Attenuation of Sepsis-Induced Cardiomyopathy by Regulation of MicroRNA-23b Is Mediated Through Targeting of MyD88-Mediat
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ORIGINAL ARTICLE
Attenuation of Sepsis-Induced Cardiomyopathy by Regulation of MicroRNA-23b Is Mediated Through Targeting of MyD88-Mediated NF-κB Activation Chao Cao,1,2 Yan Zhang,2 Yanfen Chai,1 Lijun Wang,1 Chengfen Yin,3 Songtao Shou,1 and Heng Jin 1,2,4
Myocardial cell injury or cardiomyopathy is associated with excessive inflammatory response and apoptosis of cardiac myocytes during sepsis. MicroRNA-23b (miR-23b) is a multifunctional miRNA that is considered to regulate immunosuppression in sepsis. The aim of this study was to examine the effect of miR-23b on cardiomyopathy induced by sepsis and to explore the potential mechanism involved. Sprague-Dawley rats were subjected to cecal ligation and puncture (CLP), and the level of miR-23b at different time points was measured by quantitative real-time polymerase chain reaction (qPCR). Then, we overexpressed miR-23b in vivo and in vitro. The rats were subjected to CLP 7 days after transfection. Cardiac function, inflammatory response, and heart tissues were examined 3 days thereafter. In an in vitro experiment, H9C2 cardiomyoblasts were stimulated with lipopolysaccharide (LPS) after transfection of miR-23b, following which apoptosis and the level of NF-κB were analyzed. The expression of miR-23b was upregulated during polymicrobial sepsis, and transfection of miR-23b lentivirus improved the outcome of sepsis-induced cardiomyopathy by attenuating inflammatory responses and protecting Abstract—
Electronic supplementary material The online version of this article (https://doi.org/10.1007/s10753-019-00958-7) contains supplementary material, which is available to authorized users. 1
Department of Emergency Medicine, Tianjin Medical University General Hospital, Tianjin, 300054, China 2 Department of Internal Medicine, The University of Iowa Carver College of Medicine, Iowa City, IA, USA 3 Department of Critical Care Medicine, Tianjin Third Central Hospital, Tianjin, China 4 To whom correspondence should be addressed at Department of Emergency Medicine, Tianjin Medical University General Hospital, Tianjin, 300054, China. E-mail: [email protected];[email protected] ABBREVIATIONS: BNP, Brain natriuretic peptide; CK-MB, Creatine kinase-MB; CLP, Cecal ligation and puncture; CO, Cardiac output; EF, Ejection fraction; ELISA, Enzyme-linked immunosorbent assay; EMSA, Electrophoretic mobility shift assay; ICAM-1, Intercellular cell adhesion molecule 1; LPS, Lipopolysaccharide; MIF, Migration inhibitory factor; miR-23b, MicroRNA-23b; NF-κB, Nuclear factor kappaB; qPCR, Quantitative real-time polymerase chain reaction; SIC, Sepsis-induced cardiomyopathy; TLR, Toll-like receptor; VCAM-1, Vascular cell adhesion molecule 1
0360-3997/19/0000-0001/0 # 2019 Springer Science+Business Media, LLC, part of Springer Nature
Cao, Zhang, Chai, Wang, Yin, Shou, and Jin against histopathological damage. In in vitro experiments, elevated miR-23b inhibited excessive apoptosis of cardiomyocytes, which may be because activation of the NF-κB signaling pathway was inhibited by the decreased lev
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