Regular Article
Dexamethasone Enhancement of Betaglycan (TGF-β Type III Receptor) Gene Expression in Osteoblast-like Cells

https://doi.org/10.1006/excr.1994.1091Get rights and content

Abstract

Betaglycan (type III transforming growth factor-β (TGF-β) receptor) is a cell surface heparan/chondroitin sulfate proteoglycan that binds TGF-β via its core protein and is abundantly expressed in osteoblastic cells. A previous report (Centrella et al., Mol. Cell. Biol. 11, 4490-4496, 1991) showed post-translational enhancement by glucocorticoid of TGF-β binding to betaglycan. Upon the availability of the betaglycan cDNA, we investigated the effects of a glucocorticoid analogue, dexamethasone, on the regulation of betaglycan expression in osteoblast-like cells. Betaglycan mRNA was expressed as an approximately 6-kb band in MC3T3-E1 cells. The betaglycan mRNA level was enhanced severalfold by dexamethasone in these cells. The effect of dexamethasone on the betaglycan mRNA level was observed within 9 h and was sustained at least up to 48 h. The dexamethasone effect was dose-dependent, with a saturation concentration at 10-7M. Among the steroid hormones examined, dexamethasone exhibited the most potent effect on betaglycan mRNA expression, while retinoic acid also enhanced it moderately. Dexamethasone enhancement of betaglycan mRNA expression was blocked by actinomycin D, but it was not blocked by cycloheximide. Cross-linking experiments showed that dexamethasone treatment increased the binding of radiolabeled TGF-β1 to betaglycan, but did not affect binding to the type II receptor. A similar dexamethasone enhancement of betaglycan mRNA expression was also observed in a preosteoblast-like cell line, RCT1. These results suggest that dexamethasone enhances betaglycan expression at least in part via transcriptional events in osteoblasts and this would be one of the target points of glucocorticoid regulation of bone metabolism.

References (0)

Cited by (33)

  • Joint dysfunction and functional decline in middle age myostatin null mice

    2016, Bone
    Citation Excerpt :

    Cooperation between WNT and BMP signaling pathways can further enhance the pro-osteogenic effect of each other [55–57], which would predict more active tissue remodeling in the tendon–bone insertion region of the mstn−/− mice than the wt controls. TGFBR3, also named as β-glycan, remained elevated in mstn−/− mice at all ages studied, implying enhanced activation of bone and cartilage metabolism [58–60]. Within this panel of genes, DKK1 is the only negative regulator that blocks WNT interaction with its co-receptor LRP5 and LRP6 [61].

  • Camurati-Engelmann disease

    2011, Seminarios de la Fundacion Espanola de Reumatologia
  • Clinical and Basic Aspects of Glucocorticoid Action in Bone

    2008, Principles of Bone Biology: Volume 1-2, Third Edition
View all citing articles on Scopus
View full text