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PM2.5 collecting in a tire manufacturing plant affects epithelial differentiation of human umbilical cord derived mesenchymal stem cells by Wnt/beta-catenin pathway  ( SCI-EXPANDED收录)   被引量:4

文献类型:期刊文献

英文题名:PM2.5 collecting in a tire manufacturing plant affects epithelial differentiation of human umbilical cord derived mesenchymal stem cells by Wnt/beta-catenin pathway

作者:Yan, Junyan[1];Jin, Lifang[1];Lin, Derong[2];Lai, Chia-Hsiang[3];Xu, Zhongjuan[4];Wang, Renjun[5];Chen, Yi-Chun[6];Hu, Baowei[1];Lin, Chia-Hua[6]

机构:[1]Shaoxing Univ, Sch Life Sci, Shaoxing, Zhejiang, Peoples R China;[2]Shaoxing Second Hosp, Shaoxing, Zhejiang, Peoples R China;[3]Cent Taiwan Univ Sci & Technol, Dept Safety Hlth & Environm Engn, Taichung, Taiwan;[4]Chinese Acad Sci, Suzhou Inst Nanotech & Nanobion, Div Nanobiomed, Key Lab Nanobio Interface, Suzhou, Peoples R China;[5]Qufu Normal Univ, Coll Life Sci, Qufu, Shandong, Peoples R China;[6]Natl Formosa Univ, Dept Biotechnol, Huwei, Yunlin, Taiwan

年份:2020

卷号:244

外文期刊名:CHEMOSPHERE

收录:SCI-EXPANDED(收录号:WOS:000515197700053)、、WOS

基金:This work has been generously supported by the Research Fund Program of National Natural Science Foundation of China (No. 21876115), as well the scientific research start-up funding of Shaoxing University (No. 20185009).

语种:英文

外文关键词:Fine particulate matter (PM2.5); Human umbilical cord derived mesenchymal stem cell (hUCMSC); Wnt/beta-catenin pathway; Epithelial differentiation

外文摘要:Mesenchymal stem cells (MSCs) can differentiate into pulmonary epithelial cells by Wnt/beta-catenin pathway and promote lung repair. However, whether fine particulate matter (PM2.5) could affect Wnt pathway and finally reduce the ability of MSCs to differentiate into epithelial cells is still unknown. This study aimed to investigate whether PM2.5 could inhibit the epithelial differentiation of human umbilical cord-derived MSCs cells (hUCMSCs) and the related underlying mechanism. hUCMSCs were incubated with different concentrations of PM2.5. Then, the cell viability, reactive oxygen species level, and single-cell sphere formation were assessed. The underlying mechanism of PM2.5 in epithelial differentiation of hUCMSCs was further evaluated by co-culturing hUCMSCs with A549 cells. Our results demonstrated that PM2.5 exposures could affect the expressions of beta-catenin and lung epithelial markers (zonula occludens-1 (ZO-1); cytokeratins 5 and 19) in the co-cultured hUCMSCs. The Wnt/beta-catenin pathway is involved in regulating the epithelial differentiation of MSCs. As expected, co-treatment with Wnt3a, which is the activator of the Wnt pathway, attenuated the downregulation of lung epithelial markers (ZO-1; cytokeratins 5 and 19) and paracrine factors (keratinocyte growth factor and hepatocyte growth factor) caused by PM2.5. Altogether, these results demonstrated that PM2.5 could affect the epithelial differentiation of hUCMSCs via the Wnt/beta-catenin pathway. (C) 2019 Elsevier Ltd. All rights reserved.

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