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脂肪源干细胞外体NFIC通过调节miR-204-3p/HIPK2来改善糖尿病足

Huimin Huang¹, Wufei Zhu², Zongwei Huang¹

¹Burn, Plastic and Wound Surgery Department, Yichang Central People's Hospital, The First College of Clinical Medical Science, China Three Gorges University, Yichang, China.

Journal of orthopaedic surgery and research

|September 14, 2023

概括

用核因子I/C (NFIC) 修改的人类脂肪衍生干细胞外体可以治疗糖尿病足 (DFU). 这些外体调节微RNA-204-3p (miR-204-3p) 和家庭主体相互作用蛋白激酶2 (HIPK2) 以减少高葡萄糖诱导的内皮细胞损伤.

科学领域:

内分泌学在内分泌学.
干细胞生物学干细胞生物学
分子生物学分子生物学

背景情况:

糖尿病足 (DFU) 是一种严重的糖尿病并发症,患病率和死亡率高.
人体脂肪组织衍生的介质干细胞 (ADSC) 和它们的外体细胞显示出缓解DFU的潜力.
在DFU中,ADSC衍生的外体细胞作用背后的精确分子机制在很大程度上仍未被探索.

研究的目的:

研究ADSC衍生的外体在治疗高葡萄糖 (HG) 诱导的人静脉内皮细胞 (HUVEC) 损伤中的分子机制.
阐明微RNA-204-3p (miR-204-3p) /家庭基因相互作用蛋白激酶2 (HIPK2) 轴在这个过程中的作用.
评估NFIC修饰的ADSC衍生的外体对DFU的治疗潜力.

主要方法:

用高葡萄糖和从核因子I/C (NFIC) 修饰的ADSC衍生出的外体对待HUVECs.
使用RT-qPCR量化了miR-204-3p,HIPK2和NFIC的表达水平.
细胞功能,包括增殖,亡,迁移和血管生成,通过各种测试进行了评估.
生物信息学和双露西法酶记者测试被用来验证分子相互作用.

主要成果:

在DFU患者和接受HG治疗的HUVEC中,miR-204-3p和NFIC降低,HIPK2.2增加.
过度表达miR-204-3p可以抵消HG诱导的HUVEC功能障碍.
鉴定出HIPK2是miR-204-3p的直接标,NFIC对miR-204-3p的表达进行了积极调节.
通过miR-204-3p/HIPK2通路,NFIC修饰的ADSC外体减轻了HG诱导的HUVEC损伤.

结论:

外体NFIC沉默装载的ADSC片调节miR-204-3p/HIPK2轴.
这种调制抑制了HG诱导的HUVEC增殖,迁移和血管生成.
这为DFU提供了一个有前途的基于干细胞的治疗策略.

关键词:

在ADSC中,ADSC是指ADSC.糖尿病足部糖尿病足部这就是HIPK2的原因.在HUVECEC中使用.在 NFIC 中,我们可以看到 NFIC.在 miR-204-3pp 中使用.

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