• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

多囊卵巢中窦前卵泡发生异常与颗粒细胞分裂增加有关。

Abnormal preantral folliculogenesis in polycystic ovaries is associated with increased granulosa cell division.

作者信息

Stubbs Sharron A, Stark Jaroslav, Dilworth Stephen M, Franks Stephen, Hardy Kate

机构信息

Institute of Reproductive and Developmental Biology, Imperial College London, Hammersmith Hospital, London W12 0NN, United Kingdom.

出版信息

J Clin Endocrinol Metab. 2007 Nov;92(11):4418-26. doi: 10.1210/jc.2007-0729. Epub 2007 Aug 14.

DOI:10.1210/jc.2007-0729
PMID:17698906
Abstract

CONTEXT

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women, but its etiology remains obscure. Recent data suggest that an intrinsic abnormality of early follicle development in the ovary is key to the pathogenesis of PCOS. We have recently found that in PCOS the proportion of primordial follicles is decreased with a reciprocal increase in the proportion of primary follicles.

OBJECTIVE

Our aim was to examine whether the accelerated transition of follicles from primordial to primary stages in polycystic ovaries (PCO) is due to increased granulosa cell (GC) division.

DESIGN

This study is a comparison of expression of minichromosome maintenance protein 2 (MCM2) (present in the nuclei of cells that are licensed to divide) in archive tissue from normal and PCO.

SETTING

This is a laboratory-based study.

PATIENTS

There were 16 women with regular cycles (six with normal and 10 with PCO) and five anovulatory women with PCO, classified histologically, with reference to menstrual history and ultrasound.

MAIN OUTCOME MEASURES

The presence of MCM2 expression in the GCs of 1,371 follicles was determined.

RESULTS

GC proliferation was increased in anovulatory PCO compared with both normal and ovulatory PCO, with an increased proportion of preantral follicles with MCM2-positive GCs (P <or= 0.015). The number of GCs differed significantly among the three types of ovary at the transitional (P = 0.013) and primary (P = 0.0096) stages. This was accompanied by an altered relationship (P < 0.0001) between oocyte growth and GC division/cuboidalization.

CONCLUSIONS

These findings provide evidence for increased GC proliferation in early-growing follicles in PCOS. This offers an explanation for the increased proportion of primary follicles in PCOS.

摘要

背景

多囊卵巢综合征(PCOS)是女性最常见的内分泌紊乱疾病,但其病因仍不清楚。最近的数据表明,卵巢早期卵泡发育的内在异常是PCOS发病机制的关键。我们最近发现,在PCOS中,原始卵泡的比例下降,而初级卵泡的比例相应增加。

目的

我们的目的是研究多囊卵巢(PCO)中卵泡从原始阶段到初级阶段的加速转变是否是由于颗粒细胞(GC)分裂增加所致。

设计

本研究比较了正常和PCO存档组织中微小染色体维持蛋白2(MCM2)(存在于有分裂许可的细胞核中) 的表达。

地点

这是一项基于实验室的研究。

患者

有16名月经周期规律的女性(6名正常,10名PCO)和5名无排卵的PCO女性,根据月经史和超声进行组织学分类。

主要观察指标

确定1371个卵泡的GC中MCM2表达的存在情况。

结果

与正常和排卵性PCO相比,无排卵性PCO中的GC增殖增加,有MCM2阳性GC的窦前卵泡比例增加(P≤0.015)。在过渡阶段(P = 0.013)和初级阶段(P = 0.0096),三种类型卵巢的GC数量存在显著差异。这伴随着卵母细胞生长与GC分裂/立方化之间关系的改变(P < 0.0001)。

结论

这些发现为PCOS早期生长卵泡中GC增殖增加提供了证据。这为PCOS中初级卵泡比例增加提供了解释。

相似文献

1
Abnormal preantral folliculogenesis in polycystic ovaries is associated with increased granulosa cell division.多囊卵巢中窦前卵泡发生异常与颗粒细胞分裂增加有关。
J Clin Endocrinol Metab. 2007 Nov;92(11):4418-26. doi: 10.1210/jc.2007-0729. Epub 2007 Aug 14.
2
Anti-müllerian hormone protein expression is reduced during the initial stages of follicle development in human polycystic ovaries.在人类多囊卵巢卵泡发育的初始阶段,抗苗勒管激素蛋白表达降低。
J Clin Endocrinol Metab. 2005 Oct;90(10):5536-43. doi: 10.1210/jc.2005-0907. Epub 2005 Jul 19.
3
Prolonged survival in culture of preantral follicles from polycystic ovaries.多囊卵巢窦前卵泡在培养中的长期存活。
J Clin Endocrinol Metab. 2007 May;92(5):1975-8. doi: 10.1210/jc.2006-1422. Epub 2007 Mar 6.
4
Role of Insulin-like growth factors in initiation of follicle growth in normal and polycystic human ovaries.胰岛素样生长因子在正常和多囊卵巢中卵泡生长启动中的作用。
J Clin Endocrinol Metab. 2013 Aug;98(8):3298-305. doi: 10.1210/jc.2013-1378. Epub 2013 Jun 7.
5
The rise of estradiol and inhibin B after acute stimulation with follicle-stimulating hormone predict the follicle cohort size in women with polycystic ovary syndrome, regularly menstruating women with polycystic ovaries, and regularly menstruating women with normal ovaries.促卵泡激素急性刺激后雌二醇和抑制素B的升高可预测多囊卵巢综合征患者、有卵巢多囊样改变的规律月经女性以及卵巢正常的规律月经女性的卵泡群大小。
J Clin Endocrinol Metab. 2001 Apr;86(4):1589-95. doi: 10.1210/jcem.86.4.7396.
6
Immunohistochemical study of steroidogenesis and cell proliferation in polycystic ovarian syndrome.多囊卵巢综合征中类固醇生成及细胞增殖的免疫组织化学研究
Hum Reprod. 1996 Jul;11(7):1387-92. doi: 10.1093/oxfordjournals.humrep.a019405.
7
Premature response to luteinizing hormone of granulosa cells from anovulatory women with polycystic ovary syndrome: relevance to mechanism of anovulation.多囊卵巢综合征无排卵女性颗粒细胞对促黄体生成素的过早反应:与无排卵机制的相关性
J Clin Endocrinol Metab. 1998 Nov;83(11):3984-91. doi: 10.1210/jcem.83.11.5232.
8
Gene Expression in Granulosa Cells From Small Antral Follicles From Women With or Without Polycystic Ovaries.多囊卵巢或非多囊卵巢妇女小窦卵泡颗粒细胞中的基因表达。
J Clin Endocrinol Metab. 2019 Dec 1;104(12):6182-6192. doi: 10.1210/jc.2019-00780.
9
Disordered follicle development in ovaries of prenatally androgenized ewes.产前雄激素化母羊卵巢中卵泡发育紊乱。
J Endocrinol. 2007 Feb;192(2):421-8. doi: 10.1677/joe.1.07097.
10
Stockpiling of transitional and classic primary follicles in ovaries of women with polycystic ovary syndrome.多囊卵巢综合征女性卵巢中过渡性和经典初级卵泡的储备。
J Clin Endocrinol Metab. 2004 Nov;89(11):5321-7. doi: 10.1210/jc.2004-0643.

