C-reactive protein activates the nuclear factor-κB pathway and induces vascular cell adhesion molecule-1 expression through CD32 in human umbilical vein endothelial cells and aortic endothelial cells

Yao Jen Liang, Kou Gi Shyu, Bao Wei Wang, Ling Ping Lai

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57 Citations (Scopus)

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 IκB protein and electrophoretic mobility shift assay showed a significant increase of nuclear NF-κB 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 IκB degradation, NF-κB nuclear translocation and VCAM-1 up-regulation induced by CRP were all inhibited by treatment with siRNA against CD32. SB203580, a P38 inhibitor, significantly attenuated the CRP-induced responses while SP600125 (c-jun kinase inhibitor) did not. In conclusion, CRP-induced IκB degradation, NF-κB 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.

Original languageEnglish
Pages (from-to)412-420
Number of pages9
JournalJournal of Molecular and Cellular Cardiology
Volume40
Issue number3
DOIs
Publication statusPublished - Mar 2006

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Complement Factor B
Vascular Cell Adhesion Molecule-1
Human Umbilical Vein Endothelial Cells
C-Reactive Protein
Endothelial Cells
Small Interfering RNA
Messenger RNA
Electrophoretic Mobility Shift Assay
Protein C
Immunoblotting
Northern Blotting
Atherosclerosis
Carrier Proteins
Proteins
Phosphotransferases
Up-Regulation
Western Blotting

Keywords

  • CRP
  • HUVECs
  • NF-κB
  • siRNA
  • VCAM-1

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine

Cite this

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title = "C-reactive protein activates the nuclear factor-κB pathway and induces vascular cell adhesion molecule-1 expression through CD32 in human umbilical vein endothelial cells and aortic endothelial cells",
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 IκB protein and electrophoretic mobility shift assay showed a significant increase of nuclear NF-κB 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 IκB degradation, NF-κB nuclear translocation and VCAM-1 up-regulation induced by CRP were all inhibited by treatment with siRNA against CD32. SB203580, a P38 inhibitor, significantly attenuated the CRP-induced responses while SP600125 (c-jun kinase inhibitor) did not. In conclusion, CRP-induced IκB degradation, NF-κB 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.",
keywords = "CRP, HUVECs, NF-κB, siRNA, VCAM-1",
author = "Liang, {Yao Jen} and Shyu, {Kou Gi} and Wang, {Bao Wei} and Lai, {Ling Ping}",
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T1 - C-reactive protein activates the nuclear factor-κB pathway and induces vascular cell adhesion molecule-1 expression through CD32 in human umbilical vein endothelial cells and aortic endothelial cells

AU - Liang, Yao Jen

AU - Shyu, Kou Gi

AU - Wang, Bao Wei

AU - Lai, Ling Ping

PY - 2006/3

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N2 - 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 IκB protein and electrophoretic mobility shift assay showed a significant increase of nuclear NF-κB 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 IκB degradation, NF-κB nuclear translocation and VCAM-1 up-regulation induced by CRP were all inhibited by treatment with siRNA against CD32. SB203580, a P38 inhibitor, significantly attenuated the CRP-induced responses while SP600125 (c-jun kinase inhibitor) did not. In conclusion, CRP-induced IκB degradation, NF-κB 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.

AB - 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 IκB protein and electrophoretic mobility shift assay showed a significant increase of nuclear NF-κB 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 IκB degradation, NF-κB nuclear translocation and VCAM-1 up-regulation induced by CRP were all inhibited by treatment with siRNA against CD32. SB203580, a P38 inhibitor, significantly attenuated the CRP-induced responses while SP600125 (c-jun kinase inhibitor) did not. In conclusion, CRP-induced IκB degradation, NF-κB 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.

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