Serum
Adhesion Molecule Levels in Acute Coronary Syndrome Among Indonesian Patients.
Abbreviations: HAECs, human aortic endothelial cells; TNF-[alpha], tumor necrosis factor-[alpha]; CAMs, cell
adhesion molecules; sCAMs, soluble form of cell
adhesion molecules; ICAM-1, intercellular adhesion molecule-1; VCAM-1, vascular cell adhesion molecule-1; PECAM-1, platelet endothelial cell adhesion molecule-1; sE-selectin, soluble E-selectin; sICAM-1, soluble ICAM-1; sVCAM-1, soluble VCAM-1; sPECAM-1, soluble PECAM-1; NF-[kappa]B, nuclear factor-[kappa]B; 1[kappa]B[alpha], inhibitor of NF-[kappa]B alpha; FITC-dextran, fluorescein isothiocyanate conjugated-dextran.
Lin et al., "SHP1 phosphatase-dependent T cell inhibition by CEACAM1
adhesion molecule isoforms," Immunity, vol.
Wang et al., "Induction of heme oxy-genase 1 and inhibition of tumor necrosis factor alpha-induced intercellular
adhesion molecule expression by andrographolide in EA.hy926 cells," Journal of Agricultural and Food Chemistry, vol.
Endothelial
adhesion molecules are associated with inflammation in subjects with HIV disease.
Adhesion molecules also have a role; Th1 cells express selectin ligands abundantly.
Chemokines are upregulated and increased expression of
adhesion molecules is evident.
Similar results have been described in a previous study in endothelial cells, where they have reported that dehydroepiandrosterone (DHEA), an adrenal steroid abrogated expression of
adhesion molecules in HUVEC, activated with either TNF-[alpha] or oxidized low density proteins [35].
Ito, "Circulating
adhesion molecules and severity of coronary atherosclerosis," Coronary Artery Disease, vol.
Finally, endocan and soluble
adhesion molecules were not examined in previous studies that focused on endothelial markers as prognostic parameters with regard to GVHD response to steroid treatment, and these authors did not detect any differences in pretransplant biomarkers between patients with or without later acute GVHD [35-37].
Thus, VAP-1 blockade reduced macrophage recruitment into CNV lesion indirectly via suppression of other
adhesion molecules. Previous studies have demonstrated that marked suppression of VEGF is crucial for the suppression of CNV formation in the laser-induced CNV model [51,52].
Consequently, as the endothelium and inflammatory cells play a crucial role in the development of collaterals after a sudden or slowly progressing stenosis of coronary arteries, endothelial progenitor cells and soluble
adhesion molecules determine the formation and the quality of the collaterals.
