经 IGF1 基因修饰的尿源干细胞可改善肌肉再生。

IF 1.5 Q3 UROLOGY & NEPHROLOGY American journal of clinical and experimental urology Pub Date : 2024-04-15 eCollection Date: 2024-01-01 DOI:10.62347/QSKH2686
Hualin Yi, Gang Chen, Shuai Qiu, Joshua T Maxwell, Guiting Lin, Tracy Criswell, Yuanyuan Zhang
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摘要

研究目的在这项研究中,我们旨在确定人尿衍生干细胞(USC)和基因修饰USC(旨在过表达肌原生长因子IGF1(USCIGF))对心脏毒素(CTX)损伤小鼠骨骼肌再生能力的影响:方法:我们在USC中过表达了IGF1,并研究了心脏毒素损伤肌肉组织的肌生成能力和再生功能的变化:结果:与单独表达 USC 相比,USCIGF1 激活了 IGF1-Akt-mTOR 信号通路,显著提高了体外成肌分化能力,并增强了成肌生长因子和细胞因子的分泌。此外,在体内骨骼肌损伤模型中,IGF1的过表达提高了USC与骨骼肌细胞融合形成肌管的能力,调节了促再生免疫反应和炎性细胞因子,并增加了肌生成:总之,转基因过表达 IGF1 的 USC 可通过调节肌原分化、旁分泌效应和细胞融合,以及调节体内骨骼肌损伤的免疫反应,显著促进骨骼肌再生。这项研究为评估 USC 作为骨骼肌生成过程中的非生肌细胞源的生肌功能提供了一个新的视角。USC 和 IGF1 表达的结合有望为尿失禁患者的骨骼肌损伤和相关肌肉缺陷提供一种新型高效疗法。
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Urine-derived stem cells genetically modified with IGF1 improve muscle regeneration.

Objective: In this study we aimed to determine the impact of human urine derived stem cells (USC) and genetically modified USC that were designed to overexpress myogenic growth factor IGF1 (USCIGF), on the regenerative capacity of cardiotoxin (CTX)-injured murine skeletal muscle.

Methods: We overexpressed IGF1 in USC and investigated the alterations in myogenic capacity and regenerative function in cardiotoxin-injured muscle tissues.

Results: Compared with USC alone, USCIGF1 activated the IGF1-Akt-mTOR signaling pathway, significantly improved myogenic differentiation capacity in vitro, and enhanced the secretion of myogenic growth factors and cytokines. In addition, IGF1 overexpression increased the ability of USC to fuse with skeletal myocytes to form myotubes, regulated the pro-regenerative immune response and inflammatory cytokines, and increased myogenesis in an in vivo model of skeletal muscle injury.

Conclusion: Overall, USC genetically modified to overexpress IGF1 significantly enhanced skeletal muscle regeneration by regulating myogenic differentiation, paracrine effects, and cell fusion, as well as by modulating immune responses in injured skeletal muscles in vivo. This study provides a novel perspective for evaluating the myogenic function of USC as a nonmyogenic cell source in skeletal myogenesis. The combination of USC and IGF1 expression has the potential to provide a novel efficient therapy for skeletal muscle injury and associated muscular defects in patients with urinary incontinence.

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