ALTERATIONS IN COLLAGEN SUBTYPE-III AND SUBTYPE-IV PROTEIN IN EXPERIMENTAL VENOUS BYPASS-GRAFTING

Citation
Gj. Fulton et al., ALTERATIONS IN COLLAGEN SUBTYPE-III AND SUBTYPE-IV PROTEIN IN EXPERIMENTAL VENOUS BYPASS-GRAFTING, Coronary artery disease, 9(4), 1998, pp. 191-197
Citations number
26
Categorie Soggetti
Peripheal Vascular Diseas
Journal title
ISSN journal
09546928
Volume
9
Issue
4
Year of publication
1998
Pages
191 - 197
Database
ISI
SICI code
0954-6928(1998)9:4<191:AICSAS>2.0.ZU;2-7
Abstract
Objective To examine changes in collagen III and IV protein during the development of intimal hyperplasia in experimental vein grafts. Metho ds Sixteen New Zealand White rabbits underwent reversed, jugular vein, interposition grafting of the carotid artery. Vessels were harvested 3, 7 or 28 days after operation and subjected to immunohistochemical e xamination and gelatinase assays. Results In control vein, collagen IV was expressed around adventitial blood vessels and throughout the end othelium. Compared with its presence in control veins, collagen IV pro tein was decreased in the endothelium in all 3-day vein grafts and und etectable in the endothelium and intima in 7-day vein grafts, but was present in the endothelium and intimal hyperplasia in 28-day vein graf ts. In contrast, collagen III was absent from the endothelium of contr ol vein and 3-day vein grafts, was present at low levels in the intima of 7-day vein grafts, but was absent from the endothelium and intimal hyperplasia in 28-day vein grafts. In 3-day vein grafts, areas of col lagen IV loss colocalized to areas of leukocyte infiltration. Protein extracts from 3-day vein grafts contained a 72 kDa gelatinase. Conclus ions The presence and alterations of collagen protein in veins and vei n grafts are subtype specific. Collagen III does not appear to be a no rmal component of intimal hyperplasia in vein grafts. The decrease in collagen IV protein in the endothelium of veins may be a component of the endothelial changes that follow bypass grafting, mediated by leuko cytes, the induction of gelatinase activity, or both. Coronary Artery Dis 9:191-197 (C) 1998 Lippincott-Raven Publishers.