Nuclear factor-κB immunoreactivity is present in human coronary plaque and enhanced in patients with unstable angina pectoris

Stephanie H. Wilson, Patricia Best, William D. Edwards, David Holmes, Paula J. Carlson, David S. Celermajer, Amir Lerman

Research output: Contribution to journalArticle

75 Citations (Scopus)

Abstract

Background: Nuclear factor-κB (NF-κB) is a transcription factor which plays a coordinating role in inflammation and cellular proliferation and is thought to be involved in the pathogenesis of atherosclerosis. Its role in unstable coronary plaque in humans is unknown. Methods and results: Coronary atherectomy plaque was obtained via directional coronary atherectomy from 32 patients [16 with unstable angina pectoris (UAP) and 16 with stable angina pectoris (SAP)]. The predominant pathology in UAP consisted of richly cellular areas with atheromatous gruel or loose intimal proliferative tissue within a myxoid matrix (P < 0.05 compared with SAP). By contrast, SAP plaques showed more dense fibrosis (P < 0.01 compared with UAP). Sections were then stained with a monoclonal antibody to the activated p65 subunit of NF-κB and this staining was present in 31/32 specimens, localized to smooth muscle cells, macrophages and foam cells. Staining was then graded semiquantitatively by three independent observers. Immunostaining grades for activated NF-κB were significantly higher in UAP compared with SAP (2.60 ± 0.1 vs. 1.98 ± 0.18; P < 0.01). Conclusions: NF-κB immunoreactivity is present in coronary atherosclerotic plaque and is increased among patients with unstable coronary syndromes. These data support a role for NF-κB in the pathogenesis of acute coronary syndromes in humans.

Original languageEnglish (US)
Pages (from-to)147-153
Number of pages7
JournalAtherosclerosis
Volume160
Issue number1
DOIs
StatePublished - 2002

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Stable Angina
Unstable Angina
Coronary Atherectomy
Tunica Intima
Staining and Labeling
Foam Cells
Atherosclerotic Plaques
Acute Coronary Syndrome
Smooth Muscle Myocytes
Atherosclerosis
Fibrosis
Transcription Factors
Macrophages
Monoclonal Antibodies
Cell Proliferation
Pathology
Inflammation

Keywords

  • Atherosclerosis
  • Coronary disease
  • Histopathology
  • Infection/inflammation
  • Macrophages

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Nuclear factor-κB immunoreactivity is present in human coronary plaque and enhanced in patients with unstable angina pectoris. / Wilson, Stephanie H.; Best, Patricia; Edwards, William D.; Holmes, David; Carlson, Paula J.; Celermajer, David S.; Lerman, Amir.

In: Atherosclerosis, Vol. 160, No. 1, 2002, p. 147-153.

Research output: Contribution to journalArticle

Wilson, Stephanie H. ; Best, Patricia ; Edwards, William D. ; Holmes, David ; Carlson, Paula J. ; Celermajer, David S. ; Lerman, Amir. / Nuclear factor-κB immunoreactivity is present in human coronary plaque and enhanced in patients with unstable angina pectoris. In: Atherosclerosis. 2002 ; Vol. 160, No. 1. pp. 147-153.
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AU - Celermajer, David S.

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AB - Background: Nuclear factor-κB (NF-κB) is a transcription factor which plays a coordinating role in inflammation and cellular proliferation and is thought to be involved in the pathogenesis of atherosclerosis. Its role in unstable coronary plaque in humans is unknown. Methods and results: Coronary atherectomy plaque was obtained via directional coronary atherectomy from 32 patients [16 with unstable angina pectoris (UAP) and 16 with stable angina pectoris (SAP)]. The predominant pathology in UAP consisted of richly cellular areas with atheromatous gruel or loose intimal proliferative tissue within a myxoid matrix (P < 0.05 compared with SAP). By contrast, SAP plaques showed more dense fibrosis (P < 0.01 compared with UAP). Sections were then stained with a monoclonal antibody to the activated p65 subunit of NF-κB and this staining was present in 31/32 specimens, localized to smooth muscle cells, macrophages and foam cells. Staining was then graded semiquantitatively by three independent observers. Immunostaining grades for activated NF-κB were significantly higher in UAP compared with SAP (2.60 ± 0.1 vs. 1.98 ± 0.18; P < 0.01). Conclusions: NF-κB immunoreactivity is present in coronary atherosclerotic plaque and is increased among patients with unstable coronary syndromes. These data support a role for NF-κB in the pathogenesis of acute coronary syndromes in humans.

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