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转录因子GTF2I通过介导miR-134-5p和MAT2A的表达来调节破骨细胞分化。

Transcription factor GTF2I regulates osteoclast differentiation through mediating miR-134-5p and MAT2A expressions.

作者信息

Tang Lian, Liu Yanshi, Yan Jiyuan, Yuan Lin, Wang Zhaojun, Li Zhong

机构信息

Department of Orthopedics Affiliated Hospital of Southwest Medical University Luzhou Sichuan China.

Department of Clinical Skills Center Affiliated Hospital of Southwest Medical University Luzhou Sichuan China.

出版信息

J Cell Commun Signal. 2025 Apr 3;19(2):e70010. doi: 10.1002/ccs3.70010. eCollection 2025 Jun.

DOI:10.1002/ccs3.70010
PMID:40191097
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11968177/
Abstract

This study explored the possible effect of transcription factor GTF2I on the differentiation of osteoclasts and its regulation on the miR-134-5p/MAT2A axis. RANKL-induced osteoclasts were measured for expressions of GTF2I, miR-134-5p, and MAT2A. The number and size of osteoclasts were assessed after TRAP staining. The expressions of osteoclast differentiation biomarkers, NFATC1, TRAP, and CTSK, were detected as well. The relationships of the GTF2I/miR-134-5p/MAT2A axis were verified by ChIP, dual luciferase, and RNA pull-down assay. In vivo experiments were conducted on ovariectomized (OVX)-treated mice to determine the effect of GTF2I overexpression on osteoclast differentiation and bone loss. RANKL-induced osteoclasts had suppressed expressions of GTF2I and miR-134-5p and increased expression of MAT2A. GTF2I overexpression or miR-134-5p overexpression contributed to decreased cell number and size and suppressed cell differentiation, whereas such an effect can be abolished by overexpression of MAT2A. GTF2I can bind the miR-134-5p promoter to regulate its expression, whereas miR-134-5p can negatively regulate MAT2A expression. The protective effect of GTF2I overexpression against bone loss and cell differentiation was verified by in vivo experiments. Collectively, these results indicate that GTF2I can mediate miR-134-5p expression to increase MAT2A expression, contributing to the suppression of osteoclast differentiation.

摘要

本研究探讨了转录因子GTF2I对破骨细胞分化的可能影响及其对miR-134-5p/MAT2A轴的调控作用。检测了RANKL诱导的破骨细胞中GTF2I、miR-134-5p和MAT2A的表达。通过TRAP染色评估破骨细胞的数量和大小。还检测了破骨细胞分化生物标志物NFATC1、TRAP和CTSK的表达。通过染色质免疫沉淀（ChIP）、双荧光素酶和RNA下拉实验验证了GTF2I/miR-134-5p/MAT2A轴的关系。对去卵巢（OVX）处理的小鼠进行体内实验，以确定GTF2I过表达对破骨细胞分化和骨质流失的影响。RANKL诱导的破骨细胞中GTF2I和miR-134-5p的表达受到抑制，而MAT2A的表达增加。GTF2I过表达或miR-134-5p过表达导致细胞数量和大小减少，细胞分化受到抑制，而MAT2A过表达可消除这种作用。GTF2I可结合miR-134-5p启动子来调节其表达，而miR-134-5p可负向调节MAT2A的表达。体内实验验证了GTF2I过表达对骨质流失和细胞分化的保护作用。总的来说，这些结果表明GTF2I可介导miR-134-5p的表达以增加MAT2A的表达，从而抑制破骨细胞分化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6d8/11968177/77c0286ce027/CCS3-19-e70010-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6d8/11968177/23e5da58e422/CCS3-19-e70010-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6d8/11968177/12296bb6b5d4/CCS3-19-e70010-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6d8/11968177/05e01340dad1/CCS3-19-e70010-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6d8/11968177/7570f87d9cd8/CCS3-19-e70010-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6d8/11968177/eade8d84b4c6/CCS3-19-e70010-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6d8/11968177/ab736e588bfc/CCS3-19-e70010-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6d8/11968177/77c0286ce027/CCS3-19-e70010-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6d8/11968177/23e5da58e422/CCS3-19-e70010-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6d8/11968177/12296bb6b5d4/CCS3-19-e70010-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6d8/11968177/05e01340dad1/CCS3-19-e70010-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6d8/11968177/7570f87d9cd8/CCS3-19-e70010-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6d8/11968177/eade8d84b4c6/CCS3-19-e70010-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6d8/11968177/ab736e588bfc/CCS3-19-e70010-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6d8/11968177/77c0286ce027/CCS3-19-e70010-g003.jpg

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