Enforced expression of miR-125b attenuates LPS-induced acute lung injury.


The acute respiratory distress syndrome (ARDS), a severe form of acute lung injury (ALI) in humans, is a leading cause of morbidity and mortality in critically ill patients. Despite decades of research, few therapeutic strategies for clinical ARDS have emerged. Recent evidence implicated a potential role of miR-125b in development of ALI. Here we evaluated the miR-125b-based strategy in treatment of ARDS using the murine model of lipopolysaccharide (LPS)-induced ALI. We found that up-regulation of miR-125b expression maintained the body weight and survival of ALI mice, and significantly reduced LPS-induced pulmonary inflammation as reflected by reductions in total cell and neutrophil counts, proinflammatory cytokines, as well as chemokines in BAL fluid. Further, enforced expression of miR-125b resulted in remarkable reversal of LPS-induced increases in lung permeability as assessed by reductions in total protein, albumin and IgM in BAL fluid, and ameliorated the histopathology changes of lung in LPS-induced ALI mice. Of interest, serum miR-125b expression was also decreased and inversely correlated with the disease severity in patients with ARDS. Our findings strongly demonstrated that enforced expression of miR-125b could effectively ameliorate the LPS-induced ALI, suggesting a potential application for miR-125b-based therapy to treat clinical ARDS.

DOI: 10.1016/j.imlet.2014.06.008

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@article{Guo2014EnforcedEO, title={Enforced expression of miR-125b attenuates LPS-induced acute lung injury.}, author={Zhongliang Guo and Yutong Gu and Chunhong Wang and Jie Zhang and Shan Shan and Xia Gu and Kailing Wang and Yang Han and Tao Ren}, journal={Immunology letters}, year={2014}, volume={162 1 Pt A}, pages={18-26} }