Effect of C-reactive protein on vascular cells

Evidence for a proinflammatory, proatherogenic role

Senthil Kumar Venugopal, Sridevi Devaraj, Ishwarlal Jialal

Research output: Contribution to journalArticle

152 Citations (Scopus)

Abstract

Purpose of review: C-reactive protein (CRP) is the prototypic downstream marker of inflammation. High levels of CRP predict future cardiovascular risk in apparently healthy men and women. Recent evidence from different cell types suggests that CRP is not only a risk marker but may also be a participant in atherogenesis. This review will focus on the effects of CRP on different cells involved in atherosclerosis. Recent findings: CRP is shown to induce matrix metalloproteinase-1 (MMP-1) expression through the FcγRII and extracellular signal-related kinase pathway in U937 cells. MMPs are implicated in plaque instability. A recent report shows that CRP does not induce tissue factor in human monocytes directly, disputing the previous concept that CRP induces tissue factor in monocytes. CRP is shown to upregulate interleukin-8 in human aortic endothelial cells via nuclear factor-κB. CRP promotes monocyte chemoattractant protein-1-mediated chemotaxis by upregulating CC-chemokine receptor 2 expression in human monocytes. Also CRP is shown to attenuate endothelial progenitor cell survival, differentiation, and function via inhibiting nitric oxide. Human CRP transgenic animal models show that CRP promotes atherothrombosis and increases plasminogen activator inhibitor-1. Also, the classic dogma that CRP is produced exclusively in liver is challenged by recent data on the extrahepatic production of CRP in different cells including atherosclerotic lesions. Summary: All this recent evidence along with earlier reports support a role for CRP in atherosclerosis.

Original languageEnglish (US)
Pages (from-to)33-37
Number of pages5
JournalCurrent Opinion in Nephrology and Hypertension
Volume14
Issue number1
DOIs
StatePublished - Jan 2005

Fingerprint

C-Reactive Protein
Blood Vessels
Monocytes
Atherosclerosis
Thromboplastin
CCR2 Receptors
U937 Cells
Matrix Metalloproteinase 1
Genetically Modified Animals
Chemokine CCL2
Plasminogen Activator Inhibitor 1
Chemotaxis
Matrix Metalloproteinases
Interleukin-8
Cell Differentiation
Cell Survival
Nitric Oxide
Phosphotransferases
Up-Regulation
Endothelial Cells

Keywords

  • Adhesion molecule
  • Atherosclerosis
  • C-reactive protein
  • Endothelium
  • Vascular dysfunction

ASJC Scopus subject areas

  • Nephrology
  • Internal Medicine

Cite this

Effect of C-reactive protein on vascular cells : Evidence for a proinflammatory, proatherogenic role. / Venugopal, Senthil Kumar; Devaraj, Sridevi; Jialal, Ishwarlal.

In: Current Opinion in Nephrology and Hypertension, Vol. 14, No. 1, 01.2005, p. 33-37.

Research output: Contribution to journalArticle

Venugopal, Senthil Kumar ; Devaraj, Sridevi ; Jialal, Ishwarlal. / Effect of C-reactive protein on vascular cells : Evidence for a proinflammatory, proatherogenic role. In: Current Opinion in Nephrology and Hypertension. 2005 ; Vol. 14, No. 1. pp. 33-37.
@article{a2c3b905c20247929450a4824ec9b8ec,
title = "Effect of C-reactive protein on vascular cells: Evidence for a proinflammatory, proatherogenic role",
abstract = "Purpose of review: C-reactive protein (CRP) is the prototypic downstream marker of inflammation. High levels of CRP predict future cardiovascular risk in apparently healthy men and women. Recent evidence from different cell types suggests that CRP is not only a risk marker but may also be a participant in atherogenesis. This review will focus on the effects of CRP on different cells involved in atherosclerosis. Recent findings: CRP is shown to induce matrix metalloproteinase-1 (MMP-1) expression through the FcγRII and extracellular signal-related kinase pathway in U937 cells. MMPs are implicated in plaque instability. A recent report shows that CRP does not induce tissue factor in human monocytes directly, disputing the previous concept that CRP induces tissue factor in monocytes. CRP is shown to upregulate interleukin-8 in human aortic endothelial cells via nuclear factor-κB. CRP promotes monocyte chemoattractant protein-1-mediated chemotaxis by upregulating CC-chemokine receptor 2 expression in human monocytes. Also CRP is shown to attenuate endothelial progenitor cell survival, differentiation, and function via inhibiting nitric oxide. Human CRP transgenic animal models show that CRP promotes atherothrombosis and increases plasminogen activator inhibitor-1. Also, the classic dogma that CRP is produced exclusively in liver is challenged by recent data on the extrahepatic production of CRP in different cells including atherosclerotic lesions. Summary: All this recent evidence along with earlier reports support a role for CRP in atherosclerosis.",
keywords = "Adhesion molecule, Atherosclerosis, C-reactive protein, Endothelium, Vascular dysfunction",
author = "Venugopal, {Senthil Kumar} and Sridevi Devaraj and Ishwarlal Jialal",
year = "2005",
month = "1",
doi = "10.1097/00041552-200501000-00006",
language = "English (US)",
volume = "14",
pages = "33--37",
journal = "Current Opinion in Nephrology and Hypertension",
issn = "1062-4821",
publisher = "Lippincott Williams and Wilkins",
number = "1",