引用本文的文献

1
Role of Granulosa Cell Dysfunction in Women Infertility Associated with Polycystic Ovary Syndrome and Obesity.颗粒细胞功能障碍在多囊卵巢综合征和肥胖相关女性不孕症中的作用。
Biomolecules. 2025 Jun 24;15(7):923. doi: 10.3390/biom15070923.
2
Hyperandrogen-induced imbalance of FOXO4-AR regulatory loop contributes to ovulatory disorders in polycystic ovary syndrome.高雄激素诱导的FOXO4-AR调节环失衡导致多囊卵巢综合征的排卵障碍。
Mol Ther Nucleic Acids. 2025 Apr 20;36(2):102543. doi: 10.1016/j.omtn.2025.102543. eCollection 2025 Jun 10.
3
Elevated expression of microRNA-155, microRNA-383, and microRNA-9 in Iranian patients with polycystic ovary syndrome.
伊朗多囊卵巢综合征患者中微小RNA - 155、微小RNA - 383和微小RNA - 9的表达升高。
Biochem Biophys Rep. 2025 Mar 31;42:101997. doi: 10.1016/j.bbrep.2025.101997. eCollection 2025 Jun.
4
MiR-145-5p regulates granulosa cell proliferation by targeting the gene in KGN cells.MiR-145-5p通过靶向KGN细胞中的 基因来调节颗粒细胞增殖。 (原文中“the gene”部分缺失具体基因名称)
J Reprod Dev. 2024 Dec 13;70(6):372-378. doi: 10.1262/jrd.2024-053. Epub 2024 Sep 22.
5
LncRNA PKD1P6 modulates ovarian granulosa cell survival of hyperandrogenic polycystic ovary syndrome by targeting miR-135b-5p and inhibiting ERK1/2 signaling.长链非编码RNA PKD1P6通过靶向miR-135b-5p并抑制ERK1/2信号传导来调节高雄激素性多囊卵巢综合征的卵巢颗粒细胞存活。
Heliyon. 2024 Aug 14;10(16):e36321. doi: 10.1016/j.heliyon.2024.e36321. eCollection 2024 Aug 30.
6
Whole transcriptome analysis revealed the regulatory network and related pathways of non-coding RNA regulating ovarian atrophy in broody hens.全转录组分析揭示了非编码RNA调控抱窝母鸡卵巢萎缩的调控网络及相关通路。
Front Vet Sci. 2024 May 29;11:1399776. doi: 10.3389/fvets.2024.1399776. eCollection 2024.
7
High levels of fatty acid-binding protein 5 excessively enhances fatty acid synthesis and proliferation of granulosa cells in polycystic ovary syndrome.多囊卵巢综合征中,脂肪酸结合蛋白5的高表达过度增强了颗粒细胞的脂肪酸合成和增殖。
J Ovarian Res. 2024 Feb 19;17(1):44. doi: 10.1186/s13048-024-01368-6.
8
LncRNA SNHG5 adversely governs follicular growth in PCOS via miR-92a-3p/CDKN1C axis.长链非编码RNA SNHG5通过miR-92a-3p/CDKN1C轴对多囊卵巢综合征的卵泡生长产生不利影响。
iScience. 2023 Nov 23;27(2):108522. doi: 10.1016/j.isci.2023.108522. eCollection 2024 Feb 16.
9
Dysfunction of Human Estrogen Signaling as a Novel Molecular Signature of Polycystic Ovary Syndrome.人类雌激素信号功能障碍作为多囊卵巢综合征的一种新型分子特征。
Int J Mol Sci. 2023 Nov 24;24(23):16689. doi: 10.3390/ijms242316689.
10
The neonatal southern white rhinoceros ovary contains oogonia in germ cell nests.新生南部白犀牛的卵巢中含有生殖细胞巢中的卵原细胞。
Commun Biol. 2023 Oct 17;6(1):1049. doi: 10.1038/s42003-023-05256-5.