Synovial fluid mitochondrial DNA concentration reflects the degree of cartilage damage after naturally occurring articular injury.
Synovial fluid mitochondrial DNA concentration reflects the degree of cartilage damage after naturally occurring articular injury.
复制标题
滑液线粒体DNA浓度反映了自然发生的关节损伤后软骨损伤的程度。
DOI:
10.1016/j.joca.2023.03.013
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发表时间:
2023
影响因子:
7
通讯作者:
Delco,ML
中科院分区:
文献类型:
--
作者:
Seewald,LA;Sabino,IG;Montney,KL;Delco,ML
ObjectiveTo evaluate mitochondrial DNA (mtDNA) release from injured chondrocytes and investigate the utility of synovial fluid mtDNA concentration in early detection of posttraumatic osteoarthritis.MethodWe measured mtDNA release using four models of osteoarthritis:in vitrointerleukin-1β stimulation of cultured equine chondrocytes,ex vivomechanical impact of bovine cartilage explants,in vivomechanical impact of equine articular cartilage, and naturally occurring equine intraarticular fracture. In ourin vivomodel, one group was treated with an intraarticular injection of the mitoprotective peptide SS-31 following cartilage injury. mtDNA content was quantified using qPCR. For naturally occurring cases of joint injury, clinical data (radiographs, arthroscopic video footage) were scored for criteria associated with degenerative joint disease.ResultsChondrocytes released mtDNA in the acute time frame following inflammatory and mechanical cellular stressin vitro. mtDNA was increased in equine synovial fluid following experimental and naturally occurring injury to the joint surface. In naturally occurring posttraumatic osteoarthritis, we found a strong positive correlation between the degree of cartilage damage and mtDNA concentration (r= 0.80,P= 0.0001). Finally, impact-induced mtDNA release was mitigated by mitoprotective treatment.ConclusionChanges in synovial fluid mtDNA occur following joint injury and correlate with the severity of cartilage damage. Mitoprotection mitigates increases in synovial fluid mtDNA suggesting that mtDNA release may reflect mitochondrial dysfunction. Further investigation of mtDNA as a potentially sensitive marker of early articular injury and response to mitoprotective therapy is warranted.