期刊
ENDOCRINE JOURNAL
卷 69, 期 9, 页码 1117-1129出版社
JAPAN ENDOCRINE SOC
DOI: 10.1507/endocrj.EJ21-0653
关键词
Human umbilical cord mesenchymal stem cell; Exosomes; HCP5; Musashi RNA-binding protein 2; Oestrogen receptor alpha 1
资金
- Hainan Province Science and Technology Special Fund
- Hainan Province Clinical Medical Center
- [ZDYF2020131]
This study found that HCP5 and hucMSCs-exo play important roles in promoting ovarian granulosa cell proliferation and inhibiting cell apoptosis. HCP5 targeted MSI2, leading to increased expression of ESR1 and enhanced proliferation of OGCs.
HCP5 has been reported to be downregulated in ovarian granulosa cells (OGCs) and to facilitate cell proliferation. Human umbilical cord mesenchymal stem cell exosome (hucMSCs-exo) treatment can prevent OGCs apoptosis in vitro. However, the functional mechanism of HCP5 and hucMSCs-exo requires further exploration. Fluorescence-activated cell sorting (FACS) was performed to measure the expression of markers related to hucMSCs. The osteogenic and adipogenic potential of hucMSCs was measured by alkaline phosphatase (ALP) and Alizarin red and by oil red-O staining, respectively. Real-time quantitative polymerase chain reaction (RT-qPCR) and Western blotting were used to detect the mRNA and protein levels, respectively. Cell proliferation and apoptosis were measured by Cell Counting Kit-8 (CCK-8) assay, colony formation assay and flow cytometry. The interaction of HCP5/musashi RNA-binding protein 2 (MSI2) and oestrogen receptor alpha 1 (ESR1) mRNA was analysed using RNA pulldown and RIP assays. HucMSCs and exosomes were successfully isolated and identified. HucMSC-derived exosomes promoted the proliferation of OGCs and ESR1 expression and inhibited cell apoptosis. HCP5 overexpression in exosomes further enhanced these effects. MSI2 knockdown led to the opposite results. HCP5 targeted MSI2, and MSI2 knockdown reduced the decreases in HCP5 and ESR1 expression. Mechanistically, HCP5 in HucMSC-derived exosomes promoted ESR1 expression by binding to MSI2, which promoted the proliferation of OGCs.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据