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白细胞介素 32γ 通过增加成骨细胞中的 miR-29a 刺激骨形成并预防骨质疏松症的发生。

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

机构信息

Department of Biomedical Sciences, University of Ulsan College of Medicine, Asan Medical Center, Seoul 05505, Korea.

Department of Rheumatology, University of Ulsan College of Medicine, Asan Medical Center, Seoul 05505, Korea.

出版信息

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

DOI:10.1038/srep40240
PMID:28079119
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5228062/
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.

摘要

白细胞介素 32 伽马 (IL-32γ) 是一种新发现的细胞因子，在炎症组织中升高，并有助于人类炎症性风湿性疾病中骨骼的致病特征。然而，IL-32γ 的作用及其对骨代谢的直接参与尚不清楚。我们研究了 IL-32γ 在骨重塑中的分子机制以及骨质疏松症患者中 IL-32γ 与疾病活动之间的假设相关性。与野生型 (WT) 小鼠相比，过表达人 IL-32γ 的转基因 (TG) 小鼠随着年龄的增长，骨丢失减少，骨形成增加，成骨细胞的成骨能力增强，这是通过 miR-29a 的上调引起的，导致 Dickkopf-1 (DKK1) 表达减少。与 WT 小鼠相比，IL-32γ TG 小鼠对去卵巢 (OVX) 诱导的骨质疏松症具有保护作用。人类患者的血浆 IL-32γ 水平与骨密度 (BMD) 相关，与 DKK1 水平升高相关。这些结果表明，IL-32γ 对骨丢失起保护作用，为 IL-32γ 与 DKK1 作为骨代谢标志物之间的负相关提供了临床证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a5/5228062/c8fe28065be5/srep40240-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a5/5228062/06dc9b0c39ba/srep40240-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a5/5228062/6960492be3ba/srep40240-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a5/5228062/52a696619f8f/srep40240-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a5/5228062/016d161ddb8b/srep40240-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a5/5228062/c8fe28065be5/srep40240-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a5/5228062/06dc9b0c39ba/srep40240-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a5/5228062/6960492be3ba/srep40240-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a5/5228062/52a696619f8f/srep40240-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a5/5228062/016d161ddb8b/srep40240-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5a5/5228062/c8fe28065be5/srep40240-f5.jpg

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