Environmental Noise Induces Endoplasmic Reticulum Stress Response and Cardiac Hypertrophy in Rats

• Published in: American journal of hypertension Vol. 25; no. 3; p. 396
• Main Authors: Hu, Zhong-wei, Zhao, Lian-you, Liu, Sha-sha, Shang, Fu-jun, Ai, Yong-fei, Huai, Yong, Li, Wei
• Format: Journal Article
• Language: English
• Published: Oxford University Press 01.03.2012
• DOI: 10.1038/ajh.2012.6a
• ISSN: 0895-7061

Objective To study the effects of environmental noise on myocardial expression of endoplasmic reticulum (ER) stress response proteins, glucose-regulated protein 78 (GRP78) and C/EBP-homologous protein (CHOP), and cardiac hypertrophy in rats. Methods Forty male SD rats were divided randomly into two groups: the noise stress group (n = 20), the control group (n = 20). The noise stress group was further divided into 4 subgroups (n = 5 per group): 2, 4, 6 and 8 weeks of noise stress. Mean arterial pressure (MAP) was measured through carotid cannulation. LV posterior wall thickness (LVPWT), ejection fraction (EF) and E/A were assessed by echocardiography. LV to body mass index (LVMI) was calculated. Protein levels of GRP78 and CHOP were evaluated by immunohistochemistry and Western blotting. Myocardial apoptosis was detected by TUNEL staining. Results MAP was significantly higher in the noise stress group compared to the control group (P<0.01). LVPWT and LVMI were significantly increased after 4, 6 and 8 weeks of noice stress compared with the control group (P<0.05). While E/A and EF values in noise stress group decreased at week 2 and week 6, respectively, protein levels of GRP78 in the myocardium increased, reached its peak at week 4, and then declined. The protein levels of CHOP were increased in a time-dependent manner. Furthermore, myocardial apoptosis was also increased in the noise stress groups. Conclusion Environmental noise activates ER stress in the heart. The increased expression of GRP78 and CHOP may contribute to cardiac hypertrophy and myocardial apoptosis induced by noise stress.