C-reactive protein stimulates myeloperoxidase release from polymorphonuclear cells and monocytes: Implications for acute coronary syndromes

Uma Singh, Sridevi Devaraj, Ishwarlal Jialal

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

Background: C-reactive protein (CRP), the prototypic marker of inflammation, is present in atherosclerotic plaques and appears to promote atherogenesis. Also, CRP has been localized to monocytes and tissue mac- rophages, which are present in the necrotic core of lesions prone to plaque rupture. Leukocyte-derived myeloperoxidase (MPO), primarily hosted in human polymorphonuclear cells (PMNs), has also been shown to be present in human atherosclerotic lesions. Because MPO and CRP concentrations are increased in acute coronary syndrome (ACS) patients and predict poor outcomes, we tested the effect of CRP on MPO release from PMNs and monocytes. methods: We treated human PMNs and monocytes with CRP (25 and 50 mg/L for 6 h) and measured MPO release as total mass and activity in culture superna- tants. We also measured nitro-tyrosinylation (NO 2-Tyr) of LDL as an indicator of biological activity of CRP-mediated MPO release. Furthermore, we explored the effect of human CRP on MPO release in the rat sterile pouch model. results: CRP treatment significantly increased release of MPO (both mass and activity) from human PMNs as well as monocytes (P < 0.05) and caused NO 2-Tyr of LDL. Human CRP injection in rats resulted in increased concentrations of MPO in pouch exudates (P < 0.05), thus confirming our in vitro data. conclusions: CRP stimulates MPO release both in vitro and in vivo, providing further cogent data for the proinflammatory effect of CRP. These results might further support the role of CRP in ACS.

Original languageEnglish (US)
Pages (from-to)361-364
Number of pages4
JournalClinical Chemistry
Volume55
Issue number2
DOIs
StatePublished - Feb 1 2009

Fingerprint

Acute Coronary Syndrome
C-Reactive Protein
Peroxidase
Monocytes
Rats
Macrophages
Exudates and Transudates
Atherosclerotic Plaques
Bioactivity
Human Activities
Rupture
Atherosclerosis
Leukocytes
Tissue
Inflammation

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Biochemistry, medical

Cite this

C-reactive protein stimulates myeloperoxidase release from polymorphonuclear cells and monocytes : Implications for acute coronary syndromes. / Singh, Uma; Devaraj, Sridevi; Jialal, Ishwarlal.

In: Clinical Chemistry, Vol. 55, No. 2, 01.02.2009, p. 361-364.

Research output: Contribution to journalArticle

@article{8732d951918d4b219d620e2b006f4e75,
title = "C-reactive protein stimulates myeloperoxidase release from polymorphonuclear cells and monocytes: Implications for acute coronary syndromes",
abstract = "Background: C-reactive protein (CRP), the prototypic marker of inflammation, is present in atherosclerotic plaques and appears to promote atherogenesis. Also, CRP has been localized to monocytes and tissue mac- rophages, which are present in the necrotic core of lesions prone to plaque rupture. Leukocyte-derived myeloperoxidase (MPO), primarily hosted in human polymorphonuclear cells (PMNs), has also been shown to be present in human atherosclerotic lesions. Because MPO and CRP concentrations are increased in acute coronary syndrome (ACS) patients and predict poor outcomes, we tested the effect of CRP on MPO release from PMNs and monocytes. methods: We treated human PMNs and monocytes with CRP (25 and 50 mg/L for 6 h) and measured MPO release as total mass and activity in culture superna- tants. We also measured nitro-tyrosinylation (NO 2-Tyr) of LDL as an indicator of biological activity of CRP-mediated MPO release. Furthermore, we explored the effect of human CRP on MPO release in the rat sterile pouch model. results: CRP treatment significantly increased release of MPO (both mass and activity) from human PMNs as well as monocytes (P < 0.05) and caused NO 2-Tyr of LDL. Human CRP injection in rats resulted in increased concentrations of MPO in pouch exudates (P < 0.05), thus confirming our in vitro data. conclusions: CRP stimulates MPO release both in vitro and in vivo, providing further cogent data for the proinflammatory effect of CRP. These results might further support the role of CRP in ACS.",
author = "Uma Singh and Sridevi Devaraj and Ishwarlal Jialal",
year = "2009",
month = "2",
day = "1",
doi = "10.1373/clinchem.2008.109207",
language = "English (US)",
volume = "55",
pages = "361--364",
journal = "Clinical Chemistry",
issn = "0009-9147",
publisher = "American Association for Clinical Chemistry Inc.",
number = "2",

