Cardiomyocyte-specific deletion of Senp2 contributes to CVB3 viral replication and inflammation |
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| Institution: | 1. Department of Children''s Genetics and Infectious Diseases Laboratory, Dongguan Institute of Pediatrics, Dongguan, Guangdong 510000, China;2. Department of Respiratory Medicine, Dongguan Children''s Hospital, Dongguan, Guangdong 510000, China;3. The Department of Biochemistry and Molecular & Cell Biology, The Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medical, Shanghai 200025, China |
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| Abstract: | Viral myocarditis (VMC) is characterized by cardiac inflammation and excessive inflammatory responses after viral infection. SENP2, a deSUMO-specific protease, has been reported to regulate antiviral innate immunity. This study aimed to investigate whether SENP2 affects CVB3-induced VMC. We generated a CVB3-induced VMC mouse model in 6-week-old cardiomyocyte-specific Senp2 knockout mice. The mice were sacrificed at days 0, 2, 4 and 6 after CVB3 infection. The survival rate, body weight, myocardial histopathological changes, viral load, cytokine levels and antiviral gene expression in cardiac tissues of both groups were investigated. Our study indicated that the expression of Senp2 in primary cardiomyocytes was upregulated by CVB3 infection. Moreover, deletion of Senp2 in the heart exacerbated CVB3 infection-induced myocarditis, facilitated CVB3 viral replication and downregulated the expression of antiviral proteins. In conclusion, our findings suggest a protective role for SENP2 in CVB3-induced VMC. |
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