Abstract 15275: Altered Extracellular Matrix Proteoglycan- Decorin, Collagens and Elastin Deposition May Enhance Atherosclerosis in Human Peripheral Artery Disease: Implication of Morphological Predictors in Restenotic Plaque Progression

Abstract

Introduction: In coronary artery restenosis, reduced proteoglycan-decorin deposition in extracellular matrix (ECM) was shown to be associated with alterations in the types of collagens in ECM. However, in Peripheral Artery Disease (PAD) restenosis, these ECM changes have not been carefully characterized. Alterations in proteoglycan-decorin expression in the ECM may change the fibrillar architecture of collagens, and may alter the type of collagen deposition. HYPOTHESIS: We hypothesize that in PAD restenotic plaques, decreased deposition of proteoglycan-decorin is associated with increased type III collagen and elastin with decreased type I collagen content when compared to de novo control plaques. Methods: Thirteen restenotic and thirteen de novo superficial femoral artery plaques were obtained in-vivo during peripheral artery interventional procedure and compared histopathologically for ECM changes. Protein expression profiles of decorin, type I and type III collagen, and elastin deposition were evaluated and graded by immunohistochemistry. H& E stain was used to characterize the plaque morphology and stellate cell grade by scoring. Results: (See figure and table). In restenotic atheroma decorin, and type I collagen were decreased (p= 0.0001 for all comparisons). Type III collagen and elastin content were increased (p= 0.0001 for all comparisons) compared to de novo plaques. Conclusions: In PAD restenosis, we observed a reduction in decorin with an increase in type III collagen and simultaneous decrease in type I collagen as reported in CAD restenosis. Reparative injurious processes may underlie the associated observation in reduced proteoglycan-decorin in the ECM and altered types of collagen content. Additional molecular biological studies will address the mechanistic mediators which cause these ECM compositional changes.