Abstract
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.
Highlights
Fibroblasts are widely distributed in various tissues and actively involved in tissue damage repair, remodeling and fibrosis
We found that activin A promoted L929 cell adhesion, migration and TGF-β1 release in a dose-dependent manner, proving further that activin A was a chemokine for fibroblasts in the process of tissue repair and fibrosis
The results showed that activin A significantly promoted the adhesion of L929 cells in a dose-dependent manner (Figure 1A)
Summary
Fibroblasts are widely distributed in various tissues and actively involved in tissue damage repair, remodeling and fibrosis. Fibroblasts are involved in tissue remodeling in the late stage of inflammation through cell proliferation, adhesion, migration and collagen synthesis (Sun et al, 2014; Burr et al, 2020), while abnormal activation of fibroblasts may result in scar formation and tissue fibrosis (Bai et al, 2015; Nagpal et al, 2016). Activin A regulates cell proliferation, differentiation, apoptosis and migration in an autocrine/paracrine manner, and plays a critical role in embryonic development, neuroprotection, tissue remodeling and immune response (Aleman-Muench and Soldevila, 2012; van den Ameele et al, 2012; Kaiser et al, 2013; Donovan et al, 2017). As an important factor in inducing liver, kidney and lung fibrosis, activin A is reported to be tightly associated with the occurrence and development of numerous fibrotic diseases (Hardy et al, 2015; Hruska et al, 2017; Zhang et al, 2018)
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