期刊
IMMUNOLOGY LETTERS
卷 162, 期 1, 页码 18-26出版社
ELSEVIER
DOI: 10.1016/j.imlet.2014.06.008
关键词
Acute respiratory distress syndrome; Acute lung injury; miR-125b
类别
资金
- National Natural Science Foundation of China [81372347, 81370174]
- Shanghai Committee of Science and Technology [134119a4900]
- Shanghai Pudong New Area Academic Leader in Health System [PWRd2010-01]
- Basic Research Program - Shanghai Committee of Science and Technology [11JC1410900]
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. (C) 2014 Elsevier B.V. All rights reserved.
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