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Fig. 8 | Cell Communication and Signaling

Fig. 8

From: Endothelial colony-forming cell-derived exosomal miR-21-5p regulates autophagic flux to promote vascular endothelial repair by inhibiting SIPL1A2 in atherosclerosis

Fig. 8

ECFC-derived exosomes promote reendothelialization and rescue intimal hyperplasia in a rat atherosclerosis model in a miR-21-5p-dependent manner. A A flowchart illustrating experiments to evaluate the therapeutic effects of ECFC-exosomes in a rat atherosclerosis model. B The injured areas of carotid arteries in rats with different treatments were evaluated using Evans blue staining. Biological replicates = 6, and technical replicates = 1. C Morphology of the carotid arteries in the rats with different treatments was evaluated by HE staining. The red arrows indicate the endothelial layers, and the black arrows indicate intimal hyperplasia. Biological replicates = 6, and technical replicates = 1. D Concentrations of TC, TG, LDL-c, and HDL-c in serum samples at the end of the in vivo experiment. Sham, control rat; Model, high-fat diet combined with balloon injury to construct atherosclerotic rat model of vascular injury; Exos-miR inh atherosclerotic rat model of vascular injury treated with ECFCs-exosomes transfected with miR-21-5p inhibitor, Exos-NC inh atherosclerotic rat model of vascular injury treated with ECFCs-exosomes transfected with NC inhibitor. Biological replicates = 6, and technical replicates = 3. Significant differences between different treatment groups are indicated as *P < 0.05 and **P < 0.01

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Cell Communication and Signaling

ISSN: 1478-811X