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Tannic acid modulates fibroblast proliferation and differentiation in response to pro‐fibrotic stimuli
Author(s) -
Pattarayan Dhamotharan,
Sivanantham Ayyanar,
Bethunaickan Ramalingam,
Palanichamy Rajaguru,
Rajasekaran Subbiah
Publication year - 2018
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.26866
Subject(s) - fibroblast , myofibroblast , extracellular matrix , microbiology and biotechnology , matrix metalloproteinase , smad , chemistry , tannic acid , fibrosis , cellular differentiation , cell growth , wound healing , transforming growth factor , biology , cancer research , immunology , pathology , biochemistry , medicine , gene , in vitro , organic chemistry
In response to tissue injury, fibroblasts migrate into the wound, where they undergo proliferation and differentiation. The persistence of these differentiated fibroblasts (myofibroblasts) is associated with excessive scarring in various organs. We aimed to investigate the effects of Tannic acid (TA) on fibroblast proliferation and differentiation, and found that TA inhibited fibroblast differentiation as assessed by reduced expression of α‐smooth muscle actin, N‐cadherin, and type‐1‐collagen. TA also prevented the TGF‐β1‐induced alteration in the expression of two classes of genes involved in the remodeling of extracellular matrix (ECM) proteins, namely matrix metalloproteinases (Mmp‐2 and ‐9) and tissue inhibitors of metalloproteinases (Timp‐1 and ‐3). Further, TA suppressed TGF‐β1‐induced cell proliferation and induced cell cycle arrest at G0/G1 phase via targeting Cyclins expression. Finally, TA exerted its inhibitory effects by decreasing the phosphorylation of Smad and ERK signaling. In sum, our results suggesting that TA may be a potential therapeutic agent for pathological fibrosis.