Expression of mouse ovarian insulin growth factor system components during follicular development and atresia.
Expression of mouse ovarian insulin growth factor system components during follicular development and atresia.
复制标题
DOI：
10.1210/endo.139.12.6367
复制
发表时间：
1998
期刊：
影响因子：
4.8
通讯作者：
S. Wandji;T. Wood;Jennifer Crawford;S. Levison;J. Hammond
中科院分区：
文献类型：
--
作者：
S. Wandji;T. Wood;Jennifer Crawford;S. Levison;J. Hammond
胰岛素生长因子I（IGF-I）似乎是完成小鼠卵泡发育所必需的。然而，对卵泡发育和黄体化过程中IGF系统成分的变化知之甚少。本研究确定了特定IGF系统成分的基因表达与小鼠卵泡生长、存活或闭锁之间的关系。使用了来自三种不同品系（129、C57和MF 1）的未成熟小鼠，接受或不接受促性腺激素治疗（2.5 IU PMSG/2.5 IU人CG（hCG））。菌株在所有测量参数中相似。细胞凋亡，检测原位标记的缺口DNA，出现之前的形态学迹象的闭锁。在健康卵泡中，IGF-I转录在初级卵泡阶段较低，但在窦前晚期和窦早期阶段增加到最大值（P < 0.001），与激素治疗无关。偶尔，在凋亡卵泡中也检测到IGF-I转录物，但根据形态学标准评估，其作为闭锁的函数而降低（P < 0.05）。IGF结合蛋白-4（IGFBP-4）mRNA仅表达于凋亡卵泡和闭锁卵泡（P < 0.001）。另一方面，IGFBP-5转录水平在健康初级和次级卵泡的颗粒细胞中升高，但在随后的卵泡阶段和闭锁卵泡中降低（P < 0.001）。相反，IGFBP-2 mRNA在颗粒细胞中组成型表达。PMSG/hCG处理诱导IGFBP-2转录物在卵巢上皮中出现。PMSG/hCG诱导排卵后，IGFBP-2和-4和IGF-I型受体mRNA在几乎所有的黄体细胞中强烈表达，而IGFBP-3和-5转录本选择性地定位于黄体中的某些细胞类型。相反，IGF-I mRNA在黄体中基本上检测不到。本研究对小鼠卵巢IGF系统的生理学和解剖学进行了最全面、最详细的分析，结果表明：1）IGFBP-5-与缓慢生长和未成熟的腔前卵泡的存活有关; 2）IGF-I与快速生长的大腔前卵泡和腔卵泡的生长和存活有关; 3）IGFBP-4是小鼠卵泡的致闭锁候选因子; 4）排卵剂量的PMSG/hCG上调卵巢黄体中IGFBP-2 mRNA的表达; 5）IGF-I型受体和IGFBP-2至IGFBP-5的转录本在小鼠黄体中高度表达，但IGF-I的转录本不高度表达。
Insulin growth factor I (IGF-I) appears necessary for the completion of follicular development in mice. However, little is known about changes in the IGF system components during follicular development and luteinization. This study determined the relation between gene expression of specific IGF system components and follicular growth, survival, or atresia in mice. Immature mice from three different strains (129, C57, and MF1), with or without gonadotropin treatment (2.5 IU PMSG/2.5 IU human CG (hCG)], were used. The strains were similar in all parameters measured. Apoptosis, as detected by in situ labeling of nicked DNA, preceded the appearance of morphological signs of atresia. In healthy follicles, IGF-I transcripts were low during the primary follicular stage but increased to a maximum in the late preantral and early antral stages (P < 0.001) irrespective of hormone treatment. Occasionally, IGF-I transcripts were also detected in apoptotic follicles but decreased (P < 0.05) as a function of atresia as assessed by morphological criteria. IGF binding protein-4 (IGFBP-4) messenger RNA (mRNA) expression in granulosa cells was restricted to apoptotic and atretic follicles (P < 0.001). IGFBP-5 transcript levels, on the other hand, were elevated in granulosa cells of healthy primary and secondary follicles but decreased in subsequent follicular stages and in atretic follicles (P < 0.001). Conversely, IGFBP-2 mRNA was constitutively expressed in granulosa cells. PMSG/hCG treatment induced the appearance of IGFBP-2 transcripts in the ovarian interstitium. Following PMSG/hCG-induced ovulation, IGFBP-2 and -4 and IGF type-I receptor mRNAs were strongly expressed in virtually all luteal cells, whereas IGFBP-3 and -5 transcripts were selectively localized to some cell types in the corpus luteum. Conversely, IGF-I mRNA was essentially undetectable in the corpus luteum. This study represents the most comprehensive and detailed analysis of the physiology and anatomy of the mouse ovarian IGF system, and shows that 1) IGFBP-5-is linked to the survival of the slow growing and immature preantral follicles; 2) IGF-I is associated with the growth and survival of the rapidly growing large preantral and antral follicles; 3) IGFBP-4 is an atretogenic candidate for mouse ovarian follicles; 4) ovulatory doses of PMSG/hCG up-regulate IGFBP-2 mRNA expression in the ovarian interstitium; and 5) transcripts of IGF type-I receptor and IGFBP-2 through -5, but not those of IGF-I are highly expressed in the mouse corpus luteum.