Blood-Brain Barrier and Immune Cell Transmigration: VCAM-1/CD106 Signaling Pathways
Click on one of the other molecules below to see the signaling pathways activated by that molecule and the changes it induces in the integrity of the blood-brain barrier (BBB). Click on Overview to see the generalized process of immune cell transmigration across the BBB during neuroinflammation.
Get Print Copy(VLA-4)
(VLA-4)
(LFA-1)
(LFA-1)
Ca2+ Channel
Ca2+ Channel
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Stress Fiber Formation
Increased Centripetal Tension
Cell Retraction
Stress Fiber Formation
Increased Centripetal Tension
Cell Retraction
Oxidase
Oxidase
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MMP-9
MMP-9
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Tight Junction Protein
Degradation
Tight Junction Protein
Degradation
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Receptor Endocytosis
Receptor Endocytosis
Overview of VCAM-1/CD106 Signaling and its Primary Biological Effects in Brain Endothelial Cells
The BBB is a selective diffusion barrier that is composed of specialized endothelial cells (ECs) that are linked by tight junctions (TJs) and adherens junctions (AJs). These junction complexes can be remodeled during neuroinflammation to form interendothelial gaps that peripheral immune cells will pass through to enter the central nervous system (CNS). Engagement of adhesion molecules on the surface of ECs by leukocyte integrins activates diverse signaling pathways in ECs that result in the dynamic reorganization of junction complexes and EC retraction. Vascular Cell Adhesion Molecule 1 (VCAM-1/CD106) is an Ig-like adhesion receptor that binds the leukocyte Integrin alpha 4 beta 1 (VLA-4). This induces clustering of VCAM-1/CD106 and activation of intracellular signaling pathways that induce phosphorylation of TJ proteins, resulting in their disassembly and/or redistribution from the cell border. Additionally, VCAM-1/CD106 signaling promotes the production of matrix metalloproteases (MMPs) that degrade junction proteins. VCAM-1/CD54 signaling also induces reorganization of F-Actin microfilaments into stress fibers, which increases centripetal tension inside the cell resulting in cell retraction.
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