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摘要
Purpose: The main aim of the present study was to establish whether mesenchymal stem cell microvesicles (MSC MVs) exert antifibrotic effects and investigate the mechanisms underlying these effects in a mouse model of acute respiratory distress syndrome @@@ Methods: An ARDS-associated pulmonary fibrosis model was established in mice by an intratracheal injection of lipopolysaccharide (LPS). At 1, 3, and 7 days after LPS-mediated injury, the lungs of mice treated with MSC MVs and untreated controls were carefully excised and fibrosis was assessed based on the extent of collagen deposition. In addition, the development of epithelial-mesenchymal transition (EMT) was evaluated based on loss of E-cadherin and zona occludens-1 (ZO-1) along with the acquisition of alpha-smooth muscle actin (alpha-SMA) and N-cadherin. Nuclear translocation and beta-catenin expression analyses were also used to evaluate activation of the Wnt/beta-catenin signaling pathway. @@@ Results: Blue-stained collagen fibers were evident as early as 7 days after LPS injection. Treatment with MSC MVs suppressed pathological progression to a significant extent. MSC MVs markedly reversed the upregulation of N-cadherin and alpha-SMA and attenuated the downregulation of E-cadherin and ZO-1. The expression and nuclear translocation of beta-catenin were clearly decreased on day 7 after MSC MV treatment. @@@ Conclusion: Analyses indicated that MSC MVs could ameliorate ARDS-associated early pulmonary fibrosis via the suppression of EMT and might be related to Wnt/beta-catenin transition signaling.y
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单位南方医科大学; 中国科学院研究生院
