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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
Summary
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.
- 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.
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