Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Mismatch Repair01:20

Mismatch Repair

5.2K
Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
5.2K
Animal Mitochondrial Genetics02:59

Animal Mitochondrial Genetics

8.0K
Among all the organelles in an animal cell, only mitochondria have their own independent genomes. Animal mitochondrial DNA is a double-stranded, closed-circular molecule with around 20,000 base pairs. Mitochondrial DNA is unique in that one of its two strands, the heavy, or H, -strand is guanine rich, whereas the complementary strand is cytosine rich and called the light, or L, -strand. Compared to nuclear DNA, mitochondrial DNA has a very low percentage of non-coding regions and is marked by...
8.0K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Association between progression of knee osteoarthritis pathology and gait changes over two years: Data from the IMI-APPROACH cohort.

Osteoarthritis imaging·2026
Same author

Impact of quantified knee positioning on the measurement of minimal joint space width using statistical shape models: A cross-sectional and longitudinal analysis in the IMI-APPROACH.

Osteoarthritis imaging·2026
Same author

Vasoactive intestinal peptide advances chondrogenesis and modulates pathogenic mediators in human osteoarthritis.

Journal of molecular medicine (Berlin, Germany)·2026
Same author

Abatacept versus hydroxychloroquine for prevention of rheumatoid arthritis in individuals with palindromic rheumatism: a randomized open-label trial.

Nature medicine·2026
Same author

Progression of bone and joint space deformity in patients with mild knee osteoarthritis: Data from the IMI-APPROACH cohort.

Osteoarthritis and cartilage open·2026
Same author

Butyrate extends health and lifespan in mice with mitochondrial deficiency.

Nature communications·2026

Related Experiment Video

Updated: Sep 6, 2025

Establishment of a Surgically-induced Model in Mice to Investigate the Protective Role of Progranulin in Osteoarthritis
07:58

Establishment of a Surgically-induced Model in Mice to Investigate the Protective Role of Progranulin in Osteoarthritis

Published on: February 25, 2014

28.8K

mtDNA variability determines spontaneous joint aging damage in a conplastic mouse model.

Morena Scotece1, Carlos Vaamonde-García1,2, Ana Victoria Lechuga-Vieco3,4,5

  • 1Unidad de Genómica, Grupo de Investigación de Reumatología (GIR), Instituto de Investigación Biomédica de A Coruña (INIBIC), Complexo Hospitalario Universitario de A Coruña (CHUAC), Sergas, Universidade da Coruña (UDC), A Coruña 15006, Spain.

Aging
|July 2, 2022
PubMed
Summary

Mitochondrial DNA (mtDNA) variations impact joint aging. This study shows manipulating mtDNA in conplastic mice reduced joint damage and aging markers, suggesting mtDNA is key for osteoarthritis and mitochondrial targets for therapy.

Keywords:
autophagyconplastic micemtDNAoxidative stresssenescence

More Related Videos

Destabilization of the Medial Meniscus and Cartilage Scratch Murine Model of Accelerated Osteoarthritis
07:06

Destabilization of the Medial Meniscus and Cartilage Scratch Murine Model of Accelerated Osteoarthritis

Published on: July 6, 2022

4.7K
A Mouse Model of Ankle-Subtalar Complex Joint Instability
09:14

A Mouse Model of Ankle-Subtalar Complex Joint Instability

Published on: October 28, 2022

1.4K

Related Experiment Videos

Last Updated: Sep 6, 2025

Establishment of a Surgically-induced Model in Mice to Investigate the Protective Role of Progranulin in Osteoarthritis
07:58

Establishment of a Surgically-induced Model in Mice to Investigate the Protective Role of Progranulin in Osteoarthritis

Published on: February 25, 2014

28.8K
Destabilization of the Medial Meniscus and Cartilage Scratch Murine Model of Accelerated Osteoarthritis
07:06

Destabilization of the Medial Meniscus and Cartilage Scratch Murine Model of Accelerated Osteoarthritis

Published on: July 6, 2022

4.7K
A Mouse Model of Ankle-Subtalar Complex Joint Instability
09:14

A Mouse Model of Ankle-Subtalar Complex Joint Instability

Published on: October 28, 2022

1.4K

Area of Science:

  • Mitochondrial biology and genetics
  • Aging research
  • Osteoarthritis pathogenesis

Background:

  • Mitochondria and their DNA (mtDNA) are implicated in aging processes.
  • mtDNA variations may influence age-related joint degeneration.
  • Conplastic mouse models allow investigation of mtDNA effects on nuclear genomes.

Purpose of the Study:

  • To investigate the impact of mtDNA variation on joint aging and damage.
  • To compare joint pathology and molecular markers in conplastic mice with differing mtDNA.
  • To explore mitochondrial oxidative phosphorylation (OXPHOS) as a therapeutic target for osteoarthritis (OA).

Main Methods:

  • Development of a conplastic mouse strain (BL/6NZB) with C57BL/6 nuclear genome and NZB mtDNA.
  • Histological analysis of knee joints and Mankin scoring at multiple ages (25, 75, 90 weeks).
  • Immunohistochemical analysis of autophagy, senescence, proliferation, oxidative damage, and apoptosis markers.

Main Results:

  • Conplastic (BL/6NZB) mice exhibited significantly lower Mankin scores, indicating reduced joint damage.
  • These mice showed altered expression of autophagy (increased LC3, Beclin-1; decreased P62) and senescence markers (decreased MMP13, beta-Galactosidase, p16).
  • BL/6NZB mice displayed higher proliferation (Ki67) and lower oxidative damage (8-oxo-dG) and apoptosis (cleaved caspase-3) markers.

Conclusions:

  • mtDNA genetic manipulation ameliorates joint aging damage in a conplastic mouse model.
  • mtDNA variability is a prognostic factor for aging-related osteoarthritis (OA).
  • Modulation of mitochondrial oxidative phosphorylation (OXPHOS) presents a potential therapeutic strategy for OA.