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Int. J. Mol. Sci. 2017, 18(5), 977; doi:10.3390/ijms18050977

miR-365 Ameliorates Dexamethasone-Induced Suppression of Osteogenesis in MC3T3-E1 Cells by Targeting HDAC4

1,2,†
,
2,†
,
2,3
,
2,4
and
2,5,*
1
Department of Pharmacology, Guangdong Medical University, Dongguan 523808, China
2
Department of Orthopaedics, Warren Alpert Medical School of Brown University/Rhode Island Hospital, Providence, RI 02903, USA
3
Department of Rheumatology, the First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, China
4
College of Pharmacy, Gannan Medical University, Ganzhou 341000, China
5
Bone and Joint Research Center, the First Affiliated Hospital and Frontier Institute of Science and Technology, Xi’an Jiaotong University, Xi’an 710061, China
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Academic Editor: Martin Pichler
Received: 4 April 2017 / Revised: 27 April 2017 / Accepted: 28 April 2017 / Published: 4 May 2017
(This article belongs to the Collection Regulation by Non-Coding RNAs)
View Full-Text   |   Download PDF [3565 KB, uploaded 4 May 2017]   |  

Abstract

Glucocorticoid administration is the leading cause of secondary osteoporosis. In this study, we tested the hypotheses that histone deacetylase 4 (HDAC4) is associated with glucocorticoid-induced bone loss and that HDAC4 dependent bone loss can be ameliorated by miRNA-365. Our previous studies showed that miR-365 mediates mechanical stimulation of chondrocyte proliferation and differentiation by targeting HDAC4. However, it is not clear whether miR-365 has an effect on glucocorticoid-induced osteoporosis. We have shown that, in MC3T3-E1 osteoblasts, dexamethasone (DEX) treatment decreased the expression of miR-365, which is accompanied by the decrease of cell viability in a dose-dependent manner. Transfection of miR-365 ameliorated DEX-induced inhibition of MC3T3-E1 cell viability and alkaline phosphatase activity, and attenuated the suppressive effect of DEX on runt-related transcription factor 2 (Runx2), osteopontin (OPN), and collagen 1a1 (Col1a1) osteogenic gene expression. In addition, miR-365 decreased the expression of HDAC4 mRNA and protein by direct targeting the 3′-untranslated regions (3′-UTR) of HDAC4 mRNA in osteoblasts. MiR-365 increased Runx2 expression and such stimulatory effect could be reversed by HDAC4 over-expression in osteoblasts. Collectively, our findings indicate that miR-365 ameliorates DEX-induced suppression of cell viability and osteogenesis by regulating the expression of HDAC4 in osteoblasts, suggesting miR-365 might be a novel therapeutic agent for treatment of glucocorticoid-induced osteoporosis. View Full-Text
Keywords: miR-365; glucocorticoid; osteoporosis; histone deacetylase 4 miR-365; glucocorticoid; osteoporosis; histone deacetylase 4
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Xu, D.; Gao, Y.; Hu, N.; Wu, L.; Chen, Q. miR-365 Ameliorates Dexamethasone-Induced Suppression of Osteogenesis in MC3T3-E1 Cells by Targeting HDAC4. Int. J. Mol. Sci. 2017, 18, 977.

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