Year: 1999
Type: article
Abstract: Animal models of arterial injury have failed to predict the efficacy of therapy to prevent restenosis after angioplasty in humans. We investigated coronary injury in cholesterol-fed dogs. Thirty-four dogs were divided into three groups, and fed a non-cholesterol (N), 5g of cholesterol/day (Ch5), or 10g of cholesterol/day fed group (Ch10) diet for three months. Serum cholesterol levels were increased by feeding cholesterol dose-dependently (131±12 in N, 187±5 in Ch5 (p<0.01), and 234 ±31 mg/dl in Ch10 (p<0.01) ). At one month after injury, the development of intima was accelerated by feeding cholesterol: intima/media area (I/M) ratio was 0.10±0.03 in N, 0.32±0.06 in Ch5, and 0.59±0.24 in Ch10 (p<0.01). Most of the neointimal cells were identified as immature smooth muscle cells (SMCs) using various smooth muscle cell (SMC) phenotypic markers. The proliferative activity which was determined by using the monoclonal antibody against proliferative cell nuclear antigen (PCNA) at 3 days after injury was increased in Ch10, compared to N (74 ±12% vs. 28± 7%, respectively, p< 0.01). These results suggested that cholesterol feeding enhances neointimal formation in a dose dependent manner by the up regulation of proliferative activity and neointimal cells have a similar profile of SMC differentiation status as the intimal cells of restenosis patients.
DOI: 10.11501/3154072
Author: 隆裕 中小路
Language: English
Subfield: Immunology
Field: Immunology and Microbiology
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W2267570194