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. 2022 Aug 11;35(4):ivac210. doi: 10.1093/icvts/ivac210

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© The Author(s) 2022. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 6. — Inhibition of microRNA-637 (miR-637) aggravated the ox-LDL-induced dysfunction in human umbilical vein endothelial cells via upregulating PACS2. (A) The protein analysis of PACS2 was carried out by Western blot in si-ctrl or si-PACS2 transfected human umbilical vein endothelial cells. (B) PACS2 protein expression was examined by Western blot following transfection of the inhibitor NC, miR-637 inhibitor, miR-637 inhibitor+si-ctrl or miR-637 inhibitor+si-PACS2. (C-H) Groups of control, ox-LDL (50 μg/ml) +inhibitor NC, ox-LDL+miR-637 inhibitor, ox-LDL+s miR-637 inhibitor+si-ctrl, ox-LDL+ miR-637 inhibitor+si-PACS2. (C-D) Cell viability (C) and angiogenesis (D) were determined through the Cell-Counting Kit-8 assay and the tube formation assay. (E-F) Cell apoptosis was assessed through flow cytometry (E) and Western blot (F). (G-H) Oxidative stress was measured by examining ROS (G) and MDA levels (H). *P < 0.05. ctrl: control; FITC: fluorescein isothiocyanate; GAPDH: oxidized low-density lipoprotein; MDA: malondialdehyde; miR-637: microRNA-637; NC: negative control; OX-LDL: oxidized low-density lipoprotein; PACS2: phosphofurin acidic cluster sorting protein 2; ROS: reactive oxygen species; si: small interfering.