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通过miR-143-3p/ADD3轴对长非编码RNASAN进行破坏,通过miR-143-3p/ADD3轴对老化脂肪基干细胞进行再生

Hewei Xiong^1,2, Sen Ren³, Jing Chen¹

¹Department of Hand Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, 430022, China.

Stem cell research & therapy

|August 22, 2023

概括

衰老的脂肪衍生干细胞 (ASCs) 显示伤口愈合能力降低. 向lncRNA SAN通过调节miR-143-3p/ADD3通路,改善皮肤修复,使老年ASC恢复青春.

科学领域:

干细胞生物学干细胞生物学
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:

衰老的脂肪衍生的干细胞 (ASCs) 在伤口愈合中降低了治疗潜力.
长非编码RNAs (lncRNAs) 与干细胞衰老有关,但它们在介质干细胞衰老中的精确作用需要进一步阐明.

研究的目的:

研究lncRNA衰老相关非编码RNA (SAN) 在ASC衰老中的作用.
阐明SAN影响ASC衰老和功能的分子机制.
评估针对SAN增强伤口修复的治疗潜力.

主要方法:

定量PCR检测SAN和miR-143-3p表达在年轻和老捐赠者的ASC中.
对于SAN和γ-adducin (ADD3) 的过度表达/敲击的lentiviral转导,以及对miR-143-3p操纵的模仿/抑制剂的使用.
检测ASC的增殖,迁移,衰老,纤维细胞迁移和内皮细胞血管生成.
双露西法酶测定,救援实验,以及体内皮肤损伤模型的评估.

主要成果:

在老年ASC中升级调节的IncRNA SAN驱动细胞衰老.
Knockdown 的 lncRNA SAN 增强 ASC 功能,抑制衰老,并促进纤维细胞迁移和血管生成.
SAN作为miR-143-3p的海绵,调节ADD3的表达.
用消耗SAN的老年ASCs治疗加速了皮肤伤口的关闭,改善了重新上皮质化,原沉积和新血管化.

结论:

在cRNA SAN中,通过miR-143-3p/ADD3通路调解ASC衰老.
针对 lncRNA SAN 提供了一个潜在的策略来复兴老化的 ASC.
这种方法可以提高ASC在伤口修复中的有效性.

关键词:

脂肪酸衍生介质干细胞 (ASCs) 是一种干细胞.非编码RNA (ncRNA) 是一种非编码RNA.衰老是一种衰老.干细胞疗法是一种干细胞疗法.伤口愈合伤口愈合

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