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Expression of intercellular adhesion molecule-1 on rat cardiac myocytes by monocyte chemoattractant protein-1
1Jichi Medical School, Tochigi, Japan.
Insights
Monocyte chemoattractant protein-1 (MCP-1) produced by cardiac myocytes promotes neutrophil adhesion via intercellular adhesion molecule-1 (ICAM-1), suggesting MCP-1's role in cardiac inflammation.
Area of Science:
- Cardiovascular Biology
- Immunology
- Molecular Biology
Background:
- Cardiac inflammation is implicated in myocardial infarction and myocarditis.
- Intercellular adhesion molecule-1 (ICAM-1) on cardiac myocytes may play a role in this inflammation.
- Monocyte chemoattractant protein-1 (MCP-1) is a potential mediator in this process.
Purpose of the Study:
- To investigate the role of monocyte chemoattractant protein-1 (MCP-1) in neutrophil-myocyte adhesion in vitro.
- To determine if MCP-1 influences intercellular adhesion molecule-1 (ICAM-1) expression on cardiac myocytes.
Main Methods:
- Cultured neonatal rat cardiac myocytes were analyzed for MCP-1/JE and ICAM-1 mRNA expression using northern blot.
- ICAM-1 protein levels were quantified by ELISA.
- Neutrophil-myocyte adherence assays were performed.
- Stimulation with interleukin-1 alpha, lipopolysaccharide, and hypoxia was used.
Main Results:
- MCP-1/JE transcripts were induced in myocytes by interleukin-1 alpha, lipopolysaccharide, or hypoxia.
- MCP-1 dose-dependently increased ICAM-1 expression on cardiac myocytes, detectable as early as 6 hours.
- MCP-1 significantly enhanced neutrophil adhesion to cardiac myocytes, an effect blocked by an anti-ICAM-1 antibody.
Conclusions:
- Cardiac myocytes produce MCP-1.
- MCP-1 promotes neutrophil adhesion to cardiac myocytes through ICAM-1.
- MCP-1 is implicated in cardiac inflammation associated with myocardial infarction and myocarditis.
Objective:
Cytokine induction of intercellular adhesion molecule-1 (ICAM-1) on cardiac myocytes may be a critical step in cardiac inflammation associated with acute myocardial infarction and myocarditis. The aim of this study was to investigate the involvement of monocyte chemoattractant protein-1 (MCP-1), a homologue of mouse JE, in the neutrophil-myocyte adhesion in vitro.
Methods:
MCP-1/JE and ICAM-1 mRNA expression in cultured neonatal rat cardiac myocytes was evaluated by northern blot analysis. ICAM-1 molecule content on myocytes was determined by ELISA. For adherence assay, myocytes and neutrophils were co-incubated and the number of bounded neutrophils was counted.
Results:
MCP-1/JE transcripts were not clearly observed in cultured neonatal rat cardiac myocytes; however, its transcripts were clearly detected by exposure to interleukin 1 alpha (100 U.ml-1), lipopolysaccharide (1 microgram.ml-1), or hypoxia (95% N2 + 5% CO2). In ELISA analysis, the expression of ICAM-1 molecules on cardiac myocytes was significantly stimulated by MCP-1 in a dose dependent manner, and the effect of MCP-1 was observed as early as at 6 h. In northern blot analysis, ICAM-1 mRNA expression was constitutively observed in myocytes, and the expression was markedly stimulated by exposure to MCP-1 with a peak elevation at 2 h. In adherence assay, MCP-1 stimulated the adhesion of rat neutrophils to rat cardiac myocytes, and this effect of MCP-1 was inhibited by an anti-ICAM-1 MAb.
Conclusions:
These results suggest that cardiac myocytes produce MCP-1, which could in turn promote the adhesion of neutrophils to myocytes via ICAM-1 expression, suggesting the involvement of MCP-1 in cardiac inflammation associated with acute myocardial infarction and myocarditis.
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