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基质Senp1通过调节BMP4表达促进小鼠早期卵泡发生。

Stromal Senp1 promotes mouse early folliculogenesis by regulating BMP4 expression.

作者信息

Tan Shu, Feng Boya, Yin Mingzhu, Zhou Huanjiao Jenny, Lou Ge, Ji Weidong, Li Yonghao, Min Wang

机构信息

Department of Pathology and the Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT 06519 USA.

Center for Translational Medicine, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080 China.

出版信息

Cell Biosci. 2017 Jul 25;7:36. doi: 10.1186/s13578-017-0163-5. eCollection 2017.

DOI:10.1186/s13578-017-0163-5
PMID:28770041
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5526272/
Abstract

BACKGROUND

Mammalian folliculogenesis, maturation of the ovarian follicles, require both growth factors derived from oocyte and surrounding cells, including stromal cells. However, the mechanism by which stromal cells and derived factors regulate oocyte development remains unclear.

RESULTS

We observed that SENP1, a small ubiquitin-related modifier (SUMO)-specific isopeptidase, was expressed in sm22α-positive stromal cells of mouse ovary. The sm22α-positive stromal cells tightly associated with follicle maturation. By using the sm22α-specific Cre system, we show that mice with a stromal cell-specific deletion of SENP1 exhibit attenuated stroma-follicle association, delayed oocyte growth and follicle maturation with reduced follicle number and size at early oocyte development, leading to premature ovarian failure at late stages of ovulating life. Mechanistic studies suggest that stromal SENP1 deficiency induces down-regulation of BMP4 in stromal cells concomitant with decreased expression of BMP4 receptor BMPR1b and BMPR2 on oocytes.

CONCLUSIONS

Our data support that protein SUMOylation-regulating enzyme SENP1 plays a critical role in early ovarian follicle development by regulating gene expression of BMP4 in stroma and stroma-oocyte communication.

摘要

背景

哺乳动物卵泡发生，即卵巢卵泡的成熟，需要来自卵母细胞和周围细胞（包括基质细胞）的生长因子。然而，基质细胞及其衍生因子调节卵母细胞发育的机制仍不清楚。

结果

我们观察到，小泛素相关修饰物（SUMO）特异性异肽酶SENP1在小鼠卵巢的平滑肌22α（sm22α）阳性基质细胞中表达。sm22α阳性基质细胞与卵泡成熟紧密相关。通过使用sm22α特异性Cre系统，我们发现SENP1基因在基质细胞中特异性缺失的小鼠表现出基质与卵泡的关联减弱、卵母细胞生长延迟以及卵泡成熟延迟，在早期卵母细胞发育阶段卵泡数量和大小减少，导致排卵后期卵巢早衰。机制研究表明，基质细胞中SENP1的缺失会导致基质细胞中骨形态发生蛋白4（BMP4）的下调，同时卵母细胞上BMP4受体BMPR1b和BMPR2的表达也会降低。

结论

我们的数据支持，蛋白质SUMO化调节酶SENP1通过调节基质中BMP4的基因表达以及基质与卵母细胞的通讯，在早期卵巢卵泡发育中起关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5154/5526272/826a98e980b4/13578_2017_163_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5154/5526272/47abcb04b150/13578_2017_163_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5154/5526272/8bd40a5164a5/13578_2017_163_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5154/5526272/5d4fadd1e9d7/13578_2017_163_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5154/5526272/f8f1e4dbab61/13578_2017_163_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5154/5526272/fcc0a382f6f6/13578_2017_163_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5154/5526272/826a98e980b4/13578_2017_163_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5154/5526272/47abcb04b150/13578_2017_163_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5154/5526272/8bd40a5164a5/13578_2017_163_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5154/5526272/5d4fadd1e9d7/13578_2017_163_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5154/5526272/f8f1e4dbab61/13578_2017_163_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5154/5526272/fcc0a382f6f6/13578_2017_163_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5154/5526272/826a98e980b4/13578_2017_163_Fig6_HTML.jpg

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