Activin A as a Novel Chemokine Induces Migration of L929 Fibroblasts by ERK Signaling in Microfluidic Devices
Author
Jiang, LinglingQi, Yan
Kong, Xianghan
Wang, Runnan
Qi, Jianfei
Lin, Francis
Cui, Xueling
Liu, Zhonghui
Date
2021-05-21Journal
Frontiers in Cell and Developmental BiologyPublisher
Frontiers Media S.A.Type
Article
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Activin A, a member of the transforming growth factor-beta (TGF-β) superfamily, contributes to tissue healing and fibrosis. As the innate tissue cells, fibroblasts also play an important role in wound healing and fibrosis. Herein, this study was aimed to investigate how activin A exhibited regulatory effects on adhesion and migration of fibroblasts. We found that activin A induced the migration of fibroblast cell line L929 cells in transwell chamber and microfluidic device. Activin A also promoted L929 cells adhesion, but did not affect L929 cells viability or proliferation. In addition, activin A induced α-SMA expression and TGF-β1 release, which were factors closely related to tissue fibrosis, but had no effect on IL-6 production, a pro-inflammatory cytokine. Furthermore, activin A elevated calcium levels in L929 cells and increased p-ERK protein levels. Activin A-induced migration of L929 cells was attenuated by ERK inhibitor FR180204. To conclude, these data indicated that activin A as a novel chemokine induced the chemotactic migration of L929 cells via ERK signaling and possessed the pro-fibrosis role. These findings provide a new insight into understanding of activin A in tissue fibrosis.Rights/Terms
Copyright © 2021 Jiang, Qi, Kong, Wang, Qi, Lin, Cui and Liu.Identifier to cite or link to this item
http://hdl.handle.net/10713/15969ae974a485f413a2113503eed53cd6c53
10.3389/fcell.2021.660316
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