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Sci Rep. 2017 Jan 12;7:40240. doi: 10.1038/srep40240.

Interleukin-32 Gamma Stimulates Bone Formation by Increasing miR-29a in Osteoblastic Cells and Prevents the Development of Osteoporosis.

Author information

1
Department of Biomedical Sciences, University of Ulsan College of Medicine, Asan Medical Center, Seoul 05505, Korea.
2
Department of Rheumatology, University of Ulsan College of Medicine, Asan Medical Center, Seoul 05505, Korea.
3
Department of Endocrinology and Metabolism, University of Ulsan College of Medicine, Asan Medical Center, Seoul 05505, Korea.
4
Department of Biomedical Science and Technology, Konkuk University, Seoul 05066, Korea.

Abstract

Interleukin-32 gamma (IL-32γ) is a recently discovered cytokine that is elevated in inflamed tissues and contributes to pathogenic features of bone in human inflammatory rheumatic diseases. Nevertheless, the role of IL-32γ and its direct involvement in bone metabolism is unclear. We investigated the molecular mechanism of IL-32γ in bone remodeling and the hypothetical correlation between IL-32γ and disease activity in osteoporosis patients. Transgenic (TG) mice overexpressing human IL-32γ showed reduced bone loss with advancing age, increased bone formation, and high osteogenic capacity of osteoblast compared to wild-type (WT) mice through the upregulation of miR-29a, which caused a reduction of Dickkopf-1 (DKK1) expression. IL-32γ TG mice were protected against ovariectomy (OVX)induced osteoporosis compared with WT mice. Decreased plasma IL-32γ levels were associated with bone mineral density (BMD) in human patients linked to increased DKK1 levels. These results indicate that IL-32γ plays a protective role for bone loss, providing clinical evidence of a negative correlation between IL-32γ and DKK1 as bone metabolic markers.

PMID:
28079119
PMCID:
PMC5228062
DOI:
10.1038/srep40240
[Indexed for MEDLINE]
Free PMC Article

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