These results indicate that 15-LO activity may be involved in the early pathogenesis of atherosclerosis by inducing VCAM-1 and ICAM-1 expression and by increasing T-cell adhesion on the endothelium.
Intercellular adhesion molecule-1 (ICAM-1) plays a crucial role in lymphocyte migration and activation, and is considered important in the pathogenesis of atherosclerosis.
These studies suggest that ICAM-1 variants may modulate atherosclerosis in humans and provide support for the concept that inflammatory gene polymorphisms may influence atherosclerosis independent of plasma levels of their gene products.
These studies suggest that ICAM-1 variants may modulate atherosclerosis in humans and provide support for the concept that inflammatory gene polymorphisms may influence atherosclerosis independent of plasma levels of their gene products.
In conclusion, K469E polymorphism of the ICAM-1 gene had impact on plasma fibrinogen level independently of other clinical factors in 360 type 2 diabetic patients, suggesting that fibrinogen is a candidate which links the ICAM-1 gene polymorphism to atherosclerosis.
The results proved that PMS is a powerful agent against atherosclerosis and that PMS action could possibly be through the inhibition of the expression of ICAM-1 and VEGF in foam cells.
We studied how the levels of intercellular adhesion molecule-1 (ICAM-1), one of the key molecules in the development of atherosclerosis, might be affected by paeonol in tumor necrosis factor-alpha (TNF-alpha)-activated human umbilical vein endothelial cells (HUVECs).
K(1-5) reduced atherosclerosis and neointima formation in mice, possibly through inhibition of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 expression in endothelial cells.
Further, lipoxygenase pathway SNPs that were associated with measures of atherosclerosis were associated with markers of inflammation (CRP, ICAM-1) and calcification (MGP).
Finally, PCA administration in the apolipoprotein E (ApoE)-deficient mouse model reduced aortic VCAM-1 and ICAM-1 expression, NF-κB activity, and plasma-soluble VCAM-1 and ICAM-1 levels, with inhibiting atherosclerosis development.
This study demonstrated that DTD could inhibit the expression of ICAM-1, by significantly preventing the activation of JNK and p38, which are important factors of atherosclerosis.
By integrating human and mouse results, we predict that PPAP2B, GALNT4, MAPKAPK5, TCTN1, SRR, SNF8, and ICAM1 play a causal role in the susceptibility to atherosclerosis through a role in the vasculature.
These results suggest that Trx1 inherently suppresses VCAM-1 and ICAM-1 expression in vascular endothelia and may prevent the initiation of atherosclerosis by attenuating adhesion molecule expression.
We found that SAA (80μg/mL) induced 3.5- to 37.8-fold increases in the expression of targets known to play important roles in the initiation and progression of atherosclerosis (i.e., ICAM-1, MCP-1, MMP-9 and TF) via NF-κB regulation within one hour after exposure.
To investigate intercellular adhesion molecule-1 (ICAM1) and angiotensinogen (AGT) gene polymorphisms, as related to atherosclerosis and endothelial dysfunction, in coronary slow flow (CSF).
Intercellular adhesion molecule‑1 (ICAM‑1) is an important adhesion molecule that has a crucial role in lymphocyte migration and atherosclerosis pathogenesis activation.