Effects of Rosuvastatin on Apolipoprotein J in Balloon-Injured Carotid Artery in Rats

Abstract

BackgroundRestenosis after percutaneous coronary intervention in coronary heart disease remains an unsolved problem. Clusterin (CLU) (or Apolipoprotein [Apo] J) levels have been reported to be elevated during the progression of postangioplasty restenosis and atherosclerosis. However, its role in neointimal hyperplasia is still controversial.ObjectiveTo elucidate the role Apo J in neointimal hyperplasia in a rat carotid artery model in vivo with or without rosuvastatin administration.MethodsMale Wistar rats were randomly divided into three groups: the control group (n = 20), the model group (n = 20) and the statin intervention group (n = 32). The rats in the intervention group were given 10mg /kg dose of rosuvastatin. A 2F Fogarty catheter was introduced to induce vascular injury. Neointima formation was analyzed 1, 2, 3 and 4 weeks after balloon injury. The level of Apo J was measured by real-time PCR, immunohistochemistry and western blotting.ResultsIntimal/medial area ratio (intimal/medial, I/M) was increased after balloon-injury and reached the maximum value at 4weeks in the model group; I/M was slightly increased at 2 weeks and stopped increasing after rosuvastatin administration. The mRNA and protein levels of Apo J in carotid arteries were significantly upregulated after rosuvastatin administration as compared with the model group, and reached maximum values at 2 weeks, which was earlier than in the model group (3 weeks).ConclusionApo J served as an acute phase reactant after balloon injury in rat carotid arteries. Rosuvastatin may reduce the neointima formation through up-regulation of Apo J. Our results suggest that Apo J exerts a protective role in the restenosis after balloon-injury in rats.

Effect of Endothelial Progenitor Cells Transplantation on Neointimal Hyperplasia and Reendothelialization after Balloon Catheter Injury in Rat Carotid Arteries

“…However, other scholars declared that transplanting EPCs could not only promote reendothelialization through paracrine modes of action, but also differentiate into mature ECs [40,41]. Assessment of transplanted EPCs and reendothelialization requires sequential crossor longitudinal sectioning of the vessels [42][43][44][45], but not every section could be chosen to stain and quantify [46][47][48]. The irregular geometry of the cell distribution requires accurate tools.…”