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表达 Procr 的祖细胞负责修复小鼠卵巢表面上皮的排卵破裂。

Procr-expressing progenitor cells are responsible for murine ovulatory rupture repair of ovarian surface epithelium.

机构信息

State Key Laboratory of Cell Biology, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, 200031, China.

Reproductive Medicine Center, Changzheng Hospital, Second Military Medical University, Shanghai, 200003, China.

出版信息

Nat Commun. 2019 Oct 31;10(1):4966. doi: 10.1038/s41467-019-12935-7.

Abstract

Ovarian surface epithelium (OSE) undergoes recurring ovulatory rupture and repair. The OSE replenishing mechanism post ovulation remains unclear. Here we report that the expression of Protein C Receptor (Procr) marks a progenitor population in adult mice that is responsible for OSE repair post ovulation. Procr+  cells are the major cell source for OSE repair. The mechanism facilitating the rapid re-epithelialization is through the immediate expansion of Procr+  cells upon OSE rupture. Targeted ablation of Procr+  cells impedes the repairing process. Moreover, Procr+  cells displayed robust colony-formation capacity in culture, which we harnessed and established a long-term culture and expansion system of OSE cells. Finally, we show that Procr+  cells and previously reported Lgr5+ cells have distinct lineage tracing behavior in OSE homeostasis. Our study suggests that Procr marks progenitor cells that are critical for OSE ovulatory rupture and homeostasis, providing insight into how adult stem cells respond upon injury.

摘要

卵巢表面上皮(OSE)经历反复的排卵破裂和修复。排卵后 OSE 补充的机制尚不清楚。在这里,我们报告蛋白 C 受体(Procr)的表达标志着成年小鼠中的一个祖细胞群体,该群体负责排卵后的 OSE 修复。Procr+细胞是 OSE 修复的主要细胞来源。促进快速再上皮化的机制是通过 OSE 破裂时 Procr+细胞的立即扩增。Procr+细胞的靶向消融会阻碍修复过程。此外,Procr+细胞在培养中表现出强大的集落形成能力,我们利用这一点建立了 OSE 细胞的长期培养和扩增系统。最后,我们表明 Procr+细胞和之前报道的 Lgr5+细胞在 OSE 稳态中具有不同的谱系追踪行为。我们的研究表明,Procr 标记了对于 OSE 排卵破裂和稳态至关重要的祖细胞,为了解成年干细胞在受伤时的反应提供了线索。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4b3/6823351/62ac46caf3ef/41467_2019_12935_Fig1_HTML.jpg

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