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血小板衍生的线粒体减轻5-氟尿嘧啶诱导的对骨相关间充质干细胞的损伤。

Platelet-Derived Mitochondria Attenuate 5-FU-Induced Injury to Bone-Associated Mesenchymal Stem Cells.

作者信息

Chen Yutong, Liu Zhixin, An Ning, Zhang Jing, Meng Weicheng, Wang Wenting, Wu Xiaoshuang, Hu Xingbin, Chen Yaozhen, Yin Wen

机构信息

Department of Transfusion Medicine, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.

出版信息

Stem Cells Int. 2023 Jan 30;2023:7482546. doi: 10.1155/2023/7482546. eCollection 2023.

DOI:10.1155/2023/7482546
PMID:36756493
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9902133/
Abstract

BACKGROUND

Myelosuppression is a common condition during chemotherapy. Bone-associated mesenchymal stem cells (BA-MSCs) play an essential role in the composition of the hematopoietic microenvironment and support hematopoietic activity. However, chemotherapy-induced damage to BA-MSCs is rarely studied. Recent studies have shown that platelets promote the wound-healing capability of MSCs by mitochondrial transfer. Therefore, this study is aimed at investigating the chemotherapy-induced damage to BA-MSCs and the therapeutic effect of platelet-derived mitochondria. . We established and BA-MSC chemotherapy injury models using the chemotherapy agent 5-fluorouracil (5-FU). Changes in the mitochondrial dynamics were detected by transmission electron microscopy, and the expression of mitochondrial fusion and fission genes was analyzed by qRT-PCR. In addition, mitochondrial functions were also explored by flow cytometry and luminometer. Platelet-derived mitochondria were incubated with 5-FU-damaged BA-MSCs to repair the injury, and BA-MSC functional changes were examined to assess the therapy efficacy. The mechanism of treatment was explored by studying the expression of mitochondrial fission and fusion genes and hematopoietic regulatory factor genes in BA-MSCs.

RESULTS

Stimulation with 5-FU increased the apoptosis and suppressed cell cycle progression of BA-MSCs both and . In addition, 5-FU chemotherapy inhibited the hematopoietic regulatory ability and disrupted the mitochondrial dynamics and functions of BA-MSCs. The mitochondrial membrane potential and ATP content of 5-FU-injured BA-MSCs were decreased. Interestingly, when platelet-derived mitochondria were transferred to BA-MSCs, the 5-FU-induced apoptosis was alleviated, and the hematopoietic regulatory ability of 5-FU-injured BA-MSCs was effectively improved by upregulating the expression of mitochondrial fusion genes and hematopoietic regulatory factor genes.

CONCLUSION

BA-MSCs were severely damaged by 5-FU chemotherapy both and . Meanwhile, platelet-derived mitochondria could attenuate the 5-FU-induced injury to BA-MSCs, which provides future research directions for exploring the treatment strategies for chemotherapy-injured BA-MSCs and establishes a research basis for related fields.

摘要

背景

骨髓抑制是化疗期间的常见情况。骨相关间充质干细胞（BA-MSCs）在造血微环境的组成中起重要作用，并支持造血活性。然而，化疗对BA-MSCs的损伤很少被研究。最近的研究表明，血小板通过线粒体转移促进间充质干细胞的伤口愈合能力。因此，本研究旨在调查化疗对BA-MSCs的损伤以及血小板衍生线粒体的治疗效果。我们使用化疗药物5-氟尿嘧啶（5-FU）建立了BA-MSC化疗损伤模型。通过透射电子显微镜检测线粒体动力学变化，并通过qRT-PCR分析线粒体融合和裂变基因的表达。此外，还通过流式细胞术和发光计探索线粒体功能。将血小板衍生的线粒体与5-FU损伤的BA-MSCs孵育以修复损伤，并检查BA-MSC功能变化以评估治疗效果。通过研究BA-MSCs中线粒体裂变和融合基因以及造血调节因子基因的表达来探索治疗机制。

结果

5-FU刺激增加了BA-MSCs的凋亡并抑制了其细胞周期进程。此外，5-FU化疗抑制了造血调节能力，破坏了BA-MSCs的线粒体动力学和功能。5-FU损伤的BA-MSCs的线粒体膜电位和ATP含量降低。有趣的是，当血小板衍生的线粒体转移到BA-MSCs时，5-FU诱导的凋亡得到缓解，并且通过上调线粒体融合基因和造血调节因子基因的表达有效地改善了5-FU损伤的BA-MSCs的造血调节能力。

结论

5-FU化疗对BA-MSCs造成了严重损伤。同时，血小板衍生的线粒体可以减轻5-FU对BA-MSCs的损伤，这为探索化疗损伤的BA-MSCs的治疗策略提供了未来的研究方向，并为相关领域建立了研究基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/363d/9902133/a2adaec189a1/SCI2023-7482546.008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/363d/9902133/a2adaec189a1/SCI2023-7482546.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/363d/9902133/58c8a2d301f9/SCI2023-7482546.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/363d/9902133/ad0e33f89fa7/SCI2023-7482546.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/363d/9902133/91cff5e6ff9a/SCI2023-7482546.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/363d/9902133/8efb420dbdfd/SCI2023-7482546.007.jpg
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