Journal
ADIPOCYTE
Volume 10, Issue 1, Pages 378-393Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/21623945.2021.1938829
Keywords
Adipose-derived mesenchymal stem cells; extracellular vesicles; miR-26a; KLF9; TRAF2; KLF2; neuronal damage
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Funding
- National Natural Science Foundation of China [81870884]
- Natural Science Foundation of Hunan Province [2019JJ4545]
- Foundation of Hunan Provincial Education Department [19B477]
- Scientific Research Fund Project of Hunan Provincial Health Commission [20200018, 20200037]
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This study demonstrates that EVs derived from ASCs can inhibit neuronal damage by delivering miR-26a, which targets KLF9 to regulate the TRAF2/KLF2 axis.
Extracellular vesicles (EVs) are nano-sized vesicles secreted actively by numeorus cells and have fundamental roles in intercellular communication through shuttling functional RNAs. This study sets out to elucidate the role of microRNA-26a (miR-26a) shuttled by EVs derived from adipose-derived mesenchymal stem cells (ASCs) in neuronal damage. After extraction and identification of ASC-derived EVs (ASC-EVs), mouse cortical neuronal cells were selected to establish an in vivo cerebral ischemia/reperfusion mouse model and an in vitro oxygen glucose deprivation/reperfusion (OGD/RP) cell model. The downstream genes of miR-26a were analyzed. The gain- and loss-of function of miR-26a and KLF9 was performed in mouse and cell models. Neuronal cells were subjected to co-culture with ASC-EVs and biological behaviors were detected by flow cytometry, Motic Images Plus, TTC, TUNEL staining, qRT-PCR and western blot analysis. ASC-EVs protected neuronal cells against neuronal damage following cerebral ischemia/reperfusion, which was related to transfer of miR-26a into neuronal cells. In neuronal cells, miR-26a targeted KLF9. KLF9 could suppress the expression of TRAF2 and KLF2 to facilitate neuronal damage. In vitro and in vivo results showed that miR-26a delivered by ASC-EVs inhibited neuronal damage. In summary, ASC-EVs-derived miR-26a can arrest neuronal damage by disrupting the KLF9-meidated suppression on TRAF2/KLF2 axis.
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