介酶干细胞外基因组通过miR-125b-5p/TRAF6/NF-κB通路轴抑制核脉细胞亡

介酶干细胞外基因组通过miR-125b-5p/TRAF6/NF-κB通路轴抑制核脉细胞亡

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Yang Duan¹, Cheng Yu¹, Wenhao Kuang¹

¹Department of Spinal Surgery, Zhujiang Hospital, Southern Medical University, Guangzhou 510260, China.

Acta biochimica et biophysica Sinica

|November 15, 2023

概括

介质干细胞衍生的外体提供miR-125b-5p,以抑制细胞核的细胞亡,并减少椎间盘退化. 这项研究阐明了治疗由磁盘退化引起的腰部疼痛的关键机制.

科学领域:

生物医学工程生物医学工程
细胞生物学细胞生物学
分子生物学分子生物学

背景情况:

椎间盘退化 (IVDD) 是腰部疼痛的主要原因,其潜在机制需要进一步阐明.
介质干细胞 (MSC) 移植显示出IVDD的治疗潜力,但具体的分子途径尚未完全理解.

研究的目的:

研究由MSC衍生的外体所传递的microRNAs (miRNAs) 在IVDD治疗中的作用.
阐明MSC外生体减弱核细胞 (NPC) 退化的分子机制.

主要方法:

生物信息查和高通量测序确定了候选miRNAs.
使用TEM,NTA和西方涂料来表征MSC外体.
细胞活力,细胞亡,miRNA表达和蛋白质水平使用CCK-8,流动细胞计,TUNEL,RT-qPCR和西部斑点试验进行了评估.
一个双路西法酶记者测定和 * in vivo * 鼠标模型被用于机制验证.

主要成果:

在退化的磁盘组织中,miR-125b-5p的表达显着较低,但在MSC外体中却很高.
MSC外体有效地将miR-125b-5p传递到NPC中,抑制细胞亡并促进细胞活力.
miR-125b-5p针对TRAF6,降低其表达,并随后抑制NF-κB激活.

结论:

通过释放miR-125b-5p来减弱IVDD的MSC外基因组,该外基因组向TRAF6并抑制NF-κB通路.
这一发现为IVDD提供了一种新的治疗策略,通过利用特定miRNAs的外体输送.

关键词:

在 NF-κBB 中.在TRAF6中,灭症 (apoptosis) 是一种死亡的过程.外基因组是外基因组中的一个.在 miR-125b-5p 中使用.

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