通过 TLR4 介导的信号增强脂肪间充质干细胞的再生潜能

Demet Kaçaroğlu, Seher Yaylacı
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引用次数: 0

摘要

导言Toll 样受体 4(TLR4)是一种受体,传统上在免疫调节(免疫系统的调节)和促炎症反应的启动中发挥着重要作用。TLR4 在体内用于识别来自外部的病原体或受损细胞的分子模式。然而,近年来人们也逐渐认识到,TLR4 可影响免疫系统和干细胞(尤其是间充质干细胞)的功能。因此,了解TLR4信号如何在细胞和分子水平发挥作用,并将这一知识用于再生医学可能会很有用,特别是在治疗脂肪间充质干细胞(ADMSCs)方面。本研究旨在阐明 TLR4 介导的信号在 ADMSCs 中的多方面作用:我们采用了一套全面的检测方法,包括 MTT 检测细胞活力、流式细胞术检测表面标志物表达以及基因表达分析,结果表明 TLR4 激活可显著调节 ADMSC 生物学的关键方面。具体来说,我们发现 TLR4 信号以剂量和时间依赖的方式调节 ADMSCs 的增殖、表面标记表达和再生能力。此外,TLR4激活还能对多柔比星(DOX)诱导的细胞凋亡产生细胞保护作用:这些研究结果表明,TLR4 信号可用于增强 ADMSCs 的再生能力,使基于 ADMSC 的疗法更有效地用于组织工程和治疗目的:但需要注意的是,该领域的研究还需要更多细节和临床研究。
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Enhancing the Regenerative Potential of Adipose-Derived Mesenchymal Stem Cells Through TLR4-Mediated Signaling.

Introduction: Toll-like receptor 4 (TLR4) is a receptor that traditionally plays an important role in immunomodulation (regulation of the immune system) and the initiation of proinflammatory responses. TLR4 is used in the body to recognize molecular patterns of pathogens or damaged cells from outside. However, in recent years, it has also become clear that TLR4 can affect the immune system and the function of stem cells, especially mesenchymal stem cells. Therefore, understanding how TLR4 signaling works at the cellular and molecular level and using this knowledge in regenerative medicine could be potentially useful, especially in the treatment of adipose- derived mesenchymal stem cells (ADMSCs). How these cells can use TLR4 signaling when used to increase their regenerative potential and repair tissues is an area of research.

Aims: This study aims to elucidate the multifaceted role of TLR4-mediated signaling in ADMSCs.

Methods: Employing a comprehensive set of assays, including MTT for cell viability, flow cytometry for surface marker expression, and gene expression analysis, we demonstrate that TLR4 activation significantly modulates key aspects of ADMSC biology. Specifically, TLR4 signaling was found to regulate ADMSCs proliferation, surface marker expression, and regenerative capacity in a dose- and time-dependent manner. Furthermore, TLR4 activation conferred cytoprotective effects against Doxorubicin (DOX)-induced cellular apoptosis.

Results: These findings suggest that TLR4 signaling could be used to enhance the regenerative abilities of ADMSCs and enable ADMSC-based therapies to be used more effectively for tissue engineering and therapeutic purposes.

Conclusion: However, it is important to note that research in this area needs more details and clinical studies.

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