ICAM-1 molecular mechanism and genome wide SNP's association studies

Abstract

Macrophages transformed foam cell formation occurs as a result of leukocyte accumulation mediated through intercellular adhesion molecule 1 (ICAM1), vascular cell adhesion molecule 1 (VCAM1), and E-selectin, secreted by inflamed or damaged endothelium. The key molecule is the ICAM-1, member of the adhesion immunoglobulin super family that maps to chromosome 19 p13.2-p13.3 codes for 505 amino acids have five extracellular domains including circulatory leukocytes binding site (primarily monocytes) for recruiting it at the sites of inflammation and the tight adhesion with vascular endothelium for the above mentioned pathogenesis as an initial step. Hence the objective of the current paper is to review the Genome Wide Association (GWA) studies and summarizes its understanding of functional Single Nucleotide Polymorphism (SNP's) of ICAM-1 clinical association to provide better guidance for the clinicians and researchers of the merits, demerits of the current results and direct them to do research on larger number of population for better prospective.

Clinical, biochemical and genetic risk factors for 30-day and 5-year mortality in 518 adult patients subjected to cardiopulmonary bypass during cardiac surgery - the INFLACOR study.

“…Third, we assumed that the SNVs selected for this study were 'functional' genetic variants. However, of the SNPs studied in the INFLACOR study, currently, only ICAM1 rs5498 (Pare et al, 2011;Anbarasan et al, 2015) and TNF rs1800629 (Lee et al, 2012) were verified using GWAS. It therefore remains possible that the other analyzed SNPs are not the functional genetic variants.…”

“…ICAM-1 is a cell surface glycoprotein that belongs to the superfamily of adhesion immunoglobulins. This molecule has five extracellular domains and is typically expressed on endothelial cells and cells of the immune system (Anbarasan et al, 2015). It is crucially involved in neutrophil migration into tissues during acute inflammation and in arteriosclerotic plaque formation (Lyck & Enzmann, 2015).…”

“…The rs5498 A>G SNP studied in the INFLACOR trial is a missense upstream variant in the Exon 6 region and is one of the seven known functional polymorphisms of the ICAM1 gene. This variant causes the Lys469Glu substitution in domain 5 (Anbarasan et al, 2015). The ICAM1 rs5498 SNP was extensively examined in multiple studies for associations with several cardiovascular phenotypes with conflicting results regarding the risk allele.…”

Aspirin modulates the inflammatory response in a thrombus‑stimulated LMVEC model

“…ICAM-1 belongs to an immunoglobulin superfamily, and is a transmembrane, single chain glycoprotein expressed in leukocytes, fibroblasts and epithelial cells (27). ICAM-1 can induce the expression of inflammatory factors, including IL-1α, IL-1β, IL-6 and TNF-α, via signaling pathways involving NF-κB, thereby promoting the development of inflammation (28).…”

Peptide-biofunctionalization of biomaterials for osteochondral tissue regeneration in early stage osteoarthritis: challenges and opportunities

“…Specifically, they present an improved permeability to lipoproteins and other plasma components involved in the increase of the adhesive capacity of leukocyte adhesion molecules (integrins, Lselectin, and platelet endothelial cell adhesion molecule 1 (PECAM-1)) and endothelial adhesion molecules (including vascular cell adhesion molecule (VCAM-1), endothelial intercellular adhesion molecule-1 (ICAM-1), E-selectin and P-selectin). 50 OA is characterized by the presence of several inflammatory cytokines that are known to stimulate ICAM-1 in the synovium. 51,52 On the other hand, VCAM-1, the surface sialoglycoprotein expressed on chondrocytes and synovial fibroblasts, was shown to function as soluble predictor of the long-term risk (~15-year) of knee and hip OA.…”