Arteriogenesis Proceeds via ICAM-1/Mac-1- Mediated Mechanisms

Arteriogenesis proceeds via ICAM-1/Mac-1- mediated mechanisms.

Monocyte adhesion to shear stress-activated endothelium stands as an important initial step during arteriogenesis (collateral artery growth). Using multiple approaches, we tested the hypothesis that monocyte adhesion via intercellular adhesion molecule-1 (ICAM-1) and selectin interactions is essential for adaptive arteriogenesis. Forty-eight New Zealand White rabbits received either solvent, mo...

Mechanisms of arteriogenesis.

Patients with occlusive atherosclerotic vascular diseases have frequently developed collateral blood vessels that bypass areas of arterial obstructions. The growth of these collateral arteries has been termed "arteriogenesis" which describes the process of a small arteriole's transformation into a much larger conductance artery. In recent years, intensive investigations using various animal mod...

Mechanisms of receptor-mediated rhinovirus neutralization defined by two soluble forms of ICAM-1.

The majority of human rhinoviruses use intercellular adhesion molecule 1 (ICAM-1) as a cell surface receptor. Two soluble forms of ICAM-1, one corresponding to the entire extracellular portion [tICAM(453)] and one corresponding to the two N-terminal immunoglobulin-like domains [tICAM(185)], have been produced, and their effects on virus-receptor binding, virus infectivity, and virus integrity h...

Leukocyte-endothelial cell interactions are linked to vascular permeability via ICAM-1-mediated signaling.

Two key characteristics of the inflammatory response are the recruitment of leukocytes to inflamed tissue as well as changes in vessel permeability. We explored the relationship between these two processes using intravital confocal microscopy in cremasters of anesthetized (65 mg/kg Nembutal ip) mice. We provide direct evidence that intercellular adhesion molecule-1 (ICAM-1) links leukocyte-endo...

LFA-1-Mediated Cell Binding to ICAM-1 Glycoprotein Ligand-1 Stimulates Rolling of Th1 Cells via P-Selectin