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Fig. 7 | Cell Communication and Signaling

Fig. 7

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

Fig. 7

EPC-exosome-derived miR-21-5p targets the 3’UTR of SIPA1L2. A Venn diagram illustrating the overlapping miR-21-5p-targeted genes predicted using bioinformatics tools (miRanda, starBase, RAID and PITA) and downregulated genes in HMECs following ECFC-exosome treatment. B mRNA and protein expression of SIPA1L2 in HMECs with different treatments was determined by qRT-PCR and western blot assay, respectively. Biological replicates = 3, and technical replicates = 1–3. C The interaction between miR-21-5p and the 3’UTR of SIPA1L2 was evaluated using the dual-luciferase reporter assay. Biological replicates = 5, and technical replicates = 1. D Expression of miR-21-5p and SIPA1L2 in HMECs transfected with miR-21-5p mimics or inhibitor was determined by qRT-PCR. Biological replicates = 3, and technical replicates = 3. E mRNA and protein expression of SIPA1L2 in HMECs with different treatments was determined by qRT-PCR and western blot assay, respectively. Exos ECFC-exosomes, Exos-miR inh ECFC-exosomes were transfected with miR-21-5p inhibitor, Exos-NC inh ECFC-exosomes were transfected with NC inhibitor. Biological replicates = 3, and technical replicates = 1–3. N.S. not significant; 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