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Related Experiment Videos

Fibronectin fragments modulate monocyte VLA-5 expression and monocyte migration.

J Trial1, R E Baughn, J N Wygant

  • 1Immunology Research Laboratory and the Research Center for AIDS and HIV-Related Infections, Houston Veterans Affairs Medical Center, Department of Medicine, Baylor College of Medicine, Texas 77030, USA. jtrial@bcm.tmc.edu

The Journal of Clinical Investigation
|August 17, 1999
PubMed
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Myocardial infarction releases fibronectin fragments that degrade the VLA-5 receptor on monocytes. This reduces monocyte migration, causing accumulation in damaged heart tissue.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Extracellular Matrix Research

Background:

  • Monocyte recruitment is crucial in myocardial infarction.
  • Fibronectin (FN) and its receptor VLA-5 (alpha(5)beta(1) integrin) play roles in cell adhesion and migration.
  • Ischemia-reperfusion injury alters the cardiac microenvironment.

Purpose of the Study:

  • To investigate how ischemia-reperfusion injury affects monocyte VLA-5 expression and function.
  • To elucidate the role of fibronectin fragments in monocyte localization within infarcted myocardium.

Main Methods:

  • Studied VLA-5 surface expression and function on monocytes exposed to postreperfusion cardiac lymph.
  • Investigated the effect of purified 120-kDa cell-binding fibronectin fragments (FN120) on VLA-5 expression and monocyte migration.

Related Experiment Videos

  • Assessed monocyte migration on fibronectin-coated matrices in vitro.
  • Correlated findings with in vivo monocyte accumulation in infarcted myocardium.

    • Main Results:

    • Postreperfusion cardiac lymph containing fibronectin fragments reduced VLA-5 expression on monocytes.
    • Purified FN120 fragments induced serine proteinase-dependent proteolysis of VLA-5.
    • FN120 treatment significantly inhibited both spontaneous and MCP-1-induced monocyte migration.
    • Reduced VLA-5 expression correlated with monocyte accumulation in vivo.

    Conclusions:

    • Fibronectin fragments generated during myocardial infarction proteolytically degrade monocyte VLA-5.
    • Altered VLA-5 expression impairs monocyte migration, leading to their accumulation in infarcted areas.
    • This mechanism contributes to the inflammatory response and tissue remodeling post-myocardial infarction.