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Smurf2诱导的SMAD2降解导致毛囊干细胞分化受到抑制。

Smurf2-induced degradation of SMAD2 causes inhibition of hair follicle stem cell differentiation.

作者信息

Lin Bojie, Huang Dan, Lin Guanyu, Miao Yong, Wang Jin, Fan Zhexiang, Hu Zhiqi

机构信息

Department of Plastic and Aesthetic Surgery, Guangxi Key Laboratory of Enhanced Recovery after Surgery for Gastrointestinal Cancer, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, PR China.

Department of Plastic and Aesthetic Surgery, Nanfang Hospital of Southern Medical University, Guangzhou, 510515, PR China.

出版信息

Cell Death Discov. 2022 Apr 4;8(1):160. doi: 10.1038/s41420-022-00920-x.

DOI:10.1038/s41420-022-00920-x
PMID:35379779
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8980066/
Abstract

Hair follicle stem cells (HFSCs) are implicated in the formation of hair follicles and epidermis. This study aims to clarify the role of SMAD2 in regulating the differentiation of HFSCs, which is involved with Smurf2. Functional assays were carried out in human HFSCs to assess the effect of SMAD2 and Smurf2 with altered expression on growth dynamics of HFSCs. Ubiquitination of SMAD2 and its protein stability were assessed. The binding relationship between NANOG and DNMT1 was assessed. A mouse skin wound model was induced to verify the effects of Smurf2/SMAD2/NANOG/DNMT1 on wound healing. SMAD2 overexpression was observed in HFSCs during differentiation and its ectopic expression contributed to promotion of differentiation and apoptosis of HFSCs while arresting cell proliferation. Mechanistic investigations indicated that Smurf2 promoted the ubiquitination and degradation of SMAD2, thus causing downregulation of SMAD2 expression. By this mechanism, NANOG expression was reduced and the subsequent DNMT1 transcriptional expression was also diminished, leading to suppression of differentiation and apoptosis of HFSCs while stimulating cell proliferation. Moreover, in vivo data showed that Smurf2 upregulation limited epidermal wound healing in mice by inhibiting the SMAD2/NANOG/DNMT1 axis. Our work proposed a potential target regarding SMAD2 restoration in promoting HFSC differentiation and skin wound healing.

摘要

毛囊干细胞（HFSCs）与毛囊和表皮的形成有关。本研究旨在阐明SMAD2在调节HFSCs分化中的作用，这与Smurf2有关。在人HFSCs中进行功能测定，以评估表达改变的SMAD2和Smurf2对HFSCs生长动力学的影响。评估了SMAD2的泛素化及其蛋白质稳定性。评估了NANOG与DNMT1之间的结合关系。诱导建立小鼠皮肤伤口模型，以验证Smurf2/SMAD2/NANOG/DNMT1对伤口愈合的影响。在HFSCs分化过程中观察到SMAD2过表达，其异位表达促进了HFSCs的分化和凋亡，同时抑制细胞增殖。机制研究表明，Smurf2促进了SMAD2的泛素化和降解，从而导致SMAD2表达下调。通过这种机制，NANOG表达降低，随后DNMT1的转录表达也减少，导致HFSCs的分化和凋亡受到抑制，同时刺激细胞增殖。此外，体内数据表明，Smurf2上调通过抑制SMAD2/NANOG/DNMT1轴限制了小鼠表皮伤口愈合。我们的工作提出了一个关于恢复SMAD2以促进HFSC分化和皮肤伤口愈合的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5a8/8980066/76360d65056a/41420_2022_920_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5a8/8980066/4ff2ba0db922/41420_2022_920_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5a8/8980066/5b59501963b0/41420_2022_920_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5a8/8980066/00b940c279ed/41420_2022_920_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5a8/8980066/058361590efb/41420_2022_920_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5a8/8980066/d2c90aac3e89/41420_2022_920_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5a8/8980066/330c56fc6332/41420_2022_920_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5a8/8980066/76360d65056a/41420_2022_920_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5a8/8980066/4ff2ba0db922/41420_2022_920_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5a8/8980066/5b59501963b0/41420_2022_920_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5a8/8980066/00b940c279ed/41420_2022_920_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5a8/8980066/058361590efb/41420_2022_920_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5a8/8980066/d2c90aac3e89/41420_2022_920_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5a8/8980066/330c56fc6332/41420_2022_920_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5a8/8980066/76360d65056a/41420_2022_920_Fig7_HTML.jpg

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TNF-α suppresses sweat gland differentiation of MSCs by reducing FTO-mediated mA-demethylation of Nanog mRNA.TNF-α 通过减少 FTO 介导的 Nanog mRNA 的 mA 去甲基化来抑制 MSC 的汗腺分化。
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BMP2-mediated PTEN enhancement promotes differentiation of hair follicle stem cells by inducing autophagy.
BMP2 介导的 PTEN 增强通过诱导自噬促进毛囊干细胞的分化。
Exp Cell Res. 2019 Dec 15;385(2):111647. doi: 10.1016/j.yexcr.2019.111647. Epub 2019 Sep 25.
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PBX homeobox 1 enhances hair follicle mesenchymal stem cell proliferation and reprogramming through activation of the AKT/glycogen synthase kinase signaling pathway and suppression of apoptosis. PBX 同源盒 1 通过激活 AKT/糖原合酶激酶信号通路和抑制细胞凋亡来增强毛囊间充质干细胞的增殖和重编程。
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