2026-06-14T02:28:07Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/134182024-11-29T11:59:24Zcom_20.500.12105_19604com_20.500.12105_2051com_20.500.12105_15322col_20.500.12105_19605col_20.500.12105_16985
Repisalud
author
Scotece, Morena
author
Rego-Perez, Ignacio
author
Lechuga-Vieco, Ana V.
author
Centeno-Cortes, Alberto
author
Jimenez-Gomez, Maria Concepcion
author
Filgueira-Fernández, Purificación
author
Vaamonde-Garcia, Carlos
author
Enriquez, Jose Antonio
author
Blanco, Francisco J
funder
Instituto de Salud Carlos III
funder
Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF)
funder
Xunta de Galicia (España)
2021-10-04T07:57:35Z
2021-10-04T07:57:35Z
2021-04
Sci Rep. 2021; 11(1):9112
10.1038/s41598-021-88083-0
2045-2322
Scientific reports
33907208
http://hdl.handle.net/20.500.12105/13418
It has been suggested that mitochondrial dysfunction and mtDNA variations may contribute to osteoarthritis (OA) pathogenesis. However, the causative link to support this claim is lacking. Here, we surgically-induced OA in conplastic mice in order to evaluate the functional consequences of mtDNA haplotypes in their joint degeneration. BL/6NZB strain was developed with C57BL/6JOlaHsd nuclear genome and NZB/OlaHsdmtDNA while BL/6C57, which is the original, was developed with C57BL/6JOlaHsd nuclear genome and C57/OlaHsdmtDNA for comparison. The surgical DMM OA model was induced in both strains. Their knees were processed and examined for histopathological changes. Cartilage expression of markers of autophagy, apoptosis, oxidative stress and senescence were also analyzed by immunohistochemistry. The joints of BL/6NZB mice that were operated presented more cellularity together with a reduced OARSI histopathology score, subchondral bone, menisci score and synovitis compared to those of BL/6C57 mice. This was accompanied with higher autophagy and a lower apoptosis in the cartilage of BL/6NZB mice that were operated. Therefore, the study demonstrates the functional impact of non-pathological variants of mtDNA on OA process using a surgically-induced OA model. Conplastic (BL/6NZB ) mice develop less severe OA compared to the BL/6C57original strain. These findings demonstrate that mitochondria and mtDNA are critical targets for potential novel therapeutic approaches to treat osteoarthritis.
eng
Mitochondrial DNA impact on joint damaged process in a conplastic mouse model after being surgically induced with osteoarthritis.
journal article
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