Selective Regulation of Osteoblastic OPG and RANKL by Dehydroepiandrosterone Through Activation of the Estrogen Receptor β-mediated MAPK Signaling Pathway
| Autor: | Yudong Wang, Wang L, Tao Mf, Wan Xp, Cheng Ww |
|---|---|
| Rok vydání: | 2012 |
| Předmět: |
musculoskeletal diseases
medicine.medical_specialty MAP Kinase Signaling System Endocrinology Diabetes and Metabolism Clinical Biochemistry Estrogen receptor Dehydroepiandrosterone Apoptosis Biochemistry Cell Line Endocrinology Internal medicine medicine Estrogen Receptor beta Humans Gene Silencing RNA Messenger Viability assay Extracellular Signal-Regulated MAP Kinases Receptor Estrogen receptor beta Cell Proliferation Osteoblasts biology Chemistry RANK Ligand Biochemistry (medical) Estrogen Receptor alpha Osteoprotegerin General Medicine Enzyme Activation Androgen receptor Gene Expression Regulation RANKL biology.protein Signal transduction hormones hormone substitutes and hormone antagonists |
| Zdroj: | Hormone and Metabolic Research. 44:494-500 |
| ISSN: | 1439-4286 0018-5043 |
| Popis: | The aim of the work was to investigate the differential regulation by dehydroepiandrosterone (DHEA) of the osteoblastic production via the estrogen receptor beta (ER β)-mediated signaling pathway. Having developed hMG63-ER β cells and hMG63-shER β cells, we analyzed the regulation by DHEA of human osteoblastic viability, the receptor activator of nuclear factor kappa-B ligand (RANKL), osteoprotegerin (OPG), and the differential expression of ER β, ER α, or p-ERK1/2 (extracellular signal-regulated kinase) in hMG63, hMG63-shER β, and hMG63-ER β cells pretreated with or without U0126, flutamide, and ICI 182780, followed by DHEA culture. When the level of ER β was high, DHEA (10 - 7 mol/l) could effectively amplify the proliferation and inhibit the etoposide-induced apoptosis of hMG63 cells (p |
| Databáze: | OpenAIRE |
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