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Mesenchymal Stem Cell-Derived Exosome Inhibits High Glucose-Induced Fibroblasts Transdifferentiation Via TGF-β1/Smad2/3 Signaling Pathway
Lan Beibei1, Wang Juanjuan1, Shao Lianbo1, Zhang Yu1, Zhou Jin2, Meng Qingyou2, Han Chaoshan1, Zhu Bao1, Zhang Lulu1, Wang Yanli1, Zhang Yuqing1, Li Yangxin1*
1Institute for Cardiovascular Science, Soochow University, Suzhou 215123, China; 2The First Affiliated Hospital, Soochow University, Suzhou 215123, China
Abstract: Cardiac fibrosis is the leading cause of myocardial dysfunction in patients with diabetes. Fibroblasts transdifferentiation into myofibroblasts is a key event in cardiac fibrosis. The purpose of this study was to investigate the mechanism of high glucose-induced fibroblasts transdifferentiation and to find a way to inhibit the transdifferentiation. Our results showed that the level of α-SMA (α-smooth muscle actin) was significantly up-regulated in BJ cells (human dermal fibroblasts) treated with high glucose compared with the normal BJ cells. We found that α-SMA and collagen I protein levels， and the phosphorylation level of Smad2/3 were decreased by SB525334， an inhibitor of TGF-β1 (transforming growth factor-β1) pathway， or TGF-β1 siRNA to inhibit the activation of TGF- β1/Smad2/3 signaling pathway. SB525334 also inhibited the high glucose-induced BJ cells proliferation. Rat bone marrow mesenchymal stem cell-derived exosome (MSC-Exo) inhibited the high glucose-induced expression of α-SMA by decreasing the phosphorylation of Smad2/3. In summary， high glucose-induced fibroblasts transdifferentiation is mediated by TGF-β1/Smad2/3 signaling pathway， which can be inhibited by MSC-Exo.
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