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在hUC-MSC-EV中的微RNAhsa-let-7e-5p通过准TAB2来缓解口腔粘膜炎

Shuting Lin¹, Dong Lai¹, Yan Tian¹

¹Department of Transfusion, Central Laboratory, The Second Affiliated Hospital of Xiamen Medical College, Xiamen, China.

Scandinavian journal of immunology

|July 29, 2024

概括

介酶干细胞细胞外囊泡 (EVs) 显示出治疗口腔粘膜炎 (OM) 的前景. 这些EVs,特别是hUC-MSC-EVs,通过提供hsa-let-7e-5p来减少炎症,该hsa-let-7e-5p针对TAB2和NF-κB通路.

科学领域:

生物医学研究的研究.
干细胞生物学干细胞生物学
分子医学是分子医学.

背景情况:

口腔粘膜炎 (OM) 是癌症治疗的削弱性副作用,治疗选择很少.
介细胞干细胞 (MSC) 和它们的细胞外囊泡 (EV) 显示出OM治疗的潜力,但机制尚不清楚.

研究的目的:

调查人类带MSC衍生的EVs (hUC-MSC-EVs) 对脂多糖 (LPS) 诱导的口腔粘膜炎的保护机制.
在hUC-MSC-EV中识别特定的分子,负责它们的治疗作用.

主要方法:

净化hUC-MSC-EVs和治疗LPS诱导的人口角质细胞 (HOKs).
小RNA测序 (miRNA-seq) 用于识别hUC-MSC-EVs中的关键miRNAs.
生物信息分析用于预测miRNA目标和途径.
在体内研究,使用O.M.的仓鼠模型.

主要成果:

hUC-MSC-EV治疗显著降低了LPS诱导的HOCs中的炎症.
在hUC-MSC-EVs中,hsa-let-7e-5p被确定为一种高度表达的miRNA.
hsa-let-7e-5p针对TAB2并抑制NF-κB通路,调解抗炎作用.
在一个仓鼠模型中,hUC-MSC-EV减轻了OM症状.

结论:

hUC-MSC-EVs通过提供hsa-let-7e-5p.p.来保护口腔粘膜炎.
hsa-let-7e-5p通过准TAB2并抑制NF-κB信号通路来发挥其保护作用.
这些发现突出了使用MSC衍生的EVs治疗OM的新治疗机制.

关键词:

在 NF-κBB 中.口腔粘膜炎是一种口腔粘膜炎.TAB2 TAB2 的时间表.细胞外囊泡中的细胞外囊泡.hUC-MSC 这是一个很大的问题.这是一个hsa-let-7e-5p.这是一种炎症炎症炎症炎症.

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