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. 2023 Sep 13;80(11):2386–2396. doi: 10.1161/HYPERTENSIONAHA.123.21645

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© 2023 The Authors.

Hypertension 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 6. — siRNA-mediated reduction of PPARγ (peroxisome proliferator-activated receptor-γ) significantly decreased HO1 (heme oxygenase 1) expression that were not rescued by Rosiglitazone (Rosi). PPARγ siRNA caused a significant reduction of PPARγ gene and protein expression (A, n=3) and HO1 gene and protein expression (B, n=3) when compared with the scramble siRNA control. Scramble siRNA (Scr)-treated cells were simultaneously treated with Rosi and caused a significant increase in HO1 protein expression in comparison to the Scr-treated vehicle control (C, n=3). In the PPARγ-silenced cells, Rosi could not increase HO1 protein expression when compared with vehicle-treated PPARγ-silenced cells (C, n=3). HO1 protein expression was significantly reduced in both vehicle and Rosi-treated PPARγ-silenced cells in comparison to the Rosi and vehicle-treated Scr-treated cells, which collectively suggests a PPARγ-dependent mechanism for HO1 regulation. Relative mRNA and protein expression were determined by normalization to housekeeping genes or protein. Relative expression values for sample sets were normalized to Scr control (set equal to 1) and subsequent statistical analysis was performed by student t test to determine significant differences between groups; *P<0.05, **P<0.01, ***P<0.0001. siPPARγ indicates PPARγ siRNA.