Glucocorticoid Receptor and Sequential P53 Activation by Dexamethasone Mediates Apoptosis and Cell Cycle Arrest of Osteoblastic MC3T3-E1 Cells

• DOI: 10.1371/journal.pone.0037030
• Publication Date: 2012-06-14T17:26:54Z
• Authors: Hui Li; Wenwei Qian; Xisheng Weng; Zhihong Wu; Huihua Li; Qianyu Zhuang; Bin Feng; Yanyan Bian
• Keywords: 0303 health sciences; Osteoblasts; Base Sequence; Science; Q; Blotting, Western; Cell Cycle; R; Apoptosis; 3T3 Cells; Real-Time Polymerase Chain Reaction; Dexamethasone; 3. Good health; Mice; Mifepristone; 03 medical and health sciences; Receptors, Glucocorticoid; Medicine; Animals; Gene Silencing; Tumor Suppressor Protein p53; Research Article; DNA Primers

Glucocorticoids play a pivotal role in the proliferation of osteoblasts, but underlying mechanism has not been successfully elucidated. In this report, we have investigated molecular which elucidates inhibitory effects dexamethasone on murine osteoblastic MC3T3-E1 cells. It was found that were largely attributed to apoptosis and G1 phase arrest. Both cell cycle arrest dependent glucocorticoid receptor (GR), as they abolished by GR blocker RU486 pre-treatment interference. accompanied with p53-dependent up-regulation p21 pro-apoptotic genes NOXA PUMA. We also proved can't induce when p53 inhibited RNA These data demonstrate significantly directly treatment via aberrant activation subsequently P53 activation.