alexa Mitochondrial DNA Deletions are Associated with Upregul
ISSN: 2167-7921

Journal of Arthritis
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Research Article

Mitochondrial DNA Deletions are Associated with Upregulated Articular Nitrotyrosine in Human Femoral Head Cartilage

Jörn Zwingmann1*, Bernhard Setzer2, Markus Große Perdekamp3, Wolfgang Schlickewei4, Norbert P Südkamp1, Chingching Foocharoen5 and Ulrich A Walker2,6
1Department of Orthopedic and Trauma Surgery, Freiburg University, Germany
2Department of Rheumatology and Clinical Immunology, Freiburg University, Germany
3Institute for Forensic Medicine, Freiburg University, Germany
4St. Josef’s Hospital, Freiburg, Germany
5Department of Medicine, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand
6Department of Rheumatology, Basel University, Switzerland
*Corresponding Author : Jörn Zwingmann
Department of Orthopaedic and Trauma Surgery
University of Freiburg Medical Center
Hugstetter Strabe 55, 79106 Freiburg, Germany
Tel: +49-761-270-24010
Fax: +49-761-270-27830
E-mail: [email protected]
Rec date: February 07, 2015; Acc date: February 24, 2016; Pub date: February 29, 2016
Citation: Zwingmann J, Setzer B, Perdekamp MG, Schlickewei W, Sudkamp NP, et al. (2016) Mitochondrial DNA Deletions are Associated with Upregulated Articular Nitrotyrosine in Human Femoral Head Cartilage. J Arthritis 5:195. doi:10.4172/2167-7921.1000195
Copyright: © 2016 Zwingmann J, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Background: The pathogenesis of osteoarthritis (OA) has been linked with the elaboration of increased amounts of nitrotyrosine in cartilage as a stable marker of tyrosine nitration by nitric oxide. Reactive oxygen species (ROS) are known to damage mitochondrial DNA (mtDNA); this process is associated with aging of non-cartilaginous tissues. This study aimed to link intraarticular nitrotyrosine content, with mtDNA lesions and OA severity in order to gain insights into the contribution of nitrotyrosine and mitochondria to cartilage aging and the development of OA. Methods: Femoral heads were prospectively obtained from individuals undergoing hip arthroplasty or postmortem autopsy (22 male, 26 female, age range 16-93 years). OA severity was graded radiographically, and histologically by means of the Mankin score. Articular chondrocytes were isolated, and the ‘common’ mtDNA deletion quantified with a Polymerase Chain Reaction (PCR) technique. mtDNA copy numbers per chondrocyte were determined by quantitative PCR. Articular nitrotyrosine content in chondrocytes was quantified by ELISA. Multivariate associations between parameters were computed by linear regression analysis or Spearman rank correlations, as appropriate. Results: Articular nitrotyrosine concentrations were independently correlated with both, the age of the subjects (r=0.39, p=0.01) and the presence of the common deletion (r=0.48, p=0.004), but not with the Mankin Score (p=0.84) or wild type mtDNA copy numbers. The severity of hip OA (Mankin score) however was only correlated with patient age, but not with articular nitrotyrosine, mtDNA deletions or wild type mtDNA copy numbers. Conclusions: mtDNA lesions are correlated with articular nitrotyrosine content in hip cartilage, but a link of mitochondrial mutagenesis and NO-mediated ROS formation with the age of the subjects, or with OA severity cannot be demonstrated in this study.


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