脐带间充质干细胞外泌体miR-143-3p通过靶向COX-2延缓内皮细胞衰老。

IF 2.6 3区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES
PLoS ONE Pub Date : 2025-07-11 eCollection Date: 2025-01-01 DOI:10.1371/journal.pone.0327173
Zhi-Peng Yang, Shui-Hong Lu, Yan-Hong Pan, Zhao-Fu Liao, Yi-Tuan Xie, Heng Li, Yu-Lan Zhou, Zhen-Can Shi, Yun-Fei Qu, Zhu-Guo Wu, Chongxiang Xiong, Xing-Dong Xiong
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引用次数: 0

摘要

血管内皮细胞衰老导致内皮功能障碍,加重动脉粥样硬化。在这项研究中,我们提供了证据,证明来自人脐带间充质干细胞(hucMSC-Exos)的外泌体可以延缓内皮细胞衰老,促进内皮细胞增殖,并增强体外血管生成活性。miRNA分析显示,miR-143-3p在hucMSC-Exos中高表达,在经hucMSC-Exos处理的内皮细胞中进一步上调。沉默miR-143-3p诱导内皮细胞衰老,衰老相关β-半乳糖苷酶活性增加,细胞增殖减少,抑制小管形成;相反,过表达miR-143-3p表现出相反的效果。此外,我们发现miR-143-3p直接靶向环氧合酶-2 (COX-2)并抑制其翻译,从而延缓内皮细胞衰老。这些结果表明,hucMSC-Exos可以通过转移miR-143-3p来延缓内皮细胞衰老。总之,我们的数据证明了humsc - exos作为血管衰老干预的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Umbilical cord mesenchymal stem cell exosomal miR-143-3p delays endothelial cell senescence through targeting COX-2.

Umbilical cord mesenchymal stem cell exosomal miR-143-3p delays endothelial cell senescence through targeting COX-2.

Umbilical cord mesenchymal stem cell exosomal miR-143-3p delays endothelial cell senescence through targeting COX-2.

Umbilical cord mesenchymal stem cell exosomal miR-143-3p delays endothelial cell senescence through targeting COX-2.

Senescence of vascular endothelial cells leads to endothelial dysfunction and exacerbates atherosclerosis. In this study, we presented evidence that exosomes derived from human umbilical cord mesenchymal stem cells (hucMSC-Exos) could delay endothelial cell senescence, promote endothelial cell proliferation, and enhance angiogenic activity in vitro. The miRNA profiling analysis revealed a high expression of miR-143-3p in hucMSC-Exos, which was further upregulated in endothelial cells treated with hucMSC-Exos. Silencing miR-143-3p induced endothelial cell senescence, as evidenced by increased senescence-associated β-galactosidase activity, reduced cell proliferation, and inhibited tubular formation; conversely, overexpression of miR-143-3p exhibited opposite effects. Moreover, we found that miR-143-3p directly targeted Cyclooxygenase-2 (COX-2) and suppressed its translation, thus delaying endothelial cell senescence. These results suggested that hucMSC-Exos can delay endothelial cell senescence by transferring miR-143-3p. In summary, our data demonstrated the potential of hucMSC-Exos as an intervention against vascular aging.

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来源期刊
PLoS ONE
PLoS ONE 生物-生物学
CiteScore
6.20
自引率
5.40%
发文量
14242
审稿时长
3.7 months
期刊介绍: PLOS ONE is an international, peer-reviewed, open-access, online publication. PLOS ONE welcomes reports on primary research from any scientific discipline. It provides: * Open-access—freely accessible online, authors retain copyright * Fast publication times * Peer review by expert, practicing researchers * Post-publication tools to indicate quality and impact * Community-based dialogue on articles * Worldwide media coverage
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