The PPAR-γ antagonist T007 inhibits RANKL-induced osteoclastogenesis and counteracts OVX-induced bone loss in mice.
Cell Commun Signal
; 17(1): 136, 2019 10 26.
Article
de En
| MEDLINE
| ID: mdl-31655621
ABSTRACT
BACKGROUND:
Osteoclasts are key determinant cellular components implicated in the development and progression of disorders driven by bone damage. Herein, we studied the upshot of T007, an antagonist of peroxisome proliferator-activated receptor-gamma (PPARγ), on osteoclastogenesis using cell and animal models.RESULTS:
The in vitro assays revealed that T007 hindered the osteoclastogenesis caused by the treatment with the receptor activator of nuclear factor-κB ligand (RANKL) through inhibiting the levels of PPARγ in cells. The PPARγ siRNA partially reproduced the inhibitory action of T007. The opposite findings were produced after PPARγ overexpression. Furthermore, T007 prevented from bone loss in a mouse model of osteoporosis induced by ovariectomy (OVX). These findings implied that T007 is a potential efficient drug for the prophylaxis and cure of osteoclast-related disorders.CONCLUSIONS:
Taken together, our findings demonstrated that T007 impedes osteoclastogenesis and will be useful for the therapy of bone related diseases, essentially osteoporosis.Mots clés
Texte intégral:
1
Collection:
01-internacional
Base de données:
MEDLINE
Sujet principal:
Ostéoclastes
/
Ostéogenèse
/
Pyridines
/
Benzamides
/
Résorption osseuse
/
Ovariectomie
/
Récepteur PPAR gamma
/
Ligand de RANK
Type d'étude:
Etiology_studies
/
Prognostic_studies
Limites:
Animals
Langue:
En
Journal:
Cell Commun Signal
Année:
2019
Type de document:
Article
Pays d'affiliation:
Chine