Chronic stress: a crucial promoter of cell apoptosis in atherosclerosis

Author:

Meng Ling-bing1,Shan Meng-jie2,Yu Ze-mou3,Lv Jian4,Qi Ruo-mei5,Guo Peng6,Zhang Yuan-meng7,Gong Tao1ORCID

Affiliation:

1. Neurology Department, Beijing Hospital, National Center of Gerontology, Dong Dan, Beijing, China

2. MOH Key Laboratory of Systems Biology of Pathogens, Institute of Pathogen Biology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China

3. Department of Neurology, Peking University First Hospital, Beijing, China

4. Second Department of Surgery, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, P.R. China

5. The MOH Key Laboratory of Geriatrics, Beijing Hospital, National Center of Gerontology, Dong Dan, Beijing, China

6. Department of Orthopedics, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, P.R. China

7. Internal Medicine Department, Jinzhou Medical University, Liaoning, China

Abstract

Objective Chronic stress may lead to augmented incidence rates of coronary and cerebrovascular diseases associated with atherosclerosis. However, few studies have focused on the effect of chronic stress on atherosclerosis plaque formation. Therefore, this study was designed to directly evaluate how chronic stress affects atherosclerosis. Methods Thirty rabbits were divided into three groups: the control group, balloon-injury operation + high-fat diet model group, and chronic stress + balloon-injury operation + high-fat diet model group. Physical and social stress were induced, and proteomic methods were applied to identify specific markers. Results After protein determination, the chronic stress + balloon-injury operation + high-fat diet model group exhibited significant upregulation of the following apoptosis-related proteins: UBE2K, caspase 3, caspase 9, BAX, P53, and FAS. In particular, real-time polymerase chain reaction showed that the protein expression of caspase 9 was significantly downregulated in the stress group compared with the non-stress groups. However, the other proteins showed significantly increased expression in the stress group. Conclusion Chronic stress may promote cell apoptosis in the physiopathologic process of atherosclerosis.

Funder

National Natural Science Foundation of China

Publisher

SAGE Publications

Subject

Biochemistry (medical),Cell Biology,Biochemistry,General Medicine

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