Iron oxide nanoparticles augment the intercellular mitochondrial transfer-mediated therapy
The transfer of mitochondria between cells has recently been revealed as a spontaneous way to protect the injured cells. However, the utilization of this natural transfer process for disease treatment is so far limited by its unsatisfactory transfer efficiency and selectivity. Here, we demonstrate t...
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| Veröffentlicht in: | Science advances 2021-10, Vol.7 (40), p.eabj0534-eabj0534 |
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| creator | Huang, Ting Zhang, Tianyuan Jiang, Xinchi Li, Ai Su, Yuanqin Bian, Qiong Wu, Honghui Lin, Ruyi Li, Ni Cao, Hongcui Ling, Daishun Wang, Jinqiang Tabata, Yasuhiko Gu, Zhen Gao, Jianqing |
| description | The transfer of mitochondria between cells has recently been revealed as a spontaneous way to protect the injured cells. However, the utilization of this natural transfer process for disease treatment is so far limited by its unsatisfactory transfer efficiency and selectivity. Here, we demonstrate that iron oxide nanoparticles (IONPs) can augment the intercellular mitochondrial transfer from human mesenchymal stem cells (hMSCs) selectively to diseased cells, owing to the enhanced formation of connexin 43–containing gap junctional channels triggered by ionized IONPs. In a mouse model of pulmonary fibrosis, the IONP-engineered hMSCs achieve a remarkable mitigation of fibrotic progression because of the promoted intercellular mitochondrial transfer, with no serious safety issues identified. The present study reports a potential method of using IONPs to enable hMSCs for efficient and safe transfer of mitochondria to diseased cells to restore mitochondrial bioenergetics. |
| doi_str_mv | 10.1126/sciadv.abj0534 |
| format | Article |
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However, the utilization of this natural transfer process for disease treatment is so far limited by its unsatisfactory transfer efficiency and selectivity. Here, we demonstrate that iron oxide nanoparticles (IONPs) can augment the intercellular mitochondrial transfer from human mesenchymal stem cells (hMSCs) selectively to diseased cells, owing to the enhanced formation of connexin 43–containing gap junctional channels triggered by ionized IONPs. In a mouse model of pulmonary fibrosis, the IONP-engineered hMSCs achieve a remarkable mitigation of fibrotic progression because of the promoted intercellular mitochondrial transfer, with no serious safety issues identified. The present study reports a potential method of using IONPs to enable hMSCs for efficient and safe transfer of mitochondria to diseased cells to restore mitochondrial bioenergetics.</description><identifier>ISSN: 2375-2548</identifier><identifier>EISSN: 2375-2548</identifier><identifier>DOI: 10.1126/sciadv.abj0534</identifier><identifier>PMID: 34586849</identifier><language>eng</language><publisher>United States: American Association for the Advancement of Science</publisher><subject>Bioengineering ; Biomedicine and Life Sciences ; Life Sciences ; Materials Science ; SciAdv r-articles</subject><ispartof>Science advances, 2021-10, Vol.7 (40), p.eabj0534-eabj0534</ispartof><rights>Copyright © 2021 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. 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However, the utilization of this natural transfer process for disease treatment is so far limited by its unsatisfactory transfer efficiency and selectivity. Here, we demonstrate that iron oxide nanoparticles (IONPs) can augment the intercellular mitochondrial transfer from human mesenchymal stem cells (hMSCs) selectively to diseased cells, owing to the enhanced formation of connexin 43–containing gap junctional channels triggered by ionized IONPs. In a mouse model of pulmonary fibrosis, the IONP-engineered hMSCs achieve a remarkable mitigation of fibrotic progression because of the promoted intercellular mitochondrial transfer, with no serious safety issues identified. 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| subjects | Bioengineering Biomedicine and Life Sciences Life Sciences Materials Science SciAdv r-articles |
| title | Iron oxide nanoparticles augment the intercellular mitochondrial transfer-mediated therapy |
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