Fig. 5

MSC exosomes alleviated ER stress and inhibited p38 MAPK phosphorylation via miR-21. a Beta cells were cultured under hypoxia (37 °C, 2% O₂, 5% CO₂) with or without MSC exosomes (50 μg/mL) for 48 h. Phosphorylation of p38 MAPK and the ER stress-related proteins GRP94 and P-eIF2α in beta cells, which were induced by hypoxia, were inhibited both by MSC exosomes and miR-21 mimics. After pre-treatment with the inhibitor of miR-21, the effects of MSC exosomes were reversed. β-Actin was used as a loading control. b Densitometry assay with ImageJ. Ctrl, beta cells were cultured under hypoxia in the absence of exosomes; EXO, beta cells were maintained under hypoxia in the presence of exosomes (50 μg/mL); miR-ctrl, beta cells were maintained under hypoxia in the presence of 100 nM miRNA mimic control; miR-21, beta cells were maintained under hypoxia in the presence of 100 nM miR-21 mimics; Inhi-ctrl, beta cells were maintained under hypoxia in the presence of exosomes (50 μg/mL) pretreated with miRNA inhibitor control (100 nM); inhi-miR-21, beta cells were maintained under hypoxia in the presence of exosomes (50 μg/mL) pretreated with miR-21 inhibitor (100 nM)