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. 2022 May 20;27:40. doi: 10.1186/s11658-022-00340-w

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — Downregulating EPAS1 in HA-VSMCs promotes cell apoptosis. A–C EPAS1 was silenced in HA-VSMCs. qRT-PCR (A) and immunoblotting (C) analysis of EPAS1 in HA-VSMCs. qRT-PCR (B) and immunoblotting (C) analysis of SLC3A2 in HA-VSMCs. D Silencing SLC3A2 inhibited HA-VSMC proliferation. E, G Flow cytometry assay (E), caspase-3 activity assay (F), and Western blot analysis of cleaved caspase-3 (G) showed that silencing SLC3A2 promoted HA-VSMC apoptosis. H–K p-FAK (H), p-AKT (I), pY20CAS (J), and GTP-Rac (K) immunoblotting in HA-VSMCs. Western blot was performed three times; representative images are presented. Numbers above lanes indicate the relative protein level, normalized relative to control samples. ***P < 0.001, ****P < 0.0001 (n = 3, ANOVA analysis)