scholarly journals Effect of Fimbristylis ovata on receptor for advanced glycation end-products, proinflammatory cytokines, and cell adhesion molecule level and gene expression in U937 and bEnd.3 cell lines

2015 ◽  
Vol 14 (2) ◽  
pp. 3984-3994
Author(s):  
S. Sukjamnong ◽  
R. Santiyanont
2020 ◽  
pp. 112972982097626
Author(s):  
Maria Ticala ◽  
Crina Claudia Rusu ◽  
Diana Moldovan ◽  
Alina Ramona Potra ◽  
Dacian Calin Tirinescu ◽  
...  

Background: The preferred vascular access for hemodialysis is represented by arteriovenous fistula (AVF) due to fewer complications and more prolonged survival. Considerable efforts have been made to identify biomarkers associated with AVF dysfunction, but results are conflicting. Vascular cell adhesion molecule (VCAM-1) and advanced glycation end products are involved in atherogenesis, vascular calcification, peripheral artery disease, and neointimal hyperplasia in renal and non-renal patients. The objective of this study was to evaluate whether there is an association between VCAM-1, soluble receptor for advanced glycation end products (sRAGE), NcarboxymethylLysine (CML), and arteriovenous fistula dysfunction (AVF). Methods: VCAM-1, sRAGE, and CML were performed using the ELISA technique in 88 HD patients. Ultrasound assessment of AVF reports brachial artery blood flow (Qa), brachial resistivity index (RI), presence of calcification, and the diameter. AVF dysfunction was defined as a brachial artery Qa ⩽ 500 ml/min or RI ⩾ 0.5. Results: The median level of VCAM-1 [2676.5(2206.8–4203.9) versus 2613.2(1885.7–3161.8), p 0.026] was significantly higher in patients with AVF dysfunction compared to the rest of the patients. sRAGE and CML were higher in this group but without statistical significance. In patients with AVF dysfunction, significant positive correlations were found between VCAM-1and sRAGE ( r = 0.417, p = 0.001), RI ( r = 0.313, p = 0.046), dialysis vintage ( r = 0.540, p < 0.001), AVF vintage ( r = 0.336, p = 0.032), intima-media thickness ( r = 0.423, p = 0.006) and C-reactive protein ( r = 0.315, p = 0.045). VCAM-1 correlated inversely with cholesterol ( r = −0.312, p = 0.047), triglycerides ( r = −0.358, p = 0.021), body mass index ( r = −0.388, p = 0.012). In multivariate regression analysis, VCAM-1 ( p = 0.013) and sRAGE ( p = 0.01) remained significant predictors of RI and Qa. Logistic regression disclosed calcification, VCAM-1, as risks factors for AVF dysfunction. Conclusion: The results we obtained showed that patients with AVF dysfunction had a significantly higher level of VCAM-l. A positive correlation between VCAM-1 and sRAGE was identified in this group.


2020 ◽  
Vol 21 (15) ◽  
pp. 5315
Author(s):  
Jean-Luc Wautier ◽  
Marie-Paule Wautier

In physiology and pathophysiology the molecules involved in blood cell–blood cell and blood cell–endothelium interactions have been identified. Platelet aggregation and adhesion to the walls belonging to vessels involve glycoproteins (GP), GP llb and GP llla and the GP Ib–IX–V complex. Red blood cells (RBCs) in normal situations have little interaction with the endothelium. Abnormal adhesion of RBCs was first observed in sickle cell anemia involving vascular cell adhesion molecule (VCAM)-1, α4β1, Lu/BCAM, and intercellular adhesion molecule (ICAM)-4. More recently RBC adhesion was found to be increased in retinal-vein occlusion (RVO) and in polycythemia vera (PV). The molecules which participate in this process are phosphatidylserine and annexin V in RVO, and phosphorylated Lu/BCAM and α5 laminin chain in PV. The additional adhesion in diabetes mellitus occurs due to the glycated RBC band 3 and the advanced glycation end-product receptors. The multiligand receptor binds advanced glycation end products (AGEs) or S100 calgranulins, or β-amyloid peptide. This receptor for advanced glycation end products is known as RAGE. The binding to RAGE-activated endothelial cells leads to an inflammatory reaction and a prothrombotic state via NADPH activation and altered gene expression. RAGE blockade is a potential target for drugs preventing the deleterious consequences of RAGE activation.


Sign in / Sign up

Export Citation Format

Share Document