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. 2022 Aug 2;26(4):297. doi: 10.3892/mmr.2022.12813

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Copyright: © Wu et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 3. — GAS5 promotes SP-induced autophagy in PAECs through targeting miRNA-31-5p. (A) Putative binding site of miRNA-31-5p in 3′-UTR of GAS5. (B) Effect of SP (10 µM) on the expression of miRNA-31-5p. (C) Transfection efficiency of miRNA-31-5p mimic and inhibitor. (D) Effect of pcDNA3.1-GAS5 and siRNA-GAS5 on the expression of miRNA-31-5p. (E) Relative luciferase activity in PAECs co-transfected with mutant/wild-type plasmids containing the putative binding site of miRNA-31-5p in GAS5 and miRNA-31-5p mimic. (F) Physical communication between GAS5 and miRNA-31-5p in PAECs assessed by RNA binding protein immunoprecipitation assays. *P<0.05; **P<0.01. There were at least three replicates in each group available for analysis. GAS5, growth arrest-specific transcript 5; SP, spermidine; PAECs, pulmonary artery endothelial cells; siRNA, small interfering RNA.