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- Bouderlique, T, et al.
(author)
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AUTOPHAGY AND OSTEOARTHRITIS DEVELOPMENT
- 2015
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In: OSTEOARTHRITIS AND CARTILAGE. - : Elsevier BV. - 1063-4584. ; 23, s. A309-A309
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Conference paper (other academic/artistic)
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- Bouderlique, T, et al.
(author)
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Targeted deletion of Atg5 in chondrocytes promotes age-related osteoarthritis
- 2016
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In: Annals of the rheumatic diseases. - : BMJ. - 1468-2060 .- 0003-4967. ; 75:3, s. 627-631
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Journal article (peer-reviewed)abstract
- It has been suggested that the lysosomal recycling process called macro-autophagy plays a role in osteoarthritis development. We thus decided to genetically ablate the autophagy-indispensable Atg5 gene specifically in chondrocytes and analyse the development of osteoarthritis upon aging and in a post-traumatic model.MethodsMice lacking the Atg5 gene in their chondrocytes (Atg5cKO) were generated by crossing Atg5-floxed mice with transgenic mice that expressed cre recombinase driven by the collagen type 2 promoter. Animals were analysed at the age of 2, 6 and 12 months for age-related osteoarthritis or underwent mini-open partial medial meniscectomy at 2 months of age and were analysed 1 or 2 months after surgery. We evaluated osteoarthritis using the Osteoarthritis Research Society International (OARSI) scoring on safranin-O-stained samples. Cell death was evaluated by terminal deoxy-nucleotidyl-transferase-mediated deoxy-UTP nick end labelling (TUNEL) and by immunostaining of cleaved caspases.ResultsWe observed the development of osteoarthritis in Atg5cKO mice with aging including fibrillation and loss of proteoglycans, which was particularly severe in males. The ablation of Atg5 was associated with an increased cell death as assessed by TUNEL, cleaved caspase 3 and cleaved caspase 9. Surprisingly, no difference in the development of post-traumatic osteoarthritis was observed between Atg5cKO and control mice.ConclusionsAutophagy protects from age-related osteoarthritis by facilitating chondrocyte survival.
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- Chagin, AS, et al.
(author)
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Androgen receptor modulation does not affect longitudinal growth of cultured fetal rat metatarsal bones
- 2009
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In: Hormone research. - : S. Karger AG. - 1423-0046. ; 71:4, s. 219-227
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Journal article (peer-reviewed)abstract
- <i>Background:</i> Systemic administration of the nonaromatizable androgen oxandrolone stimulates growth in girls with Turner syndrome and boys with a constitutional delay of growth and puberty. It is unknown if oxandrolone acts locally at the growth plate level to stimulate longitudinal bone growth. <i>Methods:</i> Metatarsal bones from female and male rat fetuses (day E20) were cultured for 14 days in the presence of oxandrolone, testosterone or the androgen receptor (AR) antagonist flutamide with/without insulin-like growth-factor-I (IGF-I) or charcoal-treated serum. <i>Results:</i> The AR was found to be expressed in both male and female fetal rat metatarsal bones. Neither oxandrolone nor testosterone had any effect on metatarsal bone growth when tested at a wide concentration range (1 n<i>M</i> to 10 μ<i>M</i>), not even in the presence of IGF-I (100 ng/ml) or charcoal-treated serum (10%). Bone growth was also unaffected when the AR was blocked by flutamide. Control experiments confirmed that metatarsal bone growth was significantly stimulated by IGF-I (p < 0.001). <i>Conclusion:</i> Modulation of AR activity in the fetal rat growth plate does not affect linear bone growth. Extrapolating from these in vitro data, it could be speculated that oxandrolone stimulates longitudinal bone growth in treated children by acting indirectly rather than directly through AR activation in growth plate chondrocytes.
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- Chagin, AS, et al.
(author)
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Estrogens and growth: review
- 2007
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In: Pediatric endocrinology reviews : PER. - 1565-4753. ; 4:4, s. 329-34
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Journal article (peer-reviewed)
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