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Atherosclerosis. 2008 Jan;196(1):333-40. Epub 2006 Dec 8.

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

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Division of Cardiovascular Diseases, Mayo Clinic Rochester, 200 First Street SW, Rochester, MN, USA.



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.


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.


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).


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.

[Indexed for MEDLINE]

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