bay-11-7082 and Hyperuricemia

bay-11-7082 has been researched along with Hyperuricemia* in 1 studies

Other Studies

1 other study(ies) available for bay-11-7082 and Hyperuricemia

Article	Year
Uric acid promotes chemokine and adhesion molecule production in vascular endothelium via nuclear factor-kappa B signaling. Nutrition, metabolism, and cardiovascular diseases : NMCD, 2015, Volume: 25, Issue:2 Hyperuricemia is an important risk factor for atherosclerosis, yet the potential mechanisms are not well understood. Migration and adhesion of leukocytes to endothelial cells play key roles in initiation and development of atherosclerosis. We investigated monocyte-endothelial cell interactions and potential signaling pathways under uric acid (UA)-stimulated conditions.. Primary human umbilical vein endothelial cells (HUVECs) were cultured and exposed to different concentrations of UA for various periods. Experimental hyperuricemia rat models were established. Expression of chemoattractant protein-1 (MCP-1), interleukin 8 (IL-8), vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) were evaluated. Monocyte-endothelial cell interactions were elucidated by chemotaxis and adhesion assays, and nuclear factor-kappa B (NF-κB) pathway was studied using fluorescent microscopy and electrophoretic mobility shift assay. Results showed that high concentration of UA stimulated generation of chemokines and adhesion molecules in ex vivo and in vivo experiments. Migration and adhesion of human monocytic leukemia cell line THP-1 cells to HUVECs were promoted and activated NF-κB was significantly increased. UA-induced responses were ameliorated by organic anion transporter inhibitor probenecid and NF-κB inhibitor BAY11-7082. It was also observed that human endothelial cells expressed urate transporter-1, which was not regulated by UA.. High concentration of UA exerts unfavorable effects directly on vascular endothelium via the NF-κB signaling pathway, the process of which requires intracellular uptake of UA. Topics: Animals; Atherosclerosis; Cell Adhesion; Cell Adhesion Molecules; Cell Survival; Chemokine CCL2; Chemokines; Disease Models, Animal; Endothelial Cells; Endothelium, Vascular; Gene Expression Regulation; Human Umbilical Vein Endothelial Cells; Humans; Hyperuricemia; Intercellular Adhesion Molecule-1; Interleukin-8; Male; Monocytes; NF-kappa B; Nitriles; Organic Anion Transporters; Organic Cation Transport Proteins; Rats; Rats, Wistar; Signal Transduction; Sulfones; Uric Acid; Vascular Cell Adhesion Molecule-1	2015

Article

Year

Uric acid promotes chemokine and adhesion molecule production in vascular endothelium via nuclear factor-kappa B signaling.

Nutrition, metabolism, and cardiovascular diseases : NMCD, 2015, Volume: 25, Issue:2

Hyperuricemia is an important risk factor for atherosclerosis, yet the potential mechanisms are not well understood. Migration and adhesion of leukocytes to endothelial cells play key roles in initiation and development of atherosclerosis. We investigated monocyte-endothelial cell interactions and potential signaling pathways under uric acid (UA)-stimulated conditions.. Primary human umbilical vein endothelial cells (HUVECs) were cultured and exposed to different concentrations of UA for various periods. Experimental hyperuricemia rat models were established. Expression of chemoattractant protein-1 (MCP-1), interleukin 8 (IL-8), vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) were evaluated. Monocyte-endothelial cell interactions were elucidated by chemotaxis and adhesion assays, and nuclear factor-kappa B (NF-κB) pathway was studied using fluorescent microscopy and electrophoretic mobility shift assay. Results showed that high concentration of UA stimulated generation of chemokines and adhesion molecules in ex vivo and in vivo experiments. Migration and adhesion of human monocytic leukemia cell line THP-1 cells to HUVECs were promoted and activated NF-κB was significantly increased. UA-induced responses were ameliorated by organic anion transporter inhibitor probenecid and NF-κB inhibitor BAY11-7082. It was also observed that human endothelial cells expressed urate transporter-1, which was not regulated by UA.. High concentration of UA exerts unfavorable effects directly on vascular endothelium via the NF-κB signaling pathway, the process of which requires intracellular uptake of UA.

Topics: Animals; Atherosclerosis; Cell Adhesion; Cell Adhesion Molecules; Cell Survival; Chemokine CCL2; Chemokines; Disease Models, Animal; Endothelial Cells; Endothelium, Vascular; Gene Expression Regulation; Human Umbilical Vein Endothelial Cells; Humans; Hyperuricemia; Intercellular Adhesion Molecule-1; Interleukin-8; Male; Monocytes; NF-kappa B; Nitriles; Organic Anion Transporters; Organic Cation Transport Proteins; Rats; Rats, Wistar; Signal Transduction; Sulfones; Uric Acid; Vascular Cell Adhesion Molecule-1

2015