期刊
CNS & NEUROLOGICAL DISORDERS-DRUG TARGETS
卷 12, 期 3, 页码 392-404出版社
BENTHAM SCIENCE PUBL
DOI: 10.2174/1871527311312030012
关键词
Adhesion molecule; CNS disorders; leukocyte adhesion cascade; vascular adhesion protein-1
资金
- NIH [R01 NS060936, R01 NS053407]
Mounting evidence has been provided regarding the crucial role of leukocyte extravasation and subsequent inflammatory response in several central nervous system (CNS) disorders. The infiltrated leukocytes release pro-inflammatory mediators and activate resident cells, leading to tissue injury. Leukocyte-endothelia interaction is critical for leukocyte extravasation and migration from the intravascular space into the tissue during inflammation. The basic physiology of leukocyte-endothelia interaction has been investigated extensively. Traditionally, three kinds of adhesion molecules, selectin, integrin, and immunoglobulin families, are responsible for this multiple-step interaction. Furthermore, blocking adhesion molecule function by genetic knockout, antagonizing antibodies, or inhibitory pharmacological drugs provides neuroprotection, which is associated with a reduction in leukocyte accumulation within the tissue. Detection of the soluble form of adhesion molecules has also been proven to predict outcomes in CNS disorders. Lately, vascular adhesion protein-1, a novel adhesion molecule and endothelial cell surface enzyme, has been implicated as a brake in the rolling step of the adhesion cascade, and also a regulator of leukocyte transmigration step. In this review, we summarize the functions of traditional adhesion molecules as well as vascular adhesion protein-1 in the leukocyte adhesion cascade. We also discuss the diagnostic and therapeutic potential of adhesion molecules in CNS disorders.
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