Kruppel-like factor 10 protects against acute viral myocarditis by negatively regulating cardiac MCP-1 expression.

In this study, we report that cardiac KLF10 confers enhanced protection against viral myocarditis. We found that KLF10 expression was downregulated upon CVB3 infection. KLF10 deficiency enhanced cardiac viral replication and aggravated VMC progress. Bone marrow chimera experiments indicated that KLF10 expression in nonhematopoietic cells was involved in the pathogenesis of VMC. We further identified MCP-1 as a novel target of KLF10 in cardiomyocytes, and KLF10 cooperated with histone deacetylase 1 (HDAC1) to negatively regulate MCP-1 expression by binding its promoter, leading to activation of MCP-1 transcription and recruitment of Ly6Chigh monocytes/macrophages into the myocardium. This novel mechanism of MCP-1 regulation by KLF10 might provide new insights into the pathogenesis of VMC and a potential therapeutic target for VMC.
PMID: 32895486 [PubMed - as supplied by publisher]

Source: Cellular and Molecular Immunology - September 6, 2020 Category: Molecular Biology Authors: Yang J, Zhang H, Wang X, Guo J, Wei L, Song Y, Luo Y, Zhao Y, Subramaniam M, Spelsberg TC, Wang L, Xu W, Li M Tags: Cell Mol Immunol Source Type: research