Bcl-2/Bax gene expression in different types of carotid plaque.
- Author:
Bao-zhong MEN
1
;
Ding-biao ZHOU
;
Xiao-ming ZHANG
;
Huai-yin SHI
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; genetics; Carotid Arteries; metabolism; pathology; Carotid Artery Diseases; metabolism; Carotid Stenosis; metabolism; pathology; Endothelium, Vascular; metabolism; Humans; Macrophages; metabolism; Muscle, Smooth, Vascular; metabolism; Proto-Oncogene Proteins c-bcl-2; biosynthesis; genetics; Up-Regulation; bcl-2-Associated X Protein
- From: Acta Academiae Medicinae Sinicae 2005;27(2):241-244
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate Bcl-2/Bax gene expression in different types of carotid plaque, and examine the relationship between gene expression and atherosclerotic plaque instability and the main cause of brain ischemic events.
METHODSTotally 42 human carotid plaque specimens obtained during carotid endarterectomy were divided into stable group (n=19) and unstable group (n=23) based on histopathological studies (HE staining). Eight aortic arteries and their branches from hepatic transplantation donors were taken as control group. Bcl-2/Bax was detected by immunohistochemistry (IHC) staining (n=42) and in situ hybridization (ISH) (n=25, stable 13/unstable 12).
RESULTSBcl-2 gene expression, which was expressed in smooth muscle cells (SMC), endothelial cells (EC), macrophages (MP) and foam cells, was detected in 20 and 9 cases in unstable plaque while 11 and 4 cases in stable plaque by IHC and ISH, respectively (P < 0.05). Bax, which was expressed in SMC and MP, was detected in 18 and 11 cases in unstable plaque, while 8 and 5 cases in stable plaque by IHC and ISH, respectively (P < 0.05).
CONCLUSIONThe expression rate of Bcl-2/Bax in unstable plaques was higher than in stable plaques. Bcl-2 was one of the elements that maintain plaque stability whereas Bax was one element that facilitates plaque instability. Therefore, Bcl-2/Bax expression in different stage of atherosclerosis may be one of the molecule regulation mechanisms in carotid atherosclerosis.