ABSTRACT
The expression of BAX in carotid atherosclerosis and its regulation is far from defined. Objectives To investigate BAX expression in stable/fibrous and instable/vulnerable carotid plaque and its clinical significance. Methods Twenty-five cases of carotid plaque specimens obtained from endarterectomy were divided into two groups, stable/fibrous 14 cases, vulnerable/instable 11 cases; aortic artery and its branches from hepatic transplantation donors 6 case as control. The expression of proapoptotic BAX was detected by immunohistochemistry (IHC), in situ hybridization(ISH) and in situ TdT dUTP nick end labeling (TUNEL). Results Five cases of BAX ( + ) were detected by ICH and ISH, 4 case of TUNEL ( + ) were detected by TUNEL in stable/fibrous carotid plaque , while 10 cases were BAX ( + )by IHC(P < 0.05) , 11 cases by ISH and 9 cases by TUNEL were detected in instable/vulnerable carotid plaque ( P < 0.01 ), respectively. The intensity of BAX ( + ) cells by IHC and ISH was (8.63 +/- 2.62) and (10.32 +/- 3.12) in fibrous plaques, whereas (122 +/- 21.64) and (152 +/- 23.35) in vulnerable plaques, respectively. No expression of BAX was found in controlled group. Conclusion The higher expression of Bax in vulnerable carotid plaque may be one mechanism in molecular pathogenesis of carotid atherosclerosis which affect plaque stability and be the cause of higher incidence of stroke than fibrous carotid plaques, the regulation of BAX expression in different stage of atherosclerosis may provide targets in gene therapy for carotid atherosclerosis.
ABSTRACT
<p><b>OBJECTIVE</b>To 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.</p><p><b>METHODS</b>Totally 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).</p><p><b>RESULTS</b>Bcl-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).</p><p><b>CONCLUSION</b>The 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.</p>