作者: Theodora Koromila , Sanjeev K. Baniwal , Yae S. Song , Anthony Martin , Jian Xiong
DOI: 10.1002/JCB.24646
关键词:
摘要: The efficacy of glucocorticoids (GCs) in treating a wide range autoimmune and inflammatory conditions is blemished by severe side effects, including osteoporosis. chief mechanism leading to GC-induced osteoporosis inhibition bone formation, but the role RUNX2, master regulator osteoblast differentiation has not been well studied. We assessed effects synthetic GC dexamethasone (dex) on transcription RUNX2-stimulated genes during mesenchymal pluripotent cells into osteoblasts. Dex inhibited RUNX2 reporter gene attenuated locus-dependently RUNX2-driven expression several endogenous target genes. anti-RUNX2 activity dex was attributable decreased expression, rather physical interaction between receptor (GR), demonstrated co-immunoprecipitation assays co-immunofluorescence imaging. Investigation RUNX2/GR may lead development bone-sparing treatment modalities for management diseases.