Reduction in transforming growth factor beta receptor I expression and transcription factor CBFa1 on bone cells by glucocorticoid
Glucocorticoid in excess suppresses bone formation in vivo and disrupts bone matrix protein synthesis by osteoblasts in vitro. In contrast, transforming growth factor beta (TGF-beta) potently enhances bone matrix apposition. The rat TGF-beta type I receptor gene promoter contains cis-acting elements...
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| Veröffentlicht in: | The Journal of biological chemistry 1998-02, Vol.273 (9), p.4892-4896 |
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| container_issue | 9 |
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| container_title | The Journal of biological chemistry |
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| creator | Chang, D J Ji, C Kim, K K Casinghino, S McCarthy, T L Centrella, M |
| description | Glucocorticoid in excess suppresses bone formation in vivo and disrupts bone matrix protein synthesis by osteoblasts in vitro. In contrast, transforming growth factor beta (TGF-beta) potently enhances bone matrix apposition. The rat TGF-beta type I receptor gene promoter contains cis-acting elements for transcription factor CBFa1, which increases in parallel with osteoblast differentiation. Here we present molecular data linking these events. We show that previously unexplained effects of glucocorticoid on bone loss may be mediated in part by suppression of CBFa1, with a resultant decrease in the expression and activity of the TGF-beta type I receptor on matrix-producing bone cells. |
| doi_str_mv | 10.1074/jbc.273.9.4892 |
| format | Article |
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In contrast, transforming growth factor beta (TGF-beta) potently enhances bone matrix apposition. The rat TGF-beta type I receptor gene promoter contains cis-acting elements for transcription factor CBFa1, which increases in parallel with osteoblast differentiation. Here we present molecular data linking these events. We show that previously unexplained effects of glucocorticoid on bone loss may be mediated in part by suppression of CBFa1, with a resultant decrease in the expression and activity of the TGF-beta type I receptor on matrix-producing bone cells.</abstract><cop>United States</cop><pmid>9478931</pmid><doi>10.1074/jbc.273.9.4892</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of biological chemistry, 1998-02, Vol.273 (9), p.4892-4896 |
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| language | eng |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Activin Receptors, Type I Animals Cell Differentiation Cell Nucleus - metabolism Cloning, Molecular Core Binding Factor Alpha 1 Subunit Dexamethasone - pharmacology Gene Expression Regulation, Developmental Glucocorticoids - pharmacology Neoplasm Proteins Osteoblasts - drug effects Promoter Regions, Genetic Protein Binding Protein-Serine-Threonine Kinases - biosynthesis Protein-Serine-Threonine Kinases - genetics Rats Receptor, Transforming Growth Factor-beta Type I Receptors, Transforming Growth Factor beta - biosynthesis Receptors, Transforming Growth Factor beta - genetics Recombinant Fusion Proteins - biosynthesis Space life sciences Transcription Factors - biosynthesis Transforming Growth Factor beta - metabolism |
| title | Reduction in transforming growth factor beta receptor I expression and transcription factor CBFa1 on bone cells by glucocorticoid |
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