Ubiquitin expression in atherosclerotic lesions of wistar fatty and wistar lean rats

To clarify whether ubiquitin is expressed in atherosclerotic lesions, and, if so, the expression is influenced by diabetes mellitus, we examined atherosclerotic (AS) lesions from Wistar fatty (WF) and Wistar lean (WL) rats immunohistochemically using an antibody against ubiquitin (AUb). Ten-week-old male WF and WL rats were treated to cannulize a silicon tube from the left carotid artery (LCA) to the descending aorta under chloral hydrate anesthesia and the tube was fixed. Age-matched WF and WL rats without cannulization were served as controls. Eight weeks after operation, 1 ml of 0.1% Evans blue solution was injected to all rats from the tail vein. 15 min latter, the aortae were removed, fixed with 4% paraformaldehyde and embedded in paraffin. Immunohistochemical staining with AUb by the ABC method, hematoxylin and eosin (HE) and elastica-Goldner (EG) stains were performed. In the cannulized group, focal areas of the luminal surface of the aorta were stained blue with Evans blue and these areas were microscopically confirmed as AS lesions in all WF and WL rats. In the control group, no Evans blue staining or AS lesions were observed. The destruction of the internal elastic lamina in AS lesions were seen with EG stain in the cannulized aorta of both WF and WL rats. No significant difference of the area ratio of intima/media was present between WF and WL rats in the cannulized group. Ubiquitin immunoreactivity was observed in the nucleus and cytoplasm of cells in AS lesions of both WF and WL rats. The present study suggests that ubiquitin plays a role in the formation of AS, and the condition of diabetes mellitus has little influence on ubiquitin expression and AS formation in this experimental model.