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Oxidative Medicine and Cellular Longevity
Volume 2014 (2014), Article ID 141053, 11 pages
http://dx.doi.org/10.1155/2014/141053
Research Article

Deletion of Metallothionein Exacerbates Intermittent Hypoxia-Induced Oxidative and Inflammatory Injury in Aorta

1The Center of Cardiovascular Diseases at the First Hospital of Jilin University, 71 Xinmin Street, Changchun 130021, China
2Kosair Children’s Hospital Research Institute at the Department of Pediatrics, University of Louisville, 570 South Preston Street, Baxter I, Suite 321B, Louisville, KY 40202, USA
3Chinese-American Research Institute for Diabetic Complication, Wenzhou Medical College, Wenzhou 325035, China
4Department of Pediatrics, The Second Affiliated Hospital & Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou 325027, China
5Departments of Radiation Oncology and Pharmacology and Toxicology, University of Louisville, Louisville, KY 40202, USA

Received 5 February 2014; Revised 8 July 2014; Accepted 8 July 2014; Published 6 August 2014

Academic Editor: Narasimham L. Parinandi

Copyright © 2014 Shanshan Zhou 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.

Abstract

The present study was to explore the effect of metallothionein (MT) on intermittent hypoxia (IH) induced aortic pathogenic changes. Markers of oxidative damages, inflammation, and vascular remodeling were observed by immunohistochemical staining after 3 days and 1, 3, and 8 weeks after IH exposures. Endogenous MT was induced after 3 days of IH but was significantly decreased after 8 weeks of IH. Compared with the wild-type mice, MT knock-out mice exhibited earlier and more severe pathogenic changes of oxidative damages, inflammatory responses, and cellular apoptosis, as indicated by the significant accumulation of collagen, increased levels of connective tissue growth factor, transforming growth factor , tumor necrosis factor-alpha, vascular cell adhesion molecule 1,3-nitrotyrosine, and 4-hydroxy-2-nonenal in the aorta. These findings suggested that chronic IH may lead to aortic damages characterized by oxidative stress and inflammation, and MT may play a pivotal role in the above pathogenesis process.