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Procr细胞中的选择性YAP激活对于卵巢干细胞/祖细胞的扩增和上皮修复至关重要。

Selective YAP activation in Procr cells is essential for ovarian stem/progenitor expansion and epithelium repair.

作者信息

Wang Jingqiang, Liu Chunye, He Lingli, Xie Zhiyao, Bai Lanyue, Yu Wentao, Wang Zuoyun, Lu Yi, Gao Dong, Fu Junfen, Zhang Lei, Zeng Yi Arial

机构信息

Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, National Children's Regional Medical Center, Hangzhou, China.

State Key Laboratory of Cell Biology, CAS Center for Excellence in Molecular Cell Science, Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.

出版信息

Elife. 2022 Mar 14;11:e75449. doi: 10.7554/eLife.75449.

DOI:10.7554/eLife.75449
PMID:35285801
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8920503/
Abstract

Ovarian surface epithelium (OSE) undergoes recurring ovulatory rupture and OSE stem cells rapidly generate new cells for the repair. How the stem cell activation is triggered by the rupture and promptly turns on proliferation is unclear. Our previous study has identified that Protein C Receptor (Procr) marks OSE progenitors. In this study, we observed decreased adherent junction and selective activation of YAP signaling in Procr progenitors at OSE rupture site. OSE repair is impeded upon deletion of Yap1 in these progenitors. Interestingly, Procr+ progenitors show lower expression of Vgll4, an antagonist of YAP signaling. Overexpression of Vgll4 in Procr+ cells hampers OSE repair and progenitor proliferation, indicating that selective low Vgll4 expression in Procr+ progenitors is critical for OSE repair. In addition, YAP activation promotes transcription of the OSE stemness gene . The combination of increased cell division and Procr expression leads to expansion of Procr+ progenitors surrounding the rupture site. These results illustrate a YAP-dependent mechanism by which the stem/progenitor cells recognize the murine ovulatory rupture, and rapidly multiply their numbers, highlighting a YAP-induced stem cell expansion strategy.

摘要

卵巢表面上皮（OSE）会经历反复的排卵破裂，OSE干细胞会迅速产生新细胞进行修复。目前尚不清楚破裂是如何触发干细胞激活并迅速启动增殖的。我们之前的研究已确定蛋白C受体（Procr）标记OSE祖细胞。在本研究中，我们观察到在OSE破裂部位的Procr祖细胞中，黏附连接减少，YAP信号通路选择性激活。在这些祖细胞中删除Yap1会阻碍OSE修复。有趣的是，Procr+祖细胞中Vgll4（YAP信号通路的拮抗剂）的表达较低。在Procr+细胞中过表达Vgll4会阻碍OSE修复和祖细胞增殖，这表明Procr+祖细胞中Vgll4的选择性低表达对OSE修复至关重要。此外，YAP激活促进OSE干性基因的转录。细胞分裂增加和Procr表达增加共同导致破裂部位周围Procr+祖细胞的扩增。这些结果阐明了一种YAP依赖性机制，通过该机制，干/祖细胞识别小鼠排卵破裂，并迅速增加其数量，突出了YAP诱导的干细胞扩增策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2545/8920503/bf3005aa93c6/elife-75449-sa2-fig1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2545/8920503/bf3005aa93c6/elife-75449-sa2-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2545/8920503/a248a1f79b33/elife-75449-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2545/8920503/8c5354deebb7/elife-75449-fig1-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2545/8920503/6deca9d42a62/elife-75449-fig1-figsupp2.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2545/8920503/4351e1abfe69/elife-75449-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2545/8920503/e52c5b0fcf00/elife-75449-fig3-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2545/8920503/bf30a89ce113/elife-75449-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2545/8920503/b91fadde08f6/elife-75449-fig4-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2545/8920503/82b605d03893/elife-75449-fig4-figsupp2.jpg
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