}

TY - JOUR

T1 - C-reactive protein stimulates myeloperoxidase release from polymorphonuclear cells and monocytes

T2 - Implications for acute coronary syndromes

AU - Singh, Uma

AU - Devaraj, Sridevi

AU - Jialal, Ishwarlal

PY - 2009/2/1

Y1 - 2009/2/1

N2 - Background: C-reactive protein (CRP), the prototypic marker of inflammation, is present in atherosclerotic plaques and appears to promote atherogenesis. Also, CRP has been localized to monocytes and tissue mac- rophages, which are present in the necrotic core of lesions prone to plaque rupture. Leukocyte-derived myeloperoxidase (MPO), primarily hosted in human polymorphonuclear cells (PMNs), has also been shown to be present in human atherosclerotic lesions. Because MPO and CRP concentrations are increased in acute coronary syndrome (ACS) patients and predict poor outcomes, we tested the effect of CRP on MPO release from PMNs and monocytes. methods: We treated human PMNs and monocytes with CRP (25 and 50 mg/L for 6 h) and measured MPO release as total mass and activity in culture superna- tants. We also measured nitro-tyrosinylation (NO 2-Tyr) of LDL as an indicator of biological activity of CRP-mediated MPO release. Furthermore, we explored the effect of human CRP on MPO release in the rat sterile pouch model. results: CRP treatment significantly increased release of MPO (both mass and activity) from human PMNs as well as monocytes (P < 0.05) and caused NO 2-Tyr of LDL. Human CRP injection in rats resulted in increased concentrations of MPO in pouch exudates (P < 0.05), thus confirming our in vitro data. conclusions: CRP stimulates MPO release both in vitro and in vivo, providing further cogent data for the proinflammatory effect of CRP. These results might further support the role of CRP in ACS.

AB - Background: C-reactive protein (CRP), the prototypic marker of inflammation, is present in atherosclerotic plaques and appears to promote atherogenesis. Also, CRP has been localized to monocytes and tissue mac- rophages, which are present in the necrotic core of lesions prone to plaque rupture. Leukocyte-derived myeloperoxidase (MPO), primarily hosted in human polymorphonuclear cells (PMNs), has also been shown to be present in human atherosclerotic lesions. Because MPO and CRP concentrations are increased in acute coronary syndrome (ACS) patients and predict poor outcomes, we tested the effect of CRP on MPO release from PMNs and monocytes. methods: We treated human PMNs and monocytes with CRP (25 and 50 mg/L for 6 h) and measured MPO release as total mass and activity in culture superna- tants. We also measured nitro-tyrosinylation (NO 2-Tyr) of LDL as an indicator of biological activity of CRP-mediated MPO release. Furthermore, we explored the effect of human CRP on MPO release in the rat sterile pouch model. results: CRP treatment significantly increased release of MPO (both mass and activity) from human PMNs as well as monocytes (P < 0.05) and caused NO 2-Tyr of LDL. Human CRP injection in rats resulted in increased concentrations of MPO in pouch exudates (P < 0.05), thus confirming our in vitro data. conclusions: CRP stimulates MPO release both in vitro and in vivo, providing further cogent data for the proinflammatory effect of CRP. These results might further support the role of CRP in ACS.

UR - http://www.scopus.com/inward/record.url?scp=59649113531&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=59649113531&partnerID=8YFLogxK

U2 - 10.1373/clinchem.2008.109207

DO - 10.1373/clinchem.2008.109207

M3 - Article

C2 - 19074520

AN - SCOPUS:59649113531

VL - 55

SP - 361

EP - 364

JO - Clinical Chemistry

JF - Clinical Chemistry

SN - 0009-9147

IS - 2

ER -