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来自BMSCs的外体细胞通过circ-Snhg11传递增强糖尿病伤口愈合

Tao Tang¹, Linyi Chen², Ming Zhang¹

¹Department of Vascular Surgery, The Affiliated Nanjing Drum Tower Hospital, Nanjing University Medical School, #321 Zhongshan Road, Nanjing, Jiangsu, 210008, China.

Diabetology & metabolic syndrome

|February 7, 2024

概括

骨髓干细胞外体加速糖尿病伤口愈合,通过上调circ-Snhg11. 这种机制涉及通过miR-144-3p/SLC7A11通路增强血管生成和减少铁亡.

科学领域:

再生医学是一种再生医学.
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:

从骨介质干细胞 (BMSCs) 衍生出的外体细胞在糖尿病 (DM) 模型中显示出促进皮肤伤口愈合的潜力.
这种治疗效果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BMSC外体在糖尿病伤口愈合中的作用.
阐明潜在的分子机制,重点关注循环RNA (circRNA) 的参与.

主要方法:

下一代测序 (NGS) 来识别差异表达的circRNAs.
路西法酶测定以确认RNA相互作用.
在高葡萄糖 (HG) 条件下进行免疫光染色,以评估活性氧物种 (ROS) 和内皮原生细胞 (EPC) 中的治疗作用.

主要成果:

在糖尿病小鼠中,BMSC外体治疗显著改善了伤口愈合.
NGS确定circ-Snhg11是外体细胞驱动组织修复的关键调解者.
对circ-Snhg11的降低调节降低了外体细胞的治疗疗效.
circ-Snhg11的目标是SLC7A11和miR-144-3p,影响EPC对HG诱导的损伤的保护.
在糖尿病伤口愈合中,circ-Snhg11的上调增强了血管新生和降低了铁亡 (通过GPX4).

结论:

在BMSC外体内的circ-Snhg11促进糖尿病伤口愈合.
这可以通过通过miR-144-3p/SLC7A11/GPX4轴增强抗铁亡信号来实现.
这些发现突出了circ-Snhg11作为改善血管生成和糖尿病伤口修复的治疗点.

关键词:

骨中介细胞干细胞是骨中介细胞的干细胞.糖尿病伤口愈合的治疗方法内皮原生细胞 (EPCs) 是指内皮原生细胞.外基因组是外基因组的组成部分.环-Snhg1111 在线观看

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