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用DICER1修饰的角质细胞改善伤口愈合

Srirupa Gupta Choudhury¹, Shruti Hazra², Munia Ganguli^1,3

¹CSIR-Institute of Genomics and Integrative Biology, Mathura Road, New Delhi 110025, India.

|September 29, 2025

概括

在糖尿病模型中,抑制DICER1增强了伤口愈合. 一种新纳米载体,M9-DICER1-CS-A,提高了细胞活力,促进了伤口的关闭,为受损愈合提供了一个有前途的治疗策略.

科学领域:

生物医学工程生物医学工程
分子生物学分子生物学
再生医学是一种再生医学.

背景情况:

伤口愈合障碍,在糖尿病等疾病中很常见,源于复杂的愈合过程中出现的障碍.
在停滞的糖尿病伤口中,DICER1 (一种关键的RNA处理酶) 的水平降低,这表明它在关闭受损方面发挥了作用.

研究的目的:

研究DICER1在伤口关闭中的作用.
开发和评估DICER1的新型,少有毒的基因传递系统,用于治疗伤口愈合的治疗应用.

主要方法:

使用Lipofectamine 2000和一种新的基于的纳米载体 (M9-DICER1-CS-A) 用DICER1过度表达等离子体感染HaCaT细胞.
M9-DICER1-CS-A纳米复合物的表征 (大小,PDI,表面电荷,核酸凝结/释放).
评估了细胞活力,伤口关闭率和伤口愈合基因的转移后表达. 工程细胞也被嵌入到水凝矩阵中.

主要成果:

与对照细胞相比,HaCaT细胞中的DICER1过度表达显著增加了伤口关闭和上调的伤口愈合基因.
M9-DICER1-CS-A纳米载体表现出良好的特性 (大小,同质性,电荷) 和有效的基因传递.
M9-DICER1-CS-A转染导致与Lipofectamine 2000相似的伤口关闭,但显著改善了细胞活力.
在水凝中改造的HaCaT细胞表现出持续的活力和繁殖,表明持续治疗效果的潜力.

结论:

DICER1作为关键的伤口关闭促进剂,特别是在糖尿病的背景下.
M9-DICER1-CS-A纳米载体代表了在伤口愈合中用于DICER1基因传递的更安全,更有效的替代方案.
在水凝中的DICER1工程细胞提供了一个有希望的基于细胞的治疗策略,用于治疗受损的伤口关闭.

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