Title: Rapamycin reverses connexin 43 impairment in human herpes simplex virus-1 viral myocarditis

Authors: Zidun Wang, Xiaofeng Hou, Libin Qiu, Jingcheng Chen, Xiaorong Li, Kai Gu, Fengxiang Zhang, Bing Yang, Minglong Chen, Kejiang Cao

Institution: Department of Cardiology, the First Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu 210036, China.

Abstract: We sought to observe the electrophysiology associated protein connexin 43 (Cx43) impairment in an in vitro cell model of HSV-1 viral myocarditis, and to preliminarily investigate the therapeutic effect of rapamycin on electrophysiological function in the same model. Harvested from the Vero cells, HSV-1 virion-supernatants in­fected neonatal rat ventricular cardiomyocytes (NRVM) in different plaque-forming units (PFU). Cytopathic ef­fect (CPE) of NRVM was observed post-infection. The expression of Cx43 was evaluated by Western blotting assay and RT-PCR. The effect of rapamycin on Cx43 expression and some key proteins of Akt signaling pathway were detected by Western blotting assay. Post-infection, CPE was appeared in the infected NRVM, and the HSV- 1 specific product glycoprotein D (HSV-1 gD) was detected by Western blotting assay. The Cx43 expression was down-regulated by HSV-1 post-infection, and rapamycin pre-treatment could reverse Cx43 impairment by the down-regulation of Akt signaling pathway. HSV-1 could infect the NRVM, and down-regulate the targeted cells Cx43 expression level. Rapamycin could reverse such electrophysiologic impairment by up-regulating Cx43 ex­pression and Akt signaling inhibition.

Keywords: viral myocarditis, herpes simplex virus-1, connexin 43, rapamycin, Akt signaling pathway

Full Text: PDFJBR-2013-0020.pdf

J Biomed Res published on June 12th, 2013, doi:10.7555/JBR.27. 20130020