Till sidans topp

Sidansvarig: Webbredaktion
Sidan uppdaterades: 2012-09-11 15:12

Tipsa en vän
Utskriftsversion

Retinoids stimulate perio… - Göteborgs universitet Till startsida
Webbkarta
Till innehåll Läs mer om hur kakor används på gu.se

Retinoids stimulate periosteal bone resorption by enhancing the protein RANKL, a response inhibited by monomeric glucocorticoid receptor.

Artikel i vetenskaplig tidskrift
Författare H Herschel Conaway
Amir Pirhayati
Emma Persson
Ulrika Pettersson
Olle Svensson
Catharina Lindholm
Petra Henning
Jan Tuckermann
Ulf H Lerner
Publicerad i The Journal of biological chemistry
Volym 286
Nummer/häfte 36
Sidor 31425-36
ISSN 1083-351X
Publiceringsår 2011
Publicerad vid Centre for Bone and Arthritis Research
Institutionen för medicin
Institutionen för medicin, avdelningen för invärtesmedicin
Sidor 31425-36
Språk en
Länkar dx.doi.org/10.1074/jbc.M111.247734
Ämnesord Animals, Animals, Newborn, Bone Resorption, chemically induced, Mice, Osteoprotegerin, Periosteum, pathology, RANK Ligand, agonists, antagonists & inhibitors, Receptors, Glucocorticoid, physiology, Receptors, Retinoic Acid, Retinoids, pharmacology, Tretinoin, pharmacology
Ämneskategorier Endokrinologi, Invärtesmedicin

Sammanfattning

Increased vitamin A (retinol) intake has been suggested to increase bone fragility. In the present study, we investigated effects of retinoids on bone resorption in cultured neonatal mouse calvarial bones and their interaction with glucocorticoids (GC). All-trans-retinoic acid (ATRA), retinol, retinalaldehyde, and 9-cis-retinoic acid stimulated release of (45)Ca from calvarial bones. The resorptive effect of ATRA was characterized by mRNA expression of genes associated with osteoclast differentiation, enhanced osteoclast number, and bone matrix degradation. In addition, the RANKL/OPG ratio was increased by ATRA, release of (45)Ca stimulated by ATRA was blocked by exogenous OPG, and mRNA expression of genes associated with bone formation was decreased by ATRA. All retinoid acid receptors (RARα/β/γ) were expressed in calvarial bones. Agonists with affinity to all receptor subtypes or specifically to RARα enhanced the release of (45)Ca and mRNA expression of Rankl, whereas agonists with affinity to RARβ/γ or RARγ had no effects. Stimulation of Rankl mRNA by ATRA was competitively inhibited by the RARα antagonist GR110. Exposure of calvarial bones to GC inhibited the stimulatory effects of ATRA on (45)Ca release and Rankl mRNA and protein expression. This inhibitory effect was reversed by the glucocorticoid receptor (GR) antagonist RU 486. Increased Rankl mRNA stimulated by ATRA was also blocked by GC in calvarial bones from mice with a GR mutation that blocks dimerization (GR(dim) mice). The data suggest that ATRA enhances periosteal bone resorption by increasing the RANKL/OPG ratio via RARα receptors, a response that can be inhibited by monomeric GR.

Sidansvarig: Webbredaktion|Sidan uppdaterades: 2012-09-11
Dela:

På Göteborgs universitet använder vi kakor (cookies) för att webbplatsen ska fungera på ett bra sätt för dig. Genom att surfa vidare godkänner du att vi använder kakor.  Vad är kakor?