What question did this study set out to answer?

To determine whether monocyte chemoattractant protein-1 (MCP-1/CCL2) critically regulates inflammatory responses, cellular recruitment, and tissue repair during myocardial infarct healing.

March 18, 2005Circulation Research

CCL2/Monocyte Chemoattractant Protein-1 Regulates Inflammatory Responses Critical to Healing Myocardial Infarcts

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Why the study?

Does MCP-1 gene disruption or antibody neutralization alter inflammatory responses and left ventricular remodeling in a murine model of reperfused myocardial infarction?

Key Points

To determine whether monocyte chemoattractant protein-1 (MCP-1/CCL2) critically regulates inflammatory responses, cellular recruitment, and tissue repair during myocardial infarct healing.
Evaluated the effects of targeted MCP-1 gene knockout (MCP-1-/-) and antibody-mediated neutralization in a closed-chest mouse model of reperfused myocardial infarction.
Analyzed leukocyte infiltration kinetics, cytokine mRNA expression, myofibroblast accumulation, angiogenesis, and post-infarction left ventricular remodeling compared to wild-type controls.
MCP-1-/- mice exhibited delayed and reduced macrophage infiltration, impaired differentiation marked by decreased Osteopontin-1, and prolonged replacement of damaged myocardium with granulation tissue, while neutrophil infiltration remained unaffected.
Deficiency of MCP-1 suppressed mRNA levels of TNF-alpha, IL-1beta, TGF-beta2, TGF-beta3, and IL-10, and diminished myofibroblast accumulation without altering infarct angiogenesis.
Despite delayed clearance of dead cardiomyocytes, MCP-1-deficient mice showed attenuated adverse left ventricular remodeling with an infarct size similar to wild-type animals.

Structured PICO

Does MCP-1 gene disruption or antibody neutralization alter inflammatory responses and left ventricular remodeling in a murine model of reperfused myocardial infarction?

Population

Murine closed-chest model of reperfused myocardial infarction

Intervention

MCP-1 gene disruption (MCP-1-/-) or MCP-1 antibody inhibition

Comparator

Wild-type animals

Outcome

Myocardial infarct healing (macrophage infiltration, granulation tissue replacement, left ventricular remodeling, and infarct size)surrogate

MCP-1 plays a critical role in macrophage recruitment and activation during infarct healing, and its absence attenuates post-infarction left ventricular remodeling despite prolonging the inflammatory phase.

Discussion

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Implication

Hypothesis-generating for MCP-1 targeting to limit post-MI remodeling; leaves open translation to clinical use.

Cite This Study

Dewald et al. (2005) studied this question.

synapsesocial.com/papers/69ffcc4ed1d8b50f8e9a116d https://doi.org/10.1161/01.res.0000163017.13772.3a

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CCL2/Monocyte Chemoattractant Protein-1 Regulates Inflammatory Responses Critical to Healing Myocardial Infarcts

Key Points

Structured PICO

Discussion

Implication

Cite This Study

CCL2/Monocyte Chemoattractant Protein-1 Regulates Inflammatory Responses Critical to Healing Myocardial Infarcts

Key Points

Structured PICO

Discussion

Implication

Cite This Study

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Also Consider