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. 2022 Jul 28;131(5):424–441. doi: 10.1161/CIRCRESAHA.122.321187

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© 2022 The Authors.

Circulation Research is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 3. — Regulation of UCP2 (uncoupling protein 2) by inflammation and vasoprotective agents. A–C, Real-time quantitative polymerase chain reaction (qPCR) data showing UCP2 mRNA expression is inhibited by proinflammatory mediators IL (interleukin)-1β (10 ng/mL), lysophosphatidylcholine (LPC; 100 μmol/L), and phorbol 12-myristate 13-acetate (PMA; 1 μmol/L), nonparametric Mann-Whitney test. D, Human umbilical vein ECs (HUVECs) treated with simvastatin (SMV, 1 μmol/L), rosuvastatin (RSV, 10 μmol/L), and resveratrol (RES, 50 μmol/L) for 24 h showed upregulated expression of UCP2 mRNA, nonparametric Mann-Whitney test. E, Opposite regulation of UCP2 promoter activity in HUVECs transfected with UCP2 promoter plasmid (581 bp in length) by IL-1β and vasoprotective agents RSV and RES. Two-way ANOVA, Tukey post hoc. F, KLF2 (Krüppel-like factor 2) knockdown in HUVECs by KLF2-shRNA abolished induction of UCP2 mRNA by treatment with SMV, RSV, and RES for 24 h. Two-way ANOVA, Tukey post hoc. G, SMV treatment antagonized the inhibitory effect of IL-1β on UCP2 mRNA expression. Two-way ANOVA, Tukey post hoc. PBS indicates phosphate-buffered saline.