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Joint Bone Spine
Volume 80, n° 6
pages 613-620 (décembre 2013)
Doi : 10.1016/j.jbspin.2013.01.001
accepted : 3 January 2013
Sirt1-deficient mice exhibit an altered cartilage phenotype
 

Odile Gabay a, , Kristien J. Zaal b, Christelle Sanchez c, Mona Dvir-Ginzberg d, Viktoria Gagarina a, Yingjie Song e, Xiao Hong He f, Michael W. McBurney f
a Cartilage Biology and Orthopedic Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, 50 South Drive, Bethesda, MD, USA 
b Light Imaging Section, Office of Science & Technology, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, USA 
c Bone and Cartilage Research Unit, Institute of Pathology B23, University of Liege, Liege, Belgium 
d Laboratory of Cartilage Biology, Institute of Dental Sciences, Faculty of Dental Medicine, Hebrew University-Hadassah Ein Kerem, Jerusalem, Israel 
e Uniformed Services University of the Health Sciences, Department of Surgery, Bethesda, MD, USA 
f Cancer Therapeutics, Ottawa Hospital Research Institute, 501 Smyth Road, Box 926, Ottawa, Ontario, Canada, K1H 8L6 

Corresponding author. Tel.: +1 301 443 5406; fax: +1 301 480 2958.
Abstract
Objective

We previously demonstrated that Sirt1 regulates apoptosis in cartilage in vitro . Here we attempt to examine in vivo cartilage homeostasis, using Sirt1 total body knockout (KO) mice.

Method

Articular cartilage was harvested from hind paws of 1-week and 3-week-old mice carrying wild type (WT) or null Sirt1 gene. Knees of Sirt1 haploinsufficient mice also were examined, at 6 months. Joint cartilage was processed for histologic examination or biochemical analyses of chondrocyte cultures.

Results

We found that articular cartilage tissue sections from Sirt1 KO mice up to 3 weeks of age exhibited low levels of type 2 collagen, aggrecan, and glycosaminoglycan content. In contrast, protein levels of MMP-13 were elevated in the Sirt1 KO mice, leading to a potential increase of cartilage breakdown, already shown in the heterozygous mice. Additional results showed elevated chondrocyte apoptosis in Sirt1 KO mice, as compared to WT controls. In addition to these observations, PTP1b (protein tyrosine phosphatase b) was elevated in the Sirt1 KO mice, in line with previous reports.

Conclusion

The findings from this animal model demonstrated that Sirt1 KO mice presented an altered cartilage phenotype, with an elevated apoptotic process and a potential degradative cartilage process.

The full text of this article is available in PDF format.

Keywords : Sirtuin 1, Cartilage, Osteoarthritis, Animal models




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