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Quantification of Monocyte Chemotactic Activity In Vivo and Characterization of Blood Monocyte Derived Macrophages
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Monocyte chemotactic protein 3 is a homing factor for circulating angiogenic cells

Mélanie Bousquenaud1, Chantal Schwartz, Frédérique Léonard

  • 1Laboratory of Cardiovascular Research, Centre de Recherche Public-Santé, 120 route d'Arlon, L1150 Luxembourg, Luxembourg.

Cardiovascular Research
|April 12, 2012
PubMed

Insights

Monocyte chemotactic protein 3 (MCP3) enhances circulating angiogenic cell (CAC) migration and blood vessel formation. This suggests MCP3 could be a therapeutic target for improving cardiac repair after ischemic events.

Area of Science:

  • Cardiovascular Research
  • Cell Biology
  • Immunology

Background:

  • Circulating angiogenic cells (CACs) are crucial for cardiac repair following ischemia.
  • The CXCR4/SDF-1α axis is a primary driver of CAC recruitment to the heart.
  • Existing CXCR4 blockade strategies only partially inhibit CAC mobilization, indicating other mechanisms are involved.

Purpose of the Study:

  • To investigate the role of monocyte chemotactic protein 3 (MCP3) in CAC mobilization and cardiac repair.
  • To determine if MCP3 can induce CAC migration and angiogenesis.

Main Methods:

  • CACs were isolated from peripheral blood mononuclear cells of healthy volunteers.
  • In vitro CAC migration assays were performed using recombinant MCP3 and neutralizing antibodies against chemokine receptors.
  • Flow cytometry was used to confirm chemokine receptor expression on CACs.
  • In vivo angiogenesis was assessed using Matrigel plugs in mice.

Main Results:

  • Recombinant MCP3 significantly increased CAC migration in a dose-dependent manner, an effect inhibited by CCR1-neutralizing antibodies.
  • CCR1 expression was confirmed on the surface of CACs.
  • Macrophage-conditioned medium containing MCP3 also induced CAC migration, partially blocked by CCR1 antibodies.
  • MCP3 stimulated blood vessel formation in vivo, an effect abrogated by anti-CCR1 antibodies.

Conclusions:

  • MCP3 directly stimulates CAC migration via the CCR1 receptor.
  • MCP3 promotes angiogenesis, indicating its potential therapeutic value in cardiac repair.
  • Targeting the MCP3 pathway may offer a novel strategy to enhance cardiac regeneration.
Abstract

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