在类固醇诱导的股骨头骨坏死模型中,miR-129-5p靶向HOXC10来控制BMSC脂肪生成和成骨。

IF 1.7 4区 医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL
American journal of translational research Pub Date : 2024-12-15 eCollection Date: 2024-01-01 DOI:10.62347/CHGJ7909
Xuezhao Li, Fangqiu Tian, Guohua Liu, Xiang Liu, Ming Fu, Zhiyin E, Cong Wang, Fapeng Gao
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引用次数: 0

摘要

背景:类固醇诱导的股骨头骨坏死(SONFH)是一种主要由骨髓间充质干细胞(BMSCs)分化成脂肪和成骨谱系的平衡受损引起的病理状况。本研究旨在探讨miR-129-5p作为SONFH进展调节因子的作用及其相关机制。方法:从大鼠SONFH模型中获取骨髓间充质干细胞。利用qPCR评估miR-129-5p水平,同时利用qPCR和Western免疫印迹法评估HOXC10表达。CCK8法检测骨髓间充质干细胞的增殖活性,qPCR和Western blot分析骨髓间充质干细胞的分化情况。结果:SONFH与miR-129-5p水平降低相关。下调miR-129-5p可促进BMSC成脂,抑制其成骨分化,增强其成脂分化。机制上,miR-129-5p被发现通过靶向HOXC10基因的表达来调节这些过程。结论:MiR-129-5p在大鼠SONFH模型中下调。miR-129-5p水平的降低通过抑制HOXC10促进骨髓间充质干细胞的脂肪形成和抑制成骨。这些发现为SONFH的预防和治疗提供了新的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
miR-129-5p targets HOXC10 to control BMSC adipogenesis and osteogenesis in a model of steroid-induced osteonecrosis of the femoral head.

Background: Steroid-induced osteonecrosis of the femoral head (SONFH) is a pathological condition primarily driven by an impaired balance in the differentiation of bone marrow mesenchymal stem cells (BMSCs) into adipogenic and osteogenic lineages. This study aimed to explore the role of miR-129-5p as a regulator of SONFH progression and associated mechanisms.

Methods: BMSCs were harvested from a rat SONFH model. qPCR was leveraged to assess miR-129-5p levels, while both qPCR and Western immunoblotting were utilized to evaluate HOXC10 expression. CCK8 assay was used to measure the proliferative activity of BMSCs, while their differentiation was analyzed using qPCR and Western blot.

Results: SONFH was associated with reduced miR-129-5p levels. Downregulation of miR-129-5p promoted BMSC adipogenesis while inhibiting their osteogenic differentiation and enhancing their adipogenesis differentiation. Mechanistically, miR-129-5p was found to regulate these processes by targeting the expression of the HOXC10 gene.

Conclusions: MiR-129-5p is downregulated in a rat SONFH model. Reduced miR-129-5p levels facilitated adipogenesis and suppressed osteogenesis in BMSCs through its inhibition of HOXC10. These findings offer novel insights into the prevention and treatment of SONFH.

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American journal of translational research
American journal of translational research ONCOLOGY-MEDICINE, RESEARCH & EXPERIMENTAL
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