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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 8. — NAT8L regulates SP-induced autophagy in PAECs in vivo. (A) Protein expression of LC3B, Beclin-1 and ATG7 in PAECs of CTEPH rats treated with SP and the combination of SP and siRNA-GAS5. (B) The abundance of LC3B in PAECs of rats with CTEPH treated with SP and the combination of SP and siRNA-GAS5, as assessed by immunofluorescence assays (scale bar: 25 µm; magnification, ×20). (C) Autophagic vacuoles in the cellular cytoplasm of PAECs of CTEPH rats treated with SP and the combination of SP and siRNA-GAS5, as evaluated by transmission electron microscopy (scale bar, 2 µm; magnification, ×10,000). Red arrows indicate the autophagic vacuoles. (D) GFP signals in PAECs as assessed by tfLC3 assays. (Scale bar, 50 µm; magnification, ×20). (E) Schematic of GAS5 regulating PAECs autophagy induced by SP. *P<0.05. There were at least three replicates in each group available for analysis. SP, spermidine; PAECs, pulmonary artery endothelial cells; siRNA, small interfering RNA; CTEPH, chronic thromboembolic pulmonary hypertension.