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缺氧通过 Notch 信号调节子宫内膜间充质基质/干细胞样细胞的自我更新。

Hypoxia Regulates the Self-Renewal of Endometrial Mesenchymal Stromal/Stem-like Cells via Notch Signaling.

机构信息

Department of Obstetrics and Gynaecology, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong 999077, China.

Shenzhen Key Laboratory of Fertility Regulation, The University of Hong Kong Shenzhen Hospital, Shenzhen 518000, China.

出版信息

Int J Mol Sci. 2022 Apr 21;23(9):4613. doi: 10.3390/ijms23094613.

Abstract

Human endometrium is an incredibly dynamic tissue undergoing cyclic regeneration and shedding during a woman's reproductive life. Endometrial mesenchymal stromal/stem-like cells (eMSC) contribute to this process. A hypoxic niche with low oxygen levels has been reported in multiple somatic stem cell types. However, the knowledge of hypoxia on eMSC remains limited. In mice, stromal stem/progenitor cells can be identified by the label-retaining technique. We examined the relationship between the label-retaining stromal cells (LRSC) and hypoxia during tissue breakdown in a mouse model of simulated menses. Our results demonstrated that LRSC resided in a hypoxic microenvironment during endometrial breakdown and early repair. Immunofluorescence staining revealed that the hypoxic-located LRSC underwent proliferation and was highly colocalized with Notch1. In vitro studies illustrated that hypoxia activated Notch signaling in eMSC, leading to enhanced self-renewal, clonogenicity and proliferation of cells. More importantly, HIF-1α played an essential role in the hypoxia-mediated maintenance of eMSC through the activation of Notch signaling. In conclusion, our findings show that some endometrial stem/progenitor cells reside in a hypoxic niche during menstruation, and hypoxia can regulate the self-renewal activity of eMSC via Notch signaling.

摘要

人类子宫内膜是一种极具活力的组织,在女性生殖期经历周期性的再生和脱落。子宫内膜间质基质/干细胞样细胞(eMSC)有助于这一过程。已有报道称,多种体干细胞类型存在低氧微环境,即低氧水平。然而,关于 eMSC 的缺氧知识仍然有限。在小鼠中,基质干细胞/祖细胞可以通过标记保留技术来鉴定。我们通过模拟月经的小鼠模型,研究了组织分解过程中标记保留的基质细胞(LRSC)与缺氧之间的关系。结果表明,LRSC 在子宫内膜分解和早期修复过程中位于低氧微环境中。免疫荧光染色显示,位于低氧部位的 LRSC 经历了增殖,并且与 Notch1 高度共定位。体外研究表明,缺氧激活了 eMSC 中的 Notch 信号通路,导致细胞的自我更新、克隆形成和增殖增强。更重要的是,HIF-1α 通过激活 Notch 信号通路,在缺氧介导的 eMSC 维持中发挥了重要作用。总之,我们的研究结果表明,一些子宫内膜干细胞/祖细胞在月经期间存在于低氧龛中,而缺氧可以通过 Notch 信号通路调节 eMSC 的自我更新活性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06f8/9104239/a29ff6811715/ijms-23-04613-g001.jpg

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