}

TY - JOUR

T1 - Effect of C-reactive protein on vascular cells

T2 - Evidence for a proinflammatory, proatherogenic role

AU - Venugopal, Senthil Kumar

AU - Devaraj, Sridevi

AU - Jialal, Ishwarlal

PY - 2005/1

Y1 - 2005/1

N2 - Purpose of review: C-reactive protein (CRP) is the prototypic downstream marker of inflammation. High levels of CRP predict future cardiovascular risk in apparently healthy men and women. Recent evidence from different cell types suggests that CRP is not only a risk marker but may also be a participant in atherogenesis. This review will focus on the effects of CRP on different cells involved in atherosclerosis. Recent findings: CRP is shown to induce matrix metalloproteinase-1 (MMP-1) expression through the FcγRII and extracellular signal-related kinase pathway in U937 cells. MMPs are implicated in plaque instability. A recent report shows that CRP does not induce tissue factor in human monocytes directly, disputing the previous concept that CRP induces tissue factor in monocytes. CRP is shown to upregulate interleukin-8 in human aortic endothelial cells via nuclear factor-κB. CRP promotes monocyte chemoattractant protein-1-mediated chemotaxis by upregulating CC-chemokine receptor 2 expression in human monocytes. Also CRP is shown to attenuate endothelial progenitor cell survival, differentiation, and function via inhibiting nitric oxide. Human CRP transgenic animal models show that CRP promotes atherothrombosis and increases plasminogen activator inhibitor-1. Also, the classic dogma that CRP is produced exclusively in liver is challenged by recent data on the extrahepatic production of CRP in different cells including atherosclerotic lesions. Summary: All this recent evidence along with earlier reports support a role for CRP in atherosclerosis.

AB - Purpose of review: C-reactive protein (CRP) is the prototypic downstream marker of inflammation. High levels of CRP predict future cardiovascular risk in apparently healthy men and women. Recent evidence from different cell types suggests that CRP is not only a risk marker but may also be a participant in atherogenesis. This review will focus on the effects of CRP on different cells involved in atherosclerosis. Recent findings: CRP is shown to induce matrix metalloproteinase-1 (MMP-1) expression through the FcγRII and extracellular signal-related kinase pathway in U937 cells. MMPs are implicated in plaque instability. A recent report shows that CRP does not induce tissue factor in human monocytes directly, disputing the previous concept that CRP induces tissue factor in monocytes. CRP is shown to upregulate interleukin-8 in human aortic endothelial cells via nuclear factor-κB. CRP promotes monocyte chemoattractant protein-1-mediated chemotaxis by upregulating CC-chemokine receptor 2 expression in human monocytes. Also CRP is shown to attenuate endothelial progenitor cell survival, differentiation, and function via inhibiting nitric oxide. Human CRP transgenic animal models show that CRP promotes atherothrombosis and increases plasminogen activator inhibitor-1. Also, the classic dogma that CRP is produced exclusively in liver is challenged by recent data on the extrahepatic production of CRP in different cells including atherosclerotic lesions. Summary: All this recent evidence along with earlier reports support a role for CRP in atherosclerosis.

KW - Adhesion molecule

KW - Atherosclerosis

KW - C-reactive protein

KW - Endothelium

KW - Vascular dysfunction

UR - http://www.scopus.com/inward/record.url?scp=12144249151&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=12144249151&partnerID=8YFLogxK

U2 - 10.1097/00041552-200501000-00006

DO - 10.1097/00041552-200501000-00006

M3 - Article

VL - 14

SP - 33

EP - 37

JO - Current Opinion in Nephrology and Hypertension

JF - Current Opinion in Nephrology and Hypertension

SN - 1062-4821

IS - 1

ER -