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在大鼠成骨细胞中,甲状旁腺激素暴露时,miR-873-3p靶向组蛋白去乙酰化酶4以刺激基质金属蛋白酶-13的表达。

miR-873-3p targets HDAC4 to stimulate matrix metalloproteinase-13 expression upon parathyroid hormone exposure in rat osteoblasts.

作者信息

Malavika Desai, Shreya Srinivasan, Raj Priya Vembar, Rohini Muthukumar, He Zhiming, Partridge Nicola C, Selvamurugan Nagarajan

机构信息

Department of Biotechnology, School of Bioengineering, SRM Institute of Science and Technology, Kattankulathur, Tamil Nadu, India.

Department of Basic Science and Craniofacial Biology, New York University College of Dentistry, New York University, New York, New York.

出版信息

J Cell Physiol. 2020 Nov;235(11):7996-8009. doi: 10.1002/jcp.29454. Epub 2020 Jan 21.

Abstract

Matrix metalloproteinase-13 (MMP-13) plays a predominant role in endochondral bone formation and bone remodeling. Parathyroid hormone (PTH) stimulates the expression of MMP-13 via Runx2, a bone transcription factor in rat osteoblastic cells (UMR106-01), and histone deacetylase 4 (HDAC4) acts as a corepressor of Runx2. Moreover, microRNAs (miRNAs) play an important role in regulating genes posttranscriptionally. Here, we hypothesized that PTH upregulates the miRNAs targeting HDAC4, which could lead to increased Runx2 activity and MMP-13 expression in rat osteoblastic cells. We identified several miRNAs that putatively target rat HDAC4 using bioinformatics tools. miR-873-3p was significantly upregulated by PTH in rat osteoblasts. miR-873-3p overexpression downregulated HDAC4 protein expression, increased Runx2 binding at the MMP-13 promoter, and increased MMP-13 messenger RNA expression in UMR106-01 cells. A luciferase reporter assay identified the direct targeting of miR-873-3p at the 3'-untranslated region of HDAC4. Thus, miR-873-3p targeted HDAC4 and relieved the corepressor effect of HDAC4 on Runx2 for MMP-13 expression in rat osteoblasts. This study advances our knowledge of posttranscriptional gene regulation occurring in bone and bone-related diseases and clarifies the role of miRNAs as diagnostic biomarkers.

摘要

基质金属蛋白酶-13(MMP-13)在软骨内骨形成和骨重塑过程中起主要作用。甲状旁腺激素(PTH)通过Runx2刺激MMP-13的表达,Runx2是大鼠成骨细胞(UMR106-01)中的一种骨转录因子,组蛋白去乙酰化酶4(HDAC4)作为Runx2的共抑制因子发挥作用。此外,微小RNA(miRNA)在转录后调控基因方面发挥重要作用。在此,我们假设PTH上调靶向HDAC4的miRNA,这可能导致大鼠成骨细胞中Runx2活性增加和MMP-13表达上调。我们使用生物信息学工具鉴定了几种可能靶向大鼠HDAC4的miRNA。在大鼠成骨细胞中,miR-873-3p被PTH显著上调。在UMR106-01细胞中,miR-873-3p过表达下调了HDAC4蛋白表达,增加了Runx2在MMP-13启动子处的结合,并增加了MMP-13信使核糖核酸的表达。荧光素酶报告基因检测确定了miR-873-3p对HDAC4 3'-非翻译区的直接靶向作用。因此,miR-873-3p靶向HDAC4并减轻了HDAC4对大鼠成骨细胞中MMP-13表达的Runx2共抑制作用。本研究增进了我们对骨及骨相关疾病中发生的转录后基因调控的认识,并阐明了miRNA作为诊断生物标志物的作用。

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