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001-es BibID:BIBFORM103130
035-os BibID:(Wos)000348962700035 (Scopus)84922169574
Első szerző:Menendez-Gutierrez, Maria Piedad
Cím:Retinoid X receptors orchestrate osteoclast differentiation and postnatal bone remodeling / María P. Menéndez-Gutiérrez, Tamás Röszer, Lucia Fuentes, Vanessa Núnez, Amelia Escolano, Juan Miguel Redondo, Nora De Clerk, Daniel Metzger, Annabel F. Valledor, Mercedes Ricote
Dátum:2015
ISSN:0021-9738
Megjegyzések:Osteoclasts are bone-resorbing cells that are important for maintenance of bone remodeling and mineral homeostasis. Regulation of osteoclast differentiation and activity is important for the pathogenesis and treatment of diseases associated with bone loss. Here, we demonstrate that retinoid X receptors (RXRs) are key elements of the transcriptional program of differentiating osteoclasts. Loss of RXR function in hematopoietic cells resulted in formation of giant, nonresorbing osteoclasts and increased bone mass in male mice and protected female mice from bone loss following ovariectomy, which induces osteoporosis in WT females. The increase in bone mass associated with RXR deficiency was due to lack of expression of the RXR-dependent transcription factor v-maf musculoaponeurotic fibrosarcoma oncogene family, protein B (MAFB) in osteoclast progenitors. Evaluation of osteoclast progenitor cells revealed that RXR homodimers directly target and bind to the Mafb promoter, and this interaction is required for proper osteoclast proliferation, differentiation, and activity. Pharmacological activation of RXRs inhibited osteoclast differentiation due to the formation of RXR/liver X receptor (LXR) heterodimers, which induced expression of sterol regulatory element binding protein-1c (SREBP-1c), resulting in indirect MAFB upregulation. Our study reveals that RXR signaling mediates bone homeostasis and suggests that RXRs have potential as targets for the treatment of bone pathologies such as osteoporosis.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Journal Of Clinical Investigation. - 125 : 2 (2015), p.809-823. -
További szerzők:Röszer Tamás (1979-) (orvos, biológus) Fuentes, Lucía Núnez, Vanessa Escolano, Amelia Redondo, Juan Miguel De Clerk, Nora Metzger, Daniel Valledor, Annabel F. Ricote, Mercedes
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001-es BibID:BIBFORM065063
035-os BibID:(Wos)000334175100018 (Scopus)84898634971
Első szerző:Röszer Tamás (orvos, biológus)
Cím:Leptin receptor deficient diabetic (db/db) mice are compromised in postnatal bone regeneration / Tamás Rőszer, Tamás Józsa, Éva D. Kiss-Tóth, Nora De Clerck, Lajos Balogh
Dátum:2014
ISSN:0302-766X
Megjegyzések:Increased fragility fracture risk with improper healing is a frequent and severe complication of insulin resistance (IR). The mechanisms impairing bone health in IR are still not fully appreciated, which gives importance to studies on bone pathologies in animal models of diabetes. Mice deficient in leptin signaling are widely used models of IR and its comorbidities. Leptin was first recognized as a hormone, regulating appetite and energy balance; however, recent studies have expanded its role showing that leptin is a link between insulin-dependent metabolism and bone homeostasis. In the light of these findings, it is intriguing to consider the role of leptin resistance in bone regeneration. In this study, we show that obese diabetic mice lacking leptin receptor (db/db) are deficient in postnatal regenerative osteogenesis. We apply an ectopic osteogenesis and a fracture healing model, both showing that db/db mice display compromised bone acquisition and regeneration capacity. The underlying mechanisms include delayed periosteal mesenchymatic osteogenesis, premature apoptosis of the cartilage callus and impaired microvascular invasion of the healing tissue. Our study supports the use of the db/db mouse as a model of IR associated bone-healing deficits and can aid further studies of mesenchymatic cell homing and differentiation, microvascular invasion, cartilage to bone transition and callus remodeling in diabetic fracture healing.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Fracture
Diabetes
Insulin resistance
LeptinBone
Megjelenés:Cell And Tissue Research. - 356 : 1 (2014), p. 195-206. -
További szerzők:Józsa Tamás (1969-) (gyermeksebész, urológus) Kiss-Tóth Éva (1983-) (biológus) De Clerk, Nora Balogh Lajos
Pályázati támogatás:OTKA 76091
OTKA
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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