Jia-Ping Wu1, Shu Nu Chang-Lee2, Cecilia Hsuan Day3, Tsung-Jung Ho4, Vijaya Padma Viswanadha5, Li-Chin Chung6, Jin-Ming Hwang7, Gwo-Ping Jong8, Wei-Wen Kuo9, Chih-Yang Huang10. 1. Graduate Institute of Basic Medical Science, China Medical University. 2. Department of Healthcare Administration, Asia University, Taichung. 3. Department of Nursing, MeiHo University, Pingtung. 4. Graduate Institute of Chinese Medicine, China Medical University, Taichung; ; Chinese Medicine Department, China Medical University Beigang Hospital, Taiwan. 5. Department of Biotechnology, Bharathiar University, Coimbatore, India. 6. Department of Hospital and Health Care Administration, Chia Nan University of Pharmacy & Science, Tainan County. 7. School of Applied Chemistry, Chung Shan Medical University. 8. Division of Cardiology, Armed Force Taichung General Hospital. 9. Department of Biological Science and Technology, China Medical University. 10. Graduate Institute of Basic Medical Science, China Medical University; ; Graduate Institute of Chinese Medicine, China Medical University, Taichung; ; Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan.
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 TGFβ1/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 TGFβ1/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. TGFβ1/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.
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 TGFβ1/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 TGFβ1/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. TGFβ1/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.
Authors: Carol G Au; Tanya L Butler; Megan C Sherwood; Jonathan R Egan; Kathryn N North; David S Winlaw Journal: Int J Exp Pathol Date: 2010-12-01 Impact factor: 1.925
Authors: Margaux A Horn; Helen K Graham; Mark A Richards; Jessica D Clarke; David J Greensmith; Sarah J Briston; Mark C S Hall; Katharine M Dibb; Andrew W Trafford Journal: J Mol Cell Cardiol Date: 2012-03-30 Impact factor: 5.000