Placenta growth factor expression in human atherosclerotic carotid plaques is related to plaque destabilization

Kevin Pilarczyk, Katherine J E Sattler, Offer Galili, Daniele Versari, Monica L. Olson, Frederic B. Meyer, Xiang Yang Zhu, Lilach O Lerman, Amir Lerman

Research output: Contribution to journalArticle

42 Citations (Scopus)

Abstract

Background and purpose: Placenta growth factor (PlGF) mediates angiogenesis and inflammation, but its role in human atherosclerosis is unknown. This study was designed to test the hypothesis that PlGF-expression in human atherosclerotic carotid plaques is related to inflammation, vascularization and clinical plaque instability. Methods: The expression of PlGF, C-reactive protein (CRP) and CD40L was analyzed with Western blots in carotid plaques of 60 patients. Cellular infiltration (CD68, CD3) and vascularization (von-Willebrand-factor) was assessed by immunohistochemistry. Results: Symptomatic patients showed higher levels of PlGF than asymptomatic patients (115.4 ± 8.2 versus 83.6 ± 10.5 densitometric units (DU), p < 0.05) and higher grading for inflammatory cells and microvessels (CD3: 2.3 ± 0.1 versus 0.6 ± 0.1, p < 0.001, CD68: 2.4 ± 0.1 versus 0.8 ± 0.1, p < 0.001, microvessels: 2.3 ± 0.1 versus 1.5 ± 0.1, p < 0.01). PlGF-expression showed a positive correlation to the expression of CRP (r = 0.5, p < 0.001) and CD40L (r = 0.4, p < 0.01). Conclusions: PlGF-expression within human atherosclerotic lesions is associated with plaque inflammation and microvascular density, suggesting a role for PlGF in plaque destabilization and, thus, in clinical manifestation of the disease.

Original languageEnglish (US)
Pages (from-to)333-340
Number of pages8
JournalAtherosclerosis
Volume196
Issue number1
DOIs
StatePublished - Jan 2008

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Atherosclerotic Plaques
CD40 Ligand
Microvessels
Inflammation
C-Reactive Protein
von Willebrand Factor
Placenta Growth Factor
Atherosclerosis
Western Blotting
Immunohistochemistry

Keywords

  • Atherosclerosis
  • Carotid arteries
  • Inflammation
  • Placenta growth factor
  • Vascularization

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Placenta growth factor expression in human atherosclerotic carotid plaques is related to plaque destabilization. / Pilarczyk, Kevin; Sattler, Katherine J E; Galili, Offer; Versari, Daniele; Olson, Monica L.; Meyer, Frederic B.; Zhu, Xiang Yang; Lerman, Lilach O; Lerman, Amir.

In: Atherosclerosis, Vol. 196, No. 1, 01.2008, p. 333-340.

Research output: Contribution to journalArticle

Pilarczyk, Kevin ; Sattler, Katherine J E ; Galili, Offer ; Versari, Daniele ; Olson, Monica L. ; Meyer, Frederic B. ; Zhu, Xiang Yang ; Lerman, Lilach O ; Lerman, Amir. / Placenta growth factor expression in human atherosclerotic carotid plaques is related to plaque destabilization. In: Atherosclerosis. 2008 ; Vol. 196, No. 1. pp. 333-340.
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abstract = "Background and purpose: Placenta growth factor (PlGF) mediates angiogenesis and inflammation, but its role in human atherosclerosis is unknown. This study was designed to test the hypothesis that PlGF-expression in human atherosclerotic carotid plaques is related to inflammation, vascularization and clinical plaque instability. Methods: The expression of PlGF, C-reactive protein (CRP) and CD40L was analyzed with Western blots in carotid plaques of 60 patients. Cellular infiltration (CD68, CD3) and vascularization (von-Willebrand-factor) was assessed by immunohistochemistry. Results: Symptomatic patients showed higher levels of PlGF than asymptomatic patients (115.4 ± 8.2 versus 83.6 ± 10.5 densitometric units (DU), p < 0.05) and higher grading for inflammatory cells and microvessels (CD3: 2.3 ± 0.1 versus 0.6 ± 0.1, p < 0.001, CD68: 2.4 ± 0.1 versus 0.8 ± 0.1, p < 0.001, microvessels: 2.3 ± 0.1 versus 1.5 ± 0.1, p < 0.01). PlGF-expression showed a positive correlation to the expression of CRP (r = 0.5, p < 0.001) and CD40L (r = 0.4, p < 0.01). Conclusions: PlGF-expression within human atherosclerotic lesions is associated with plaque inflammation and microvascular density, suggesting a role for PlGF in plaque destabilization and, thus, in clinical manifestation of the disease.",
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