期刊
JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY
卷 31, 期 5, 页码 -出版社
WILEY
DOI: 10.1002/jbt.21879
关键词
fibrosis; Galectin-3; pulmonary adventitial fibroblasts; TGF-beta 1
资金
- National Natural Science Foundation of China (Youth Fund) [81300036, 31600956]
- Heilongjiang Postdoctoral Startup Fund [LBH-Q15077]
- University Nursing Program for Young Scholars with Creative Talents in Heilongjiang Province [UNPYSCT-2015035]
- Scientific Research Project of Health and Family Commission of Heilongjiang Province [2014-433]
- Guiding Science and Technology plan project of the city of Daqing [szdy-2015-01]
Galectin-3 (Gal-3) plays a critical role in vascular inflammation and fibrosis. The role of TGF-beta 1 in mediating pulmonary vascular fibrosis is well documented; thus, we suspected that Gal-3 could be an important factor in TGF-beta 1-induced fibrosis in pulmonary adventitial fibroblasts (PAFs). We treated rats with monocrotaline (MCT) and cultured PAFs with TGF-beta 1 to stimulate fibrosis. We found that MCT injection induced vessel thickening and extracellular matrix deposition in vivo. TGF-beta 1 stimulated the production of collagen and fibronectin (Fn) protein in vitro. TGF-beta 1 promoted the expression of Gal-3 and its translocation, while silencing Gal-3 reduced Col-1a deposition. Blockage of STAT3 decreased the expression of Gal-3 induced by TGF-beta 1. Gal-3 increased Col-1a accumulation and downregulated matrix metallopeptidase 9 (MMP-9) expression in PAFs, but it did not affect Fn expression. These findings demonstrate that Gal-3 is required for TGF-beta 1-stimulated vascular fibrosis via a STAT3 signaling cascade and that MMP-9 is also involved in TGF-beta 1/ Gal-3-induced vascular fibrosis.
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