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Oxidative Medicine and Cellular Longevity
Volume 2017 (2017), Article ID 5135241, 13 pages
Research Article

Acute Exposure to Cigarette Smoking Followed by Myocardial Infarction Aggravates Renal Damage in an In Vivo Mouse Model

1Department of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut, Beirut, Lebanon
2Department of Biological and Chemical Sciences, Lebanese International University, Beirut, Lebanon
3Department of Pharmacology and Toxicology, American University of Beirut, Beirut, Lebanon
4ER045, PRASE, DSST, Lebanese University, Beirut, Lebanon
5CNRS UPR9002, Institute of Molecular and Cellular Biology, Strasbourg University, Strasbourg, France
6Department of Pathology, School of Medicine, Lebanese American University, Beirut, Lebanon
7GICC, UMR 7292, CNRS, Université François Rabelais de Tours, Tours, France
8Department of Anatomy, Cell Biology and Physiological Sciences, American University of Beirut, Beirut, Lebanon
9Department of Basic Medical Sciences, College of Medicine, Qatar University, Doha, Qatar
10Biology Department, Faculty of Sciences-I, Lebanese University, Beirut, Lebanon

Correspondence should be addressed to Ahmad Husari, Fouad A. Zouein, and Kazem Zibara

Received 31 March 2017; Revised 6 June 2017; Accepted 19 September 2017; Published 22 October 2017

Academic Editor: Andreas Daiber

Copyright © 2017 Firas Kobeissy et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Cigarette smoking (S) is a risk factor for progressive chronic kidney disease, renal dysfunction, and renal failure. In this study, the effect of smoking on kidney function was investigated in a mouse model of myocardial infarction (MI) using 4 groups: control (C), smoking (S), MI, and S+MI. Histological analysis of S+MI group showed alterations in kidney structure including swelling of the proximal convoluted tubules (PCTs), thinning of the epithelial lining, focal loss of the brush border of PCTs, and patchy glomerular retraction. Molecular analysis revealed that nephrin expression was significantly reduced in the S+MI group, whereas sodium-hydrogen exchanger-1 (NHE-1) was significantly increased, suggesting altered glomerular filtration and kidney functions. Moreover, S+MI group, but not S alone, showed a significant increase in the expression of connective tissue growth factor (CTGF) and fibrotic proteins fibronectin (FN) and α-smooth muscle actin (SMA), in comparison to controls, in addition to a significant increase in mRNA levels of IL-6 and TNF-α inflammatory markers. Finally, reactive oxygen species (ROS) production was significantly accentuated in S+MI group concomitant with a significant increase in NOX-4 protein levels. In conclusion, smoking aggravates murine acute renal damage caused by MI at the structural and molecular levels by exacerbating renal dysfunction.