Sexual dimorphism, but not testosterone itself, is responsible for ankylosing enthesitis of the ankle in B10.BR (H-2k) male mice
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
16344499
PubMed Central
PMC1797974
DOI
10.1136/ard.2005.039800
PII: S0003-4967(24)20345-9
Knihovny.cz E-zdroje
- MeSH
- ankylóza krev patofyziologie MeSH
- lidé MeSH
- myši inbrední C57BL MeSH
- myši MeSH
- orchiektomie MeSH
- pohlavní dimorfismus * MeSH
- testosteron krev fyziologie MeSH
- zadní končetina * MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- mužské pohlaví MeSH
- myši MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- testosteron MeSH
BACKGROUND: Ankylosing enthesopathy (ANKENT) with progressive stiffening of ankle and tarsal joints of the hind limbs is a naturally occurring arthropathy in B10.BR mice. Some features are similar to those of the spondyloarthropathies in humans. OBJECTIVE: To study the role of sexual dimorphism and testosterone in the development of ANKENT. METHODS: The incidence of ANKENT was observed in non-castrated, castrated, and testosterone substituted castrated male mice, and in control and testosterone treated female mice. RESULTS: ANKENT occurred only in males; it did not develop in males castrated at age 2-3 months but occurred in castrated males injected with testosterone. Females injected with testosterone did not develop ANKENT. CONCLUSION: Testosterone can replace what castration eliminates, at least in the postpubertally castrated males, but is itself not sufficient to induce joint disease.
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