MicroRNA-155 attenuates late sepsis-induced cardiac dysfunction through JNK and β-arrestin 2

摘要: // Yu Zhou 1, 2 , Yan Song 3, 1 Zahir Shaikh Hui Li Haiju Zhang Yi Caudle Shouhua Zheng 4 Dan Hu Charles Stuart and Deling Yin Department of Internal Medicine, College East Tennessee State University, Johnson City, TN 37614, USA Neurology, Renmin Hospital Wuhan 430060, China 3 Vascular Surgery, The First Affiliated Zhengzhou 450052, Thyroid Correspondence to: Yin, email: yin@etsu.edu Keywords: microRNA-155, late sepsis, cardiac dysfunction, β-arrestin 2, inflammatory Received: February 09, 2017      Accepted: April 19, Published: May 04, 2017 ABSTRACT Cardiac dysfunction is correlated with detrimental prognosis sepsis contributes to a high risk mortality. After an initial hyperinflammatory reaction, most patients enter protracted state immunosuppression (late sepsis) that alters both innate adaptive immunity. changes function in are not yet known. MicroRNA-155 (miR-155) previously found play important roles regulations immune activation function. In this study, C57BL/6 mice were operated develop into early phases, miR-155 mimic was injected through the tail vein 48 h after cecal ligation puncture (CLP). effect on CLP-induced explored sepsis. We increased expression myocardium protected against evidenced by attenuating sepsis-reduced output enhancing left ventricular systolic also observed markedly reduced infiltration macrophages neutrophils attenuated response via suppression JNK signaling pathway. Moreover, overexpression (Arrb2) exacerbated mortality Furthermore, transfection Arrb2 expression, then restored immunocompetence improved survival septic mice. conclude systemic administration attenuates improves targeting associated mediated immunosuppression.