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微小RNA-26a调控核因子κB受体活化因子配体诱导的破骨细胞形成。

MicroRNA-26a regulates RANKL-induced osteoclast formation.

作者信息

Kim Kabsun, Kim Jung Ha, Kim Inyoung, Lee Jongwon, Seong Semun, Park Yong-Wook, Kim Nacksung

机构信息

Department of Pharmacology, Medical Research Center for Gene Regulation, Chonnam National University Medical School, Gwangju 501-746, Korea.

出版信息

Mol Cells. 2015 Jan 31;38(1):75-80. doi: 10.14348/molcells.2015.2241. Epub 2014 Dec 16.

DOI:10.14348/molcells.2015.2241
PMID:25518928
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4314121/
Abstract

Osteoclasts are unique cells responsible for the resorption of bone matrix. MicroRNAs (miRNAs) are involved in the regulation of a wide range of physiological processes. Here, we examined the role of miR-26a in RANKL-induced osteoclastogenesis. The expression of miR-26a was up-regulated by RANKL at the late stage of osteoclastogenesis. Ectopic expression of an miR-26a mimic in osteoclast precursor cells attenuated osteoclast formation, actin-ring formation, and bone resorption by suppressing the expression of connective tissue growth factor/CCN family 2 (CTGF/CCN2), which can promote osteoclast formation via up-regulation of dendritic cell-specific transmembrane protein (DC-STAMP). On the other hand, overexpression of miR-26a inhibitor enhanced RANKL-induced osteoclast formation and function as well as CTGF expression. In addition, the inhibitory effect of miR-26a on osteoclast formation and function was prevented by treatment with recombinant CTGF. Collectively, our results suggest that miR-26a modulates osteoclast formation and function through the regulation of CTGF.

摘要

破骨细胞是负责骨基质吸收的独特细胞。微小RNA（miRNA）参与多种生理过程的调节。在此，我们研究了miR-26a在RANKL诱导的破骨细胞生成中的作用。在破骨细胞生成后期，RANKL上调了miR-26a的表达。在破骨细胞前体细胞中异位表达miR-26a模拟物可通过抑制结缔组织生长因子/CCN家族2（CTGF/CCN2）的表达来减弱破骨细胞形成、肌动蛋白环形成和骨吸收，CTGF/CCN2可通过上调树突状细胞特异性跨膜蛋白（DC-STAMP）促进破骨细胞形成。另一方面，miR-26a抑制剂的过表达增强了RANKL诱导的破骨细胞形成和功能以及CTGF表达。此外，用重组CTGF处理可阻止miR-26a对破骨细胞形成和功能的抑制作用。总体而言，我们的结果表明miR-26a通过调节CTGF来调节破骨细胞的形成和功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c51/4314121/e73af1e537c7/molcell-38-1-75f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c51/4314121/4dcbc20422a0/molcell-38-1-75f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c51/4314121/06953699966f/molcell-38-1-75f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c51/4314121/523263008f2a/molcell-38-1-75f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c51/4314121/184214d26d86/molcell-38-1-75f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c51/4314121/e73af1e537c7/molcell-38-1-75f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c51/4314121/4dcbc20422a0/molcell-38-1-75f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c51/4314121/06953699966f/molcell-38-1-75f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c51/4314121/523263008f2a/molcell-38-1-75f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c51/4314121/184214d26d86/molcell-38-1-75f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c51/4314121/e73af1e537c7/molcell-38-1-75f5.jpg

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3
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Microrna. 2025;14(1):9-18. doi: 10.2174/0122115366305491240708060422.
4
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5
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