Osteoclast-Derived Autotaxin, a Distinguishing Factor for Inflammatory Bone Loss.
Animals
Arthritis, Experimental
/ immunology
Arthritis, Rheumatoid
/ immunology
Bone Resorption
/ diagnostic imaging
Calcaneus
/ diagnostic imaging
Female
Femur
/ diagnostic imaging
Gene Knockdown Techniques
Humans
Male
Mice
Mice, Transgenic
Osteoclasts
/ metabolism
Ovariectomy
Phosphoric Diester Hydrolases
/ metabolism
Talus
/ diagnostic imaging
Tumor Necrosis Factor-alpha
/ genetics
X-Ray Microtomography
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:
11 2019
11 2019
Historique:
received:
23
10
2018
accepted:
29
05
2019
pubmed:
5
6
2019
medline:
23
2
2020
entrez:
5
6
2019
Statut:
ppublish
Résumé
The severity of rheumatoid arthritis (RA) correlates directly with bone erosions arising from osteoclast (OC) hyperactivity. Despite the fact that inflammation may be controlled in patients with RA, those in a state of sustained clinical remission or low disease activity may continue to accrue erosions, which supports the need for treatments that would be suitable for long-lasting inhibition of OC activity without altering the physiologic function of OCs in bone remodeling. Autotaxin (ATX) contributes to inflammation, but its role in bone erosion is unknown. ATX was targeted by inhibitory treatment with pharmacologic drugs and also by conditional inactivation of the ATX gene Ennp2 in murine OCs (ΔATX OCs present at sites of inflammation overexpressed ATX. Pharmacologic inhibition of ATX in hTNF Our results identify ATX as a novel OC factor that specifically controls inflammation-induced bone erosions and systemic bone loss. Therefore, ATX inhibition offers a novel therapeutic approach for potentially preventing bone erosion in patients with RA.
Identifiants
pubmed: 31162832
doi: 10.1002/art.41005
pmc: PMC6817375
mid: NIHMS1033521
doi:
Substances chimiques
TNF protein, human
0
Tumor Necrosis Factor-alpha
0
Phosphoric Diester Hydrolases
EC 3.1.4.-
alkylglycerophosphoethanolamine phosphodiesterase
EC 3.1.4.39
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1801-1811Subventions
Organisme : Institut National de la Santé et de la Recherche Médicale
Pays : International
Organisme : Agence Nationale de la Recherche
ID : ANR-15-CE14-0010-01
Pays : International
Organisme : Pfizer
Pays : International
Organisme : NCI NIH HHS
ID : R01 CA092160
Pays : United States
Organisme : Fondation ARC pour la Recherche sur le Cancer
ID : PJA20151203151
Pays : International
Organisme : Ligue Contre le Cancer
Pays : International
Informations de copyright
© 2019, American College of Rheumatology.
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