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http://ntur.lib.ntu.edu.tw/handle/246246/93126
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| Title: | C-Reactive Protein Activates the Nuclear Factor-Kappab Pathway and Induces Vascular Cell Adhesion Molecule-1 Expression through Cd32 in Human Umbilical Vein Endothelial Cells and Aortic Endothelial Cells |
| Authors: | 賴凌平
LAI, LING-PING |
| Contributors: | 內科 |
| Keywords: | Aorta/cytology;Blotting, Northern;Blotting, Western;C- Reactive Protein/ metabolism;Cells, Cultured;Electrophoretic Mobility Shift Assay |
| Date: | 2006 |
| Issue Date: | 2009-09-29T04:55:45Z |
| Abstract: | C-reactive protein (CRP) contributes to the process of atherosclerosis by inducing pro-inflammatory changes in endothelial cells. However, the exact receptor involved in CRP-induced endothelial changes remains unclear . Human umbilical vein endothelial cells (HUVECs) and human aortic endothelial cells (HAECs) were used for the experiments. After incubation with CRP, immunoblotting showed a significant decrease of IkappaB protein and electrophoretic mobility shift assay showed a significant increase of nuclear NF-kappaB binding capacity. These changes were associated with a significant increase of vascular cell adhesion molecule-1 (VCAM-1) expression. The mRNA level of CD32, the major binding protein for CRP in endothelial cells , increased significantly as measured by Northern blot and Western blot. When these cells were transfected with siRNA directed against CD32, the mRNA of CD32 decreased significantly. The IkappaB degradation, NF-kappaB nuclear translocation and VCAM-1 up-regulation induced by CRP were all inhibited by treatment with siRNA against CD32. SB 203580 , a P38 inhibitor, significantly attenuated the CRP-induced responses while SP600125 (c-jun kinase inhibitor) did not. In conclusion, CRP-induced IkappaB degradation, NF-kappaB nuclear translocation and VCAM- 1 protein expression in HUVECs and HAECs. CRP also increased the expression of CD32, which might serve as the receptor for CRP in endothelial cells and mediated the effects of CRP. |
| Relation: | J MOL CELL CARDIOL v.40 n.3 pp.412-420 |
| Appears in Collections: | [醫學系內科] 期刊論文
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