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. 2020 Jul 31;26:123–135. doi: 10.1016/j.jare.2020.07.015

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© 2020 The Authors. Published by Elsevier B.V. on behalf of Cairo University.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Fig. 4 — Silencing of lncRNA HIF1A-AS2 enhances cell viability, but reduces apoptosis by inhibiting ATF2 expression. (A) Viability of ECs after ox-LDL-induced inflammation determined using CCK-8 assay. (B) Viability of SMCs after ox-LDL-induced inflammation determined using CCK-8 assay. (C) Viability of HCAECs after ox-LDL-induced inflammation determined using CCK-8 assay. (D) Cell apoptosis of ECs after ox-LDL-induced inflammation determined using flow cytometry. (E) Cell apoptosis of SMCs after ox-LDL-induced inflammation determined using flow cytometry. (F) Cell apoptosis of HCAECs after ox-LDL-induced inflammation determined using flow cytometry. *p < 0.05 vs. ox-LDL-exposed cells co-transfected with si-NC + oe-NC. #p < 0.05 vs. ox-LDL-exposed cells co-transfected with si-HIF1A-AS2 + oe-NC. &p < 0.05 vs. the ox-LDL-exposed cells co-transfected with si-NC + oe-ATF2. Data (mean ± standard deviation) were obtained from three independent cell experiments and comparison among multiple groups was analyzed with one-way analysis of variance.