Human-specific duplicate CHRFAM7A gene is associated with more severe osteoarthritis and amplifies pain behaviours
Authors' conclusion
CHRFAM7A is an aggravating factor for OA-associated inflammation and tissue damage and a novel genetic risk factor and therapeutic target for pain.
Study context
- Population
- Transgenic CHRFAM7A mice; mouse and human cells; human joint tissues
- Comparison
- Transgenic CHRFAM7A (TgCHRFAM7A) mice vs wild type (WT) mice
Methodological detailstransgenic mouse models, human cells and joint tissues
- Transgenic mouse models
- Human cells and joint tissues
Main finding
As reported in the abstract
- TgCHRFAM7A mice developed more severe structural damage and increased mechanical allodynia than WT mice in the destabilisation of medial meniscus osteoarthritis (OA) model
- Decreased suppression of inflammation by α7nAchR agonist
- TgCHRFAM7A mice: higher basal sensitivity to pain stimuli and increased pain behaviour in monoiodoacetate and formalin models
- Dorsal root ganglia of TgCHRFAM7A mice: increased macrophage infiltration and fractalkine expression; compromised antinociceptive response to nicotine
- CHRNA7 and CHRFAM7A expressed in human joint tissues; CHRFAM7A/CHRNA7 ratio increased in OA cartilage
- Human chondrocytes with two copies of CHRFAM7A had reduced anti-inflammatory responses to nicotine
Original publication
Human-specific duplicate CHRFAM7A gene is associated with more severe osteoarthritis and amplifies pain behaviours. Ann Rheum Dis. Published 10 January 2023. doi:10.
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