Pathogenesis of glucocorticoid-induced avascular necrosis: A microarray analysis of gene expression in vitro

Bian,Yanyan; Qian,Wenwei; Li,Hongling; Zhao,Robert Chunhua; Shan,Wang Xing; Weng,Xisheng

doi:10.3892/ijmm.2015.2273

Pathogenesis of glucocorticoid-induced avascular necrosis: A microarray analysis of gene expression in vitro

Authors:
- Yanyan Bian
- Wenwei Qian
- Hongling Li
- Robert Chunhua Zhao
- Wang Xing Shan
- Xisheng Weng
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Affiliations: Department of Orthopedics, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, P.R. China, Institute of Basic Medical Science, Chinese Academy of Medical Sciences, Beijing 100730, P.R. China
Published online on: July 6, 2015 https://doi.org/10.3892/ijmm.2015.2273
Pages: 678-684
Copyright: © Bian et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

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Abstract

Avascular necrosis of the femoral head (ANFH) occurs following exposure to corticosteroids, and the proliferative capacity of the mesenchymal stem cells (MSCs) belonging to ANFH was reduced. The previous studies indicate that microRNA (miRNA) has an important regulatory role during proliferation and osteogenic differentiation of MSCs. Therefore, MSCs were obtained from healthy adults, and were cultured and osteogenically‑induced by different dexamethasone concentrations. The proliferation and osteogenic differentiation capacities were examined through observing cellular morphology, alkaline phosphatase and alizarin red; miRNA expression was investigated using an miRNA gene chip and miRNA of differential expressions were retrieved through a database to analyze its regulatory effect. Dexamethasone at a concentration of 10‑7 mol/l induced the proliferation and osteogenic differentiation of MSCs and resulted in evident miRNA expression profile changes. In total, 11 miRNAs were upregulated at 10‑7 mol/l while 6 were downregulated, and partial miRNA was identified to participate in the regulation of cell proliferation and cell apoptosis, MSC osteogenic differentiation, lipid metabolism and other processes.

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