Adipose-Derived Stem Cell-Derived Extracellular Vesicles Inhibit the Fibrosis of Fibrotic Buccal Mucosal Fibroblasts via the MicroRNA-375/FOXF1 Axis

Autor:	Yuxia Xiao, Bin Han, Hong Wu, Yanhui Zhang, Bo-hong Shi, De-sheng Liu
Jazyk:	angličtina
Rok vydání:	2021
Předmět:	0301 basic medicine Article Subject Cell growth Chemistry Cell Adipose tissue Cell Biology medicine.disease RC31-1245 03 medical and health sciences 030104 developmental biology 0302 clinical medicine medicine.anatomical_structure Oral submucous fibrosis Fibrosis Apoptosis 030220 oncology & carcinogenesis microRNA medicine Cancer research Stem cell Molecular Biology Internal medicine Research Article
Zdroj:	Stem Cells International, Vol 2021 (2021) Stem Cells International
ISSN:	1687-966X
DOI:	10.1155/2021/9964159
Popis:	Oral submucous fibrosis (OSF) is a precancerous lesion. Adipose-derived stem cell- (ADSC-) derived extracellular vesicles (EVs) (ADSC-EVs) regulate multiple oral diseases. Hence, this study explored the mechanism of ADSC-EVs in OSF. ADSCs were transduced with microRNA- (miR-) 375 mimic. ADSC-EVs and miR-375-overexpressed ADSC-EVs (EVs-miR-375) were extracted and identified. miR-375 expression in EVs and fibrotic buccal mucosal fibroblasts (fBMFs) was detected. EV uptake by fBMFs was observed. The targeted relationship between miR-375 and forkhead box protein F1 (FOXF1) was predicted and verified. After EVs-miR-375 treatment or FOXF1 overexpression, fBMF cell proliferation, migration, invasion, and apoptosis were evaluated, and levels of apoptosis-related proteins (cleaved-caspase-3, Bax, and Bcl-2) and fibrosis markers (α-SMA, collagen I, and collagen III) were detected. Functional rescue experiments were further performed to verify the role of the miR-375/FOXF1 axis in OSF. miR-375 was notably upregulated in EVs-miR-375 and EVs-miR-375-treated fBMFs (all P < 0.001 ). ADSC-EVs carried miR-375 into fBMFs. fBMFs can internalize ADSC-EVs. EVs-miR-375 treatment markedly inhibited fBMF cell proliferation, migration, invasion, and fibrosis and promoted apoptosis (all P < 0.01 ). Moreover, miR-375 targeted FOXF1 in fBMFs. FOXF1 overexpression promoted fBMF cell biological behaviors and fibrosis, which were reversed after EVs-miR-375 treatment ( P < 0.01 or P < 0.001 ). We highlighted that ADSC-EVs inhibited fBMF fibrosis and then suppressed OSF progression via the miR-375/FOXF1 axis.
Databáze:	OpenAIRE
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