Grishko VI et al. – Mitochondrial DNA (mtDNA) damage and poor mtDNA repair capacity for removing damage caused by oxidative stress may contribute to the pathogenesis of OA. Methods
Study to determine whether mtDNA damage was present in OA chondrocytes, and whether mtDNA repair capacity is compromised in OA chondrocytes following oxidative stress, leading to chondrocyte death
Human articular cartilage was isolated from knee joints of cadavers or OA pts
Total DNA was isolated by collagenase digestion, or from first passage chondrocytes grown in culture and exposed to ROS or RNS
mtDNA integrity and repair capacity were analyzed by quantitative Southern blot analysis
Cell viability was determined by the trypan blue exclusion method
Results
mtDNA damage was found in chondrocytes from OA pts vs normal donors
It was accompanied with reduced mtDNA repair capacity, cell viability, and increased apoptosis in OA chondrocytes following exposure to ROS and RNS
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