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Bone. 2014 Oct;67:156-65. doi: 10.1016/j.bone.2014.07.004. Epub 2014 Jul 12.

A novel microRNA regulates osteoclast differentiation via targeting protein inhibitor of activated STAT3 (PIAS3).

Author information

  • 1Institute of Endocrinology and Metabolism, Second Xiangya Hospital of Central South University, 139# Middle Renmin Road, Changsha, Hunan 410011, PR China.
  • 2Department of Endocrinology, Hunan Province Geriatric Hospital, 89# Guhan Road, Changsha, Hunan 410001, PR China.
  • 3Department of Endocrinology, Changsha Central Hospital, 161# Shaoshan Road, Changsha, Hunan 410004, PR China.
  • 4Department of Endocrinology, Xiangya Hospital of Central South University, 87# Xiangya Road, Changsha, Hunan 410008, PR China.
  • 5Department of Endocrinology, Changsha Central Hospital, 161# Shaoshan Road, Changsha, Hunan 410004, PR China. Electronic address: genqingxie@gmail.com.
  • 6Department of Endocrinology, Hunan Province Geriatric Hospital, 89# Guhan Road, Changsha, Hunan 410001, PR China; Department of Endocrinology, Xiangya Hospital of Central South University, 87# Xiangya Road, Changsha, Hunan 410008, PR China. Electronic address: run850218@163.com.
  • 7Department of Endocrinology, Xiangya Hospital of Central South University, 87# Xiangya Road, Changsha, Hunan 410008, PR China. Electronic address: jiangtiejian@gmail.com.

Abstract

MicroRNAs (miRNAs) involve in the regulation of a wide range of physiological processes. Recent studies suggested that miRNAs might play a role in osteoclast differentiation. Here, we identify a new miRNA (miR-9718) in primary mouse osteoclasts that promotes osteoclast differentiation by repressing protein inhibitor of activated STAT3 (PIAS3) at the post-transcriptional level. MiR-9718 was found to be transcribed during osteoclastogenesis, which was induced by macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor-κB ligand (RANKL). Overexpression of miR-9718 in RAW 264.7 cells promoted M-CSF and RANKL-induced osteoclastogenesis, whereas inhibition of miR-9718 attenuated it. PIAS3 was predicted to be a target of miR-9718. Luciferase reporter gene validated the prediction. Transfection of pre-miR-9718 in RAW 264.7 cells induced by both M-CSF and RANKL inhibited expression of PIAS3 protein, while the mRNA levels of PIAS3 were not attenuated. In vivo, our study showed that silencing of miR-9718 using a specific antagomir inhibited bone resorption and increased bone mass in mice receiving ovariectomy (OVX) and in sham-operated control mice. Thus, our study showed that miR-9718 played an important role in osteoclast differentiation via targeting PIAS3 both in vitro and in vivo.

Copyright © 2014 Elsevier Inc. All rights reserved.

KEYWORDS:

Bone; Differentiation; MicroRNA; Osteoclast; PIAS3

PMID:
25019593
[PubMed - indexed for MEDLINE]
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