Role of neuropeptide Y and peroxisome proliferator-activated receptor γ coactivator-1α in stress cardiomyopathy.
10.1007/s11596-012-1041-3
- Author:
Sunnassee ANANDA
1
;
Yunyun WANG
;
Shaohua ZHU
;
Rongshuai WANG
;
Xiaowei ZHOU
;
Luo ZHUO
;
Tingyi SUN
;
Liang REN
;
Qian LIU
;
Hongmei DONG
;
Yan LIU
;
Liang LIU
Author Information
1. Department of Forensic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. Alandocs@gmail.com
- Publication Type:Journal Article
- MeSH:
Animals;
Cardiomyopathies;
metabolism;
Myocytes, Cardiac;
metabolism;
Neuropeptide Y;
metabolism;
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha;
Rats;
Rats, Sprague-Dawley;
Stress, Physiological;
physiology;
Transcription Factors;
metabolism
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2012;32(6):823-828
- CountryChina
- Language:English
-
Abstract:
Death following situations of intense emotional stress has been linked to the cardiac pathology described as stress cardiomyopathy, whose pathomechanism is still not clear. In this study, we sought to determine, via an animal model, whether the transcriptional coactivator peroxisome proliferator-activated receptor γ coactivator-1alpha (PGC-1α) and the amino peptide neuropeptide Y (NPY) play a role in the pathogenesis of this cardiac entity. Male Sprague-Dawley rats in the experimental group were subjected to immobilization in a plexy glass box for 1 h, which was followed by low voltage electric foot shock for about 1 h at 10 s intervals in a cage fitted with metallic rods. After 25 days the rats were sacrificed and sections of their hearts were processed. Hematoxylin-eosin staining of cardiac tissues revealed the characteristic cardiac lesions of stress cardiomyopathy such as contraction band necrosis, inflammatory cell infiltration and fibrosis. The semi-quantitative RT-PCR analysis for PGC-1α mRNA expression showed significant overexpression of PGC1-α in the stress-subjected rats (P<0.05). Fluorescence immunohistochemistry revealed a higher production of NPY in the stress-subjected rats as compared to the control rats (P=0.0027). Thus, we are led to conclude that following periods of intense stress, an increased expression of PGC1-α in the heart and an overflow of NPY may lead to stress cardiomyopathy and even death in susceptible victims. Moreover, these markers can be used to identify stress cardiomyopathy as the cause of sudden death in specific cases.
