Secondhand Smoke Exposure Enhances Cardiac Fibrosis Effects on the Aging Rat Hearts

doi:10.6515/ACS20150824C

CNU IR > College of Smart Living > Dept. of Hospital and Health (including master's program) > Periodical Articles > Item 310902800/30935

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Title:	Secondhand Smoke Exposure Enhances Cardiac Fibrosis Effects on the Aging Rat Hearts
Authors:	Wu, Jia-Ping Chang-Lee, Shu Nu Day, Cecilia Hsuan Ho, Tsung-Jung Viswanadha, Vijaya Padma Chung, Li-Chin Hwang, Jin-Ming Jong, Gwo-Ping Kuo, Wei-Wen Huang, Chih-Yang
Contributors:	China Med Univ, Grad Inst Basic Med Sci Asia Univ, Dept Healthcare Adm MeiHo Univ, Dept Nursing China Med Univ, Grad Inst Chinese Med China Med Univ, Chinese Med Dept, Beigang Hosp Bharathiar Univ, Dept Biotechnol, Coimbatore Chia Nan Univ Pharm & Sci, Dept Hosp & Hlth Care Adm Chung Shan Med Univ, Sch Appl Chem Armed Force Taichung Gen Hosp, Div Cardiol China Med Univ, Dept Biol Sci & Technol Asia Univ, Dept Hlth & Nutr Biotechnol
Keywords:	Aging Basic fibroblast growth factors Connective tissue growth factor Extracellular matrix Secondhand smoke exposure infarction
Date:	2016-09
Issue Date:	2018-01-18 11:38:15 (UTC+8)
Publisher:	Taiwan Soc Cardiology
Abstract:	Background: Examining aging rats exposed to secondhand smoke (SHS) engenders changes in left ventricular remodeling due to age- or disease-dependent alterations. Methods: Rats were placed in whole-body exposure chambers and exposed to 10 cigarettes. Filtered air was introduced into the chamber at a low rate. Rats were exposed to SHS for 30 min, twice a day, 5 days per week for 1 month. After 4 weeks SHS exposure, rats were sacrificed for morphological study with trichome staining and left ventricular remodeling related protein analysis using western blot. Results: Characteristic fibrotic morphology in the left ventricle increased significantly with aging and exposure to SHS. Exposure to SHS elevated TGF1 beta 1/p-Smad2/3/CTGF and MMP2/MMP9 protein expression levels (p < 0.05). No significant differences in FGF-2 and UPA protein expression were noted as a result of SHS exposure. However, TIMP-1, TIMP-2, TIMP-3 and TIMP-4 protein expression were suppressed by SHS exposure. We also observed increased TGF beta 1/p-Smad2/3/CTGF (p < 0.01), FGF-2/UPA (p < 0.05) and decreased TIMPs protein expression levels. Corresponding MMP2 and MMP9 upregulation occurred with aging and exposure to SHS. TGF beta 1/p-Smad2/3/CTGF and FGF-2/UPA protein expression from SHS exposure were higher than that from aging. In contrast, MMP2 and MMP9 were increased in aging rats compared with SHS exposed rats (p < 0.05); however, TIMP-1 (p < 0.01), TIMP-2 (p < 0.01) and TIMP-3 (p < 0.05) were decreased. TIMP-4 protein expression levels were decreased compared with SHS exposed rats (p < 0.01). Conclusions: Aging and SHS exposure in rats will produce elevated fibrosis. Exposure to SHS will accelerate aging and left ventricular fibrosis.
Relation:	Acta Cardiologica Sinica, v.32 n.5, pp.594-603
Appears in Collections:	[Dept. of Hospital and Health (including master's program)] Periodical Articles

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