Related Experiment Video

Updated: Jul 16, 2026

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response
12:50

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response

Published on: September 15, 2017

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

Insights

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.

More Related Videos

Simultaneous Study of the Recruitment of Monocyte Subpopulations Under Flow In Vitro09:16

Simultaneous Study of the Recruitment of Monocyte Subpopulations Under Flow In Vitro

Published on: November 26, 2018

A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation12:55

A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation

Published on: December 9, 2021

Related Concept Videos

Fibronectins Connect Cells with ECM01:25

Fibronectins Connect Cells with ECM

Fibronectin is an adhesive glycoprotein present in the extracellular matrix of embryogenic and adult tissue. These molecules primarily aid in regulating cell motility and attachment. A fibronectin molecule is composed of two identical polypeptide chains attached to each other by a pair of disulfide bonds at the C-terminal.
Both proteoglycans and collagen are attached to fibronectin proteins, which, in turn, are attached to integrin proteins. These integrin proteins interact with transmembrane...
Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
Selectins01:25

Selectins

Cell adhesion is  an essential aspect of multicellularity. While stable cell interactions usually occur between cells of the same type, transient cell interactions occur between cells of different tissue types, such as between neutrophils and endothelial cells. Selectins are one class of cell adhesion molecules (CAMs) that bind carbohydrate ligands to form transient cell adhesion. They are rod-like proteins with a long extracellular part of variable length ending with the lectin domain, which...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.