Regulation of osteoarthritis development by ADAM17/Tace in articular cartilage.
ADAM17/TACE
Articular cartilage
Mouse model
Osteoarthritis
Journal
Journal of bone and mineral metabolism
ISSN: 1435-5604
Titre abrégé: J Bone Miner Metab
Pays: Japan
ID NLM: 9436705
Informations de publication
Date de publication:
Mar 2022
Mar 2022
Historique:
received:
05
08
2021
accepted:
08
10
2021
pubmed:
10
11
2021
medline:
12
3
2022
entrez:
9
11
2021
Statut:
ppublish
Résumé
A disintegrin and metalloproteinase 17 (Adam17), also known as TNFα-converting enzyme (Tace), is a membrane-anchored protein involved in shedding of TNF, IL-6 receptor, ligands of epidermal growth factor receptor (EGFR), and Notch receptor. This study aimed to examine the role of Adam17 in adult articular cartilage and osteoarthritis (OA) pathophysiology. Adam17 expression was examined in mouse knee joints during OA development. We analyzed OA development in tamoxifen-inducible chondrocyte-specific Adam17 knockout mice of a resection of the medial meniscus and medial collateral ligament (medial) model, destabilization of the medial meniscus (DMM) model, and aging model. We analyzed downstream pathways by in vitro experiments, and further performed intra-articular administration of an Adam17 inhibitor TAPI-0 for surgically induced mouse OA. Adam17 expression in mouse articular cartilage was increased by OA progression. In all models, Adam17 knockout mice showed ameliorated progression of articular cartilage degradation. Adam17 knockout decreased matrix metallopeptidase 13 (Mmp13) expression in both in vivo and in vitro experiments, whereas Adam17 activation by phorbol-12-myristate-13-acetate (PMA) increased Mmp13 and decreased aggrecan in mouse primary chondrocytes. Adam17 activation enhanced release of soluble TNF and transforming growth factor alpha, a representative EGF ligand, from mouse primary chondrocytes, while it did not change release of soluble IL-6 receptor or nuclear translocation of Notch1 intercellular domain. Intra-articular administration of the Adam17 inhibitor ameliorated OA progression. This study demonstrates regulation of OA development by Adam17, involvement of EGFR and TNF pathways, and the possibility of Adam17 as a therapeutic target for OA.
Identifiants
pubmed: 34751824
doi: 10.1007/s00774-021-01278-3
pii: 10.1007/s00774-021-01278-3
doi:
Substances chimiques
Matrix Metalloproteinase 13
EC 3.4.24.-
Mmp13 protein, mouse
EC 3.4.24.-
ADAM17 Protein
EC 3.4.24.86
Adam17 protein, mouse
EC 3.4.24.86
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
196-207Subventions
Organisme : Japan Society for the Promotion of Science London
ID : 20H03799
Organisme : Japan Society for the Promotion of Science London
ID : 17H04310
Organisme : Japan Society for the Promotion of Science
ID : 19H05654
Organisme : Japan Society for the Promotion of Science
ID : 19H05565
Organisme : Japan Society for the Promotion of Science
ID : 19K09641
Organisme : Japan Society for the Promotion of Science
ID : 18KK0254
Organisme : Japan Society for the Promotion of Science
ID : 26462285
Informations de copyright
© 2021. The Japanese Society Bone and Mineral Research.
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