Neural stem cell-derived exosomes regulate cell proliferation, migration, and cell death of brain microvascular endothelial cells via the miR-9/Hes1 axis under hypoxia
© 2024 The Authors. Animal Models and Experimental Medicine published by John Wiley & Sons Australia, Ltd on behalf of The Chinese Association for Laboratory Animal Sciences..
BACKGROUND: Our previous study found that mouse embryonic neural stem cell (NSC)-derived exosomes (EXOs) regulated NSC differentiation via the miR-9/Hes1 axis. However, the effects of EXOs on brain microvascular endothelial cell (BMEC) dysfunction via the miR-9/Hes1 axis remain unknown. Therefore, the current study aimed to determine the effects of EXOs on BMEC proliferation, migration, and death via the miR-9/Hes1 axis.
METHODS: Immunofluorescence, quantitative real-time polymerase chain reaction, cell counting kit-8 assay, wound healing assay, calcein-acetoxymethyl/propidium iodide staining, and hematoxylin and eosin staining were used to determine the role and mechanism of EXOs on BMECs.
RESULTS: EXOs promoted BMEC proliferation and migration and reduced cell death under hypoxic conditions. The overexpression of miR-9 promoted BMEC proliferation and migration and reduced cell death under hypoxic conditions. Moreover, miR-9 downregulation inhibited BMEC proliferation and migration and also promoted cell death. Hes1 silencing ameliorated the effect of amtagomiR-9 on BMEC proliferation and migration and cell death. Hyperemic structures were observed in the regions of the hippocampus and cortex in hypoxia-induced mice. Meanwhile, EXO treatment improved cerebrovascular alterations.
CONCLUSION: NSC-derived EXOs can promote BMEC proliferation and migration and reduce cell death via the miR-9/Hes1 axis under hypoxic conditions. Therefore, EXO therapeutic strategies could be considered for hypoxia-induced vascular injury.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2024 |
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Erschienen: |
2024 |
Enthalten in: |
Zur Gesamtaufnahme - volume:7 |
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Enthalten in: |
Animal models and experimental medicine - 7(2024), 1 vom: 16. Feb., Seite 24-35 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Deng, Xiaojun [VerfasserIn] |
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Links: |
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Themen: |
Brain microvascular endothelial cells |
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Anmerkungen: |
Date Completed 26.03.2024 Date Revised 27.03.2024 published: Print-Electronic Citation Status MEDLINE |
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doi: |
10.1002/ame2.12394 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM368597458 |
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245 | 1 | 0 | |a Neural stem cell-derived exosomes regulate cell proliferation, migration, and cell death of brain microvascular endothelial cells via the miR-9/Hes1 axis under hypoxia |
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520 | |a © 2024 The Authors. Animal Models and Experimental Medicine published by John Wiley & Sons Australia, Ltd on behalf of The Chinese Association for Laboratory Animal Sciences. | ||
520 | |a BACKGROUND: Our previous study found that mouse embryonic neural stem cell (NSC)-derived exosomes (EXOs) regulated NSC differentiation via the miR-9/Hes1 axis. However, the effects of EXOs on brain microvascular endothelial cell (BMEC) dysfunction via the miR-9/Hes1 axis remain unknown. Therefore, the current study aimed to determine the effects of EXOs on BMEC proliferation, migration, and death via the miR-9/Hes1 axis | ||
520 | |a METHODS: Immunofluorescence, quantitative real-time polymerase chain reaction, cell counting kit-8 assay, wound healing assay, calcein-acetoxymethyl/propidium iodide staining, and hematoxylin and eosin staining were used to determine the role and mechanism of EXOs on BMECs | ||
520 | |a RESULTS: EXOs promoted BMEC proliferation and migration and reduced cell death under hypoxic conditions. The overexpression of miR-9 promoted BMEC proliferation and migration and reduced cell death under hypoxic conditions. Moreover, miR-9 downregulation inhibited BMEC proliferation and migration and also promoted cell death. Hes1 silencing ameliorated the effect of amtagomiR-9 on BMEC proliferation and migration and cell death. Hyperemic structures were observed in the regions of the hippocampus and cortex in hypoxia-induced mice. Meanwhile, EXO treatment improved cerebrovascular alterations | ||
520 | |a CONCLUSION: NSC-derived EXOs can promote BMEC proliferation and migration and reduce cell death via the miR-9/Hes1 axis under hypoxic conditions. Therefore, EXO therapeutic strategies could be considered for hypoxia-induced vascular injury | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a Hes1 | |
650 | 4 | |a brain microvascular endothelial cells | |
650 | 4 | |a exosomes | |
650 | 4 | |a miR‐9 | |
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700 | 1 | |a Hu, Xiaoyi |e verfasserin |4 aut | |
700 | 1 | |a Wang, Shang |e verfasserin |4 aut | |
700 | 1 | |a Zhao, Hui |e verfasserin |4 aut | |
700 | 1 | |a Wei, Yaqin |e verfasserin |4 aut | |
700 | 1 | |a Fu, Jiaqi |e verfasserin |4 aut | |
700 | 1 | |a Wu, Wenhui |e verfasserin |4 aut | |
700 | 1 | |a Liu, Jinming |e verfasserin |4 aut | |
700 | 1 | |a Zhang, Caicai |e verfasserin |4 aut | |
700 | 1 | |a Wang, Lili |e verfasserin |4 aut | |
700 | 1 | |a Yuan, Ping |e verfasserin |4 aut | |
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