Suppression of SMOC2 reduces bleomycin (BLM)-induced pulmonary fibrosis by inhibition of TGF-β1/SMADs pathway

Publication date: September 2018Source: Biomedicine & Pharmacotherapy, Volume 105Author(s): Li Luo, Chang-Cheng Wang, Xiao-Ping Song, Hong-Mei Wang, Hui Zhou, Ying Sun, Xiao-Kun Wang, Shuo Hou, Fu-Yang PeiAbstractAlthough the initiation and modulation of lung fibrosis has been widely investigated, the pathogenesis was not well understood. Secreted modular calcium-binding protein 2 (SMOC2) as the secreted protein acidic is enriched in cysteine (SPARC) family of matricellular proteins, which are important in regulating cell-matrix interactions. Here we aimed to calculate the effects and molecular mechanism of SMOC2 on the progression and severity of lung fibrosis in murine bleomycin (BLM)-induced mice. The pulmonary fibrosis was significantly induced by BLM in wild type (WT) C57BL6 mice, as evidenced by the lung sections histology and collagen accumulation using H&E and Masson Trichrome staining. Notably, SMOC2 knockout (SMOC2−/−) mice treated with BLM exhibited the decrease in inflammation accompanied by the reduction of neutrophils, macrophages and lymphocytes in bronchoalveolar lavage fluids (BALF). In addition, the levels of inflammation-associated cytokines and chemokines induced by BLM were also decreased in BALF obtained from SMOC2−/− mice. Meanwhile, SMOC2−/− suppressed the progression of pulmonary fibrosis, as evidenced by the reduction in levels of transforming growth factor-β1 (TGF-β1), α-smooth muscle actin (α-SMA), p-SMAD2 and p-SMAD3 in lung tissue...
Source: Biomedicine and Pharmacotherapy - Category: Drugs & Pharmacology Source Type: research