MEF2C alleviates acute lung injury in cecal ligation and puncture (CLP)-induced sepsis rats by up-regulating AQP1

• Wenmei Liang ^[1] ; Li Guo ^[2] ; Tonghua Liu ^[1] ; Song Qin ^[1]
  1. [1] Department of Critical Care Medicine, The Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou 563000, China.
  2. [2] Department of Critical Care Medicine, Zhongshan Torch Development Zone Hospital, Zhongshan, Guangdong 528437, China.
• Localización: Allergologia et immunopathologia: International journal for clinical and investigate allergology and clinical immunology, ISSN-e 1578-1267, ISSN 0301-0546, Vol. 49, Nº. 5, 2021, págs. 117-124
• Idioma: inglés
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• Resumen

  • Background Sepsis is a systemic inflammatory response syndrome and leads to patient’s death. Objective: To investigate the effect of myocyte enhancer factor 2 (MEF2C) on acute lung injury (ALI) with sepsis and its possible mechanism.

    Material and Methods The cecal ligation and puncture (CLP)-induced sepsis rat model was established. The lung injury was determined by lung wet–dry weight ratio, the concentration of inflammatory cytokines, including tumor necrosis factor-α (TNF-α), Interlukin (IL)-6, IL-1β, and IL-10, were measured by the enzyme-linked-immunosorbent serologic assay kit. The cell apoptosis was detected by TUNEL staining assay.

    Results Interestingly, MEF2C was down-regulated in this model. Moreover, adeno-associated virus (AAV)-MEF2C treatment markedly suppressed TNF-α, IL-1β, and IL-6 concentrations but promoted IL-10 concentration in serum in CLP-challenged rats. Besides, overexpression of MEF2C alleviates CLP-induced lung injury. Interestingly, AAV-MEF2C treatment was confirmed to suppress apoptosis in CLP-induced sepsis rats as well as promote aquaporin APQ1 expression. Mechanistically, the rescue experiments indicated that MEF2C alleviated CLP-induced lung inflammatory response and apoptosis via up-regulating AQP1.

    Conclusion In summary, overexpression of MEF2C suppressed CLP-induced lung inflammatory response and apoptosis via up-regulating AQP1, providing a novel therapeutic target for sepsis-induced ALI.