H3K9me3 loss and endogenous retroviruses (ERVs) activation as hallmarks for osteoarthritis progression and knee joint aging
Authors' conclusion
The findings suggest a compelling hypothesis that the loss of H3K9me3, either due to aging or cellular stressors, may lead to ERVs reactivation that contributes to tissue inflammation and OA progression.
Study context
- Population
- Cartilage tissues of osteoarthritis (OA) patients; post-traumatic OA mouse models
- Comparison
- Damaged cartilage vs intact cartilage
Methodological detailsERVs-centric analysis of published ATAC-seq and RNA-seq data, immunohistochemistry, post-traumatic OA mouse models
- ERVs-centric analysis of published ATAC-seq and RNA-seq data
- Immunohistochemistry
- Post-traumatic OA mouse models
Main finding
As reported in the abstract
- Chromatin accessibility and transcription of ERVs, particularly intermediate-age families (ERV1 and ERVL), enriched and elevated in OA cartilage
- H3K9me3-related heterochromatin loss might be mechanistically connected to ERV activation in OA tissue
- Global H3K9me3 levels reduced in diseased vs intact cartilage in OA patients and injury-induced OA mice
Original publication
H3K9me3 loss and ERVs activation as hallmarks for osteoarthritis progression and knee joint aging. Osteoarthritis Cartilage. Published 15 August 2024. doi:10.
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