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sup] ICAM-1 has been widely known for its effect in endothelial dysfunction.
Synthesis and secretion of ICAM-1 can be induced by interleukin-1 (IL-1) and tumor necrosis factor-[alpha] (TNF-[alpha]), and it functions as a ligand for lyphocyte function associated antigen 1 (LFA-1) (integrin) receptor found on leukocytes.
CerbB2 was negative in the cases with negative ICAM-1 whereas estrogen receptor and progesterone receptor were positive in the cases with positive VCAM-1.
Coronary atherosclerosis causes release of inflammatory cytokines which in turn generate increased expression of CAMS like soluble ICAM-1 and SVCAM.
In addition, ICAM-1 and VCAM-1 serve as signaling molecules that promote the production of reactive oxygen species (ROS), a key player of TNF-[alpha]-induced increased permeability (van Wetering et al.
To assess their anti-inflammatory effects, we evaluated their ability to reduce the expression and secretion of the adhesion molecules ICAM-1 and VCAM-1 in HUVEC exposed to the proinflammatory cytokine TNF-[alpha].
A variety of cells such as vascular endothelial cells leukocytes epithelial cells can express ICAM-1 and vascular endothelial cells have the strongest expression.
A study published in 1992 looked at differing forms of zinc lozenges and found that some of them were so tightly bound to their carrier by zinc chelators that they would not release enough free zinc in the throat to block the ICAM-1 receptor.
Determination of the ICAM-1 mRNA level in lung tissues
The data obtained from this study is useful to verify the reliability of ICAM-1 and VCAM-1 as SLE disease monitoring and flare predictor tools and the potential of antiC1q antibody as SLE global activity biomarker .
The genes evaluated for both extracts included BCL-2, p53, PDGF, ICAM-1, ERCC1, TNF[alpha], and VEGF.
Circulating soluble ICAM-1 (sICAM-1) is the result of cleavage of membrane-bound ICAM-1.
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