Sodium Thiosulfate Prevents Chondrocyte Mineralization and Reduces the Severity of Murine Osteoarthritis.

Details

Ressource 1Download: BIB_7920E7051A8B.P001.pdf (3973.68 [Ko])
State: Public
Version: author
Serval ID
serval:BIB_7920E7051A8B
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Sodium Thiosulfate Prevents Chondrocyte Mineralization and Reduces the Severity of Murine Osteoarthritis.
Journal
PloS one
Author(s)
Nasi S., Ea H.K., Lioté F., So A., Busso N.
ISSN
1932-6203 (Electronic)
ISSN-L
1932-6203
Publication state
Published
Issued date
2016
Peer-reviewed
Oui
Volume
11
Number
7
Pages
e0158196
Language
english
Notes
Publication types: Journal Article
Publication Status: epublish
Abstract
Calcium-containing crystals participate in the pathogenesis of OA. Sodium thiosulfate (STS) has been shown to be an effective treatment in calcification disorders such as calciphylaxis and vascular calcification. This study investigated the effects and mechanisms of action of STS in a murine model of OA and in chondrocyte calcification.
Hydroxyapatite (HA) crystals-stimulated murine chondrocytes and macrophages were treated with STS. Mineralization and cellular production of IL-6, MCP-1 and reactive oxygen species (ROS) were assayed. STS's effects on genes involved in calcification, inflammation and cartilage matrix degradation were studied by RT-PCR. STS was administered in the menisectomy model of murine OA, and the effect on periarticular calcific deposits and cartilage degeneration was investigated by micro-CT-scan and histology.
In vitro, STS prevented in a dose-dependent manner calcium crystal deposition in chondrocytes and inhibited Annexin V gene expression. In addition, there was a reduction in crystal-induced IL-6 and MCP-1 production. STS also had an antioxidant effect, diminished HA-induced ROS generation and abrogated HA-induced catabolic responses in chondrocytes. In vivo, administration of STS reduced the histological severity of OA, by limiting the size of new periarticular calcific deposits and reducing the severity of cartilage damage.
STS reduces the severity of periarticular calcification and cartilage damage in an animal model of OA via its effects on chondrocyte mineralization and its attenuation of crystal-induced inflammation as well as catabolic enzymes and ROS generation. Our study suggests that STS may be a disease-modifying drug in crystal-associated OA.

Keywords
Animals, Bone Marrow Cells/cytology, Calcium/chemistry, Calcium Phosphates/chemistry, Cartilage/pathology, Cartilage, Articular/pathology, Chemokine CCL2/metabolism, Chondrocytes/cytology, Crystallization, Female, Gene Expression Regulation, Humans, Interleukin-6/metabolism, Macrophages/cytology, Mice, Mice, Inbred C57BL, Osteoarthritis/therapy, Reactive Oxygen Species/metabolism, Thiosulfates/pharmacology, X-Ray Microtomography
Pubmed
Web of science
Open Access
Yes
Create date
19/07/2016 17:47
Last modification date
20/01/2021 18:12
Usage data