mtDNA haplogroup J Modulates telomere length and Nitric Oxide production
Open Access
- 15 December 2011
- journal article
- research article
- Published by Springer Nature in BMC Musculoskeletal Disorders
- Vol. 12 (1) , 283
- https://doi.org/10.1186/1471-2474-12-283
Abstract
Oxidative stress due to the overproduction of nitric oxide (NO) and other oxygen reactive species (ROS), play a main role in the initiation and progression of the OA disease and leads to the degeneration of mitochondria. Therefore, the goal of this work is to describe the difference in telomere length of peripheral blood leukocytes (PBLs) and Nitric Oxide (NO) production between mitochondrial DNA (mtDNA) haplogroup J and non-J carriers, as indirect approaches of oxidative stress.Keywords
This publication has 44 references indexed in Scilit:
- Association between mitochondrial DNA variations and Alzheimer's disease in the ADNI cohortNeurobiology of Aging, 2010
- Role of European mitochondrial DNA haplogroups in the prevalence of hip osteoarthritis in Galicia, Northern SpainAnnals of the Rheumatic Diseases, 2010
- Mitochondria as metabolizers and targets of nitriteNitric Oxide, 2009
- Diminished mitochondrial DNA integrity and repair capacity in OA chondrocytesOsteoarthritis and Cartilage, 2008
- Reactive nitrogen and oxygen species in interleukin-1-mediated DNA damage associated with osteoarthritisOsteoarthritis and Cartilage, 2007
- Effects of Purifying and Adaptive Selection on Regional Variation in Human mtDNAScience, 2004
- Mitochondrial respiratory activity is altered in osteoarthritic human articular chondrocytesArthritis & Rheumatism, 2003
- Relative expression software tool (REST(C)) for group-wise comparison and statistical analysis of relative expression results in real-time PCRNucleic Acids Research, 2002
- The expression and regulation of nitric oxide synthase in human osteoarthritis-affected chondrocytes: evidence for up-regulated neuronal nitric oxide synthase.The Journal of Experimental Medicine, 1995
- Nitric oxide and energy production in articular chondrocytesJournal of Cellular Physiology, 1994