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B-Dependent Proinflammatory Factors but not of Collagen I in a Rabbit Model of Atherosclerosis
From the Research Laboratory*
and Division of
Cardiology,
Fundación Jiménez
Díaz, Autonoma University, Madrid, and the Division of
Pathology,
Hospital Clínico,
Madrid, Spain
Increasing evidence supports an association between inflammation
and plaque rupture. Macrophages and vascular smooth muscle cells are a
source of cytokines and growth factors, which contribute to
ongoing inflammation during atherogenesis. In a rabbit model of
atherosclerosis, we evaluated the effect of the ACE inhibitor
quinapril on different parameters implicated in the pathogenesis of the
plaque, such as the presence of chemokines
(interleukin-8, monocyte chemoattractant protein-1),
collagen I, and vascular smooth muscle cell proliferation
(PDGF-B). Since nuclear factor 
B (NF-B) has been implicated in
the control of chemokine transcription and cell proliferation,
we also investigated its activation and localization in the lesion.
Quinapril administration for 28 days caused a down-regulation in
arterial expression of interleukin-8 and monocyte chemoattractant
protein-1 (mRNA and protein). However, collagen I expression
(mRNA and protein) was not modified. PDGF-B expression was reduced in
both the intima and the media. Active NF-B, found in both
macrophages and vascular smooth muscle cells, was also reduced
by quinapril. Nevertheless, no significant changes were noted
in the mild neointima formation, although a certain trend
toward normalization was found in the quinapril-treated group. In
conclusion, our results show that quinapril treatment
attenuates several parameters associated with inflammation within the
atherosclerotic lesions that are controlled by NF-B,
although it has no effect on collagen I expression. Both effects could
contribute to the stabilization of the atherosclerotic
plaque.
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