosterone affect the forskolin-induced level of cAMP in denuded oocytes. Apparently, the oocyte is a site for the synergistic activity of steroid hormones with a cAMP-dependent process in inhibiting maturation. Results of these studies are discussed in terms of the roles of intercellular communication, cAMP, a putative maturation-inhibiting factor and steorid hormones in the inhibition of maturation of mouse oocytes.