Deletion of JNK Enhances Senescence in Joint Tissues and Increases the Severity of Age-Related Osteoarthritis in Mice.
Aging
/ metabolism
Animals
Cartilage, Articular
/ metabolism
Cellular Senescence
/ genetics
Chondrocytes
/ metabolism
Disease Models, Animal
Knee Joint
/ metabolism
Matrix Metalloproteinase 13
/ metabolism
Mice
Mice, Knockout
Mitogen-Activated Protein Kinase 8
/ genetics
Mitogen-Activated Protein Kinase 9
/ genetics
Osteoarthritis
/ diagnosis
Severity of Illness Index
Journal
Arthritis & rheumatology (Hoboken, N.J.)
ISSN: 2326-5205
Titre abrégé: Arthritis Rheumatol
Pays: United States
ID NLM: 101623795
Informations de publication
Date de publication:
10 2020
10 2020
Historique:
received:
19
03
2020
accepted:
12
05
2020
pubmed:
18
5
2020
medline:
7
1
2021
entrez:
18
5
2020
Statut:
ppublish
Résumé
To determine the role of JNK signaling in the development of osteoarthritis (OA) induced by joint injury or aging in mice. In the joint injury model, 12-week-old wild-type control, JNK1 There were no differences after DMM surgery between the wild-type and the JNK-knockout mouse groups in articular cartilage structure, toluidine blue, or osteophyte scores or in MMP-13 production in explants. All 3 knockout mouse groups had increased subchondral bone thickness and area of cartilage necrosis compared to wild-type mice. Aged JNK-knockout mice had significantly worse articular cartilage structure scores compared to the aged wild-type control mice (mean ± SD 52 ± 24 in JNK1 JNK1 and JNK2 are not required for the development of OA in the mouse DMM model. Deletion of JNK1 or JNK2 is associated with more severe age-related OA and increased cell senescence, suggesting that JNK may act as a negative regulator of senescence in the joint.
Identifiants
pubmed: 32418287
doi: 10.1002/art.41312
pmc: PMC7669715
mid: NIHMS1605433
doi:
Substances chimiques
Mitogen-Activated Protein Kinase 9
EC 2.7.1.24
Mitogen-Activated Protein Kinase 8
EC 2.7.11.24
Matrix Metalloproteinase 13
EC 3.4.24.-
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
1679-1688Subventions
Organisme : NIA NIH HHS
ID : R01 AG044034
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR049003
Pays : United States
Organisme : NIAMS NIH HHS
ID : R37 AR049003
Pays : United States
Organisme : NIAMS NIH HHS
ID : T32 AR050938
Pays : United States
Commentaires et corrections
Type : CommentIn
Type : CommentIn
Informations de copyright
© 2020, American College of Rheumatology.
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