Itokazu Maki, Takehara Toshiyuki, Toriumi Kensuke, Iwawaki Natsumi, Mori Tatsufumi, Ondoera Yuta, Higashimoto Yuji, Goto Koji, Yamada Hidekazu, Teramura Takeshi
Department of Rehabilitation Medicine, Kindai University Faculty of Medicine, Osaka, Japan.
Division of Cell Biology for Regenerative Medicine, Institute of Advanced Clinical Medicine, Kindai University Faculty of Medicine, Osaka, Japan.
Sci Rep. 2025 Jul 1;15(1):22186. doi: 10.1038/s41598-025-06982-y.
Extracellular vesicles (EVs), which carry biological mediators such as microRNAs (miRNAs) and cytokines, play a crucial role in regulating recipient tissues and are considered a key mechanism of action in cell therapy. However, it has been found that cellular aging in donor cells significantly affects the expression profiles of these mediators involved in intercellular communication. In this study, we identified miR-23b-3p as a regulator of stemness-associated genes through its targeting of TGFBR3, with its expression differing between mesenchymal stem cells (MSCs) from young and aged donors. In aged MSCs, hypermethylation of the human MIR23B promoter region led to its downregulation. Treatment with the demethylating agent valproic acid restored miR-23b-3p expression and facilitated its incorporation into EVs. Our findings indicate that aging in MSCs alters the miRNA composition of EVs, potentially disrupting intercellular communication and significantly impacting the therapeutic efficacy of cell transplantation. To address this issue, the induction of demethylation may represent a promising strategy to improve treatment outcomes of MSCs.
细胞外囊泡(EVs)携带诸如微小RNA(miRNAs)和细胞因子等生物介质,在调节受体组织中发挥关键作用,被认为是细胞治疗中的关键作用机制。然而,已发现供体细胞中的细胞衰老会显著影响这些参与细胞间通讯的介质的表达谱。在本研究中,我们通过靶向转化生长因子β受体3(TGFBR3)确定了miR-23b-3p是干性相关基因的调节因子,其在年轻和老年供体的间充质干细胞(MSCs)中的表达有所不同。在衰老的MSCs中,人MIR23B启动子区域的高甲基化导致其下调。用去甲基化剂丙戊酸处理可恢复miR-23b-3p的表达并促进其掺入EVs。我们的研究结果表明,MSCs的衰老会改变EVs的miRNA组成,可能破坏细胞间通讯并显著影响细胞移植的治疗效果。为解决这一问题,诱导去甲基化可能是改善MSCs治疗效果的一种有前景的策略。