ArticleJournal of virology2004
Coxsackievirus group B type 3 infection upregulates expression of monocyte chemoattractant protein 1 in cardiac myocytes, which leads to enhanced migration of mononuclear cells in viral myocarditis.
Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 66 citations in OpenAlex.
- Cardiomyocyte β-arrestins mediate inflammation and cGAS-STING activation in CVB3 viral myocarditis.American journal of physiology. Heart and circulatory physiology · 2026Article
- Macrophage-derived SPP1 exacerbate myocardial injury by interacting with fibroblasts in viral myocarditis.Biology direct · 2025Article
- Regulatory role of microRNAs in virus-mediated inflammation.Journal of inflammation (London, England) · 2024Review
- The Role of the Immune System in Pathobiology and Therapy of Myocarditis: A Review.Biomedicines · 2024Review
- Immunopathogenesis and immunomodulatory therapy for myocarditis.Science China. Life sciences · 2023Review
- Kruppel-like factor 10 protects against acute viral myocarditis by negatively regulating cardiac MCP-1 expression.Cellular & molecular immunology · 2021Article
- Article
- The Macrophage in Cardiac Homeostasis and Disease: JACC Macrophage in CVD Series (Part 4).Journal of the American College of Cardiology · 2018Review
- MCPIP1 inhibits coxsackievirus B3 replication by targeting viral RNA and negatively regulates virus-induced inflammation.Medical microbiology and immunology · 2018Article
- Gr-1+ Cells Other Than Ly6G+ Neutrophils Limit Virus Replication and Promote Myocardial Inflammation and Fibrosis Following Coxsackievirus B3 Infection of Mice.Frontiers in cellular and infection microbiology · 2018Article
- Mesenchymal Stromal Cells Modulate Monocytes Trafficking in Coxsackievirus B3-Induced Myocarditis.Stem cells translational medicine · 2017Article
- Article
- Effect of AMP-activated protein kinase activation on cardiac fibroblast proliferation induced by coxsackievirus B3.Experimental and therapeutic medicine · 2016Article
- Remission of CVB3-induced myocarditis with Astragaloside IV treatment requires A20 (TNFAIP3) up-regulation.Journal of cellular and molecular medicine · 2015Article
- Induction of a broad spectrum of inflammation-related genes by Coxsackievirus B3 requires Interleukin-1 signaling.Medical microbiology and immunology · 2013Article
- Immunomodulatory effects of mesenchymal stromal cells revisited in the context of inflammatory cardiomyopathy.Stem cells international · 2013Article
- Article
- Effects of yiqi huoxue recipe and Coxsackie virus B type 3 on the expression of ribosomal protein S20 in rat cardiac myocytes.Chinese journal of integrative medicine · 2011Article
- Direct gene transfer with IP-10 mutant ameliorates mouse CVB3-induced myocarditis by blunting Th1 immune responses.PloS one · 2011Article
- Mesenchymal stem cells and inflammatory cardiomyopathy: cardiac homing and beyond.Cardiology research and practice · 2011Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coxsackievirus group B type 3 (CVB3) is an important cause of viral myocarditis. The infiltration of mononuclear cells into the myocardial tissue is one of the key events in viral myocarditis. Immediately after CVB3 infects the heart, the expression of chemokine(s) by infected myocardial cells may be the first trigger for inflammatory infiltration and immune response. However, it is unknown whether CVB3 can induce the chemokine expression in cardiac myocytes. Monocyte chemoattractant protein 1 (MCP-1) is a potent chemokine that stimulates the migration of mononuclear cells. The objective of the present study was to investigate the effect of CVB3 infection on MCP-1 expression in murine cardiac myocytes and the role of MCP-1 in migration of mononuclear cells in viral myocarditis. Our results showed that the expression of MCP-1 was significantly increased in cardiac myocytes after wild-type CVB3 infection in a time- and dose-dependent manner, which resulted in enhanced migration of mononuclear cells in mice with viral myocarditis. The migration of mononuclear cells was partially abolished by antibodies specific for MCP-1 in vivo and in vitro. Administration of anti-MCP-1 antibody prevented infiltration of mononuclear cells bearing the MCP-1 receptor CCR2 in mice with viral myocarditis. Infection by UV-irradiated CVB3 induced rapid and transient expression of MCP-1 in cardiac myocytes. In conclusion, our results indicate that CVB3 infection stimulates the expression of MCP-1 in myocardial cells, which subsequently leads to migration of mononuclear cells in viral myocarditis.
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