Abstract:
:The differentiation of atrial fibroblasts into myofibroblasts is a critical event in atrial fibrosis. One of the most important factors in atrial fibroblast differentiation is transforming growth factor-β1 (TGF-β1). Accumulating evidence indicates that sodium tanshinone IIA sulfonate (STS) possesses antifibrotic properties. In this study, we therefore investigated whether STS attenuates the TGF-β1‑induced differentiation of atrial fibroblasts. TGF-β1 enhanced collagen production, collagen synthesis and the expression of collagen type I and III, as shown by hydroxyproline assay, collagen synthesis assay and western blot analysis, respectively. In addition, as shown by immunohistochemistry and western blot analysis, TGF-β1 enhanced the expression of α-smooth muscle actin (α-SMA), which is the hallmark of myofibroblast differentiation. These responses were attenuated by treatment with STS. In addition, STS suppressed the TGF-β1‑induced expression of phosphorylated (p)Smad/pSmad3 expression and nuclear translocation. Furthermore, STS suppressed extracellular signal-regulated kinase (ERK) phosphorylation. In conclusion, the current study demonstrates that STS exerts antifibrotic effects by modulating atrial fibroblast differentiation through ERK phosphorylation and the Smad pathway.
journal_name
Int J Mol Medjournal_title
International journal of molecular medicineauthors
Yang L,Hu J,Hao HZ,Yin Z,Liu G,Zou XJdoi
10.3892/ijmm.2015.2087subject
Has Abstractpub_date
2015-04-01 00:00:00pages
1026-32issue
4eissn
1107-3756issn
1791-244Xjournal_volume
35pub_type
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