Fig. 5: HP disturbs PGC1α expression and energy metabolism in an IRF1-dependent manner.
From: IRF1-mediated downregulation of PGC1α contributes to cardiorenal syndrome type 4
a qPCR analysis of the expression of the predicted transcriptional factors in H9c2 cells treated with control or HP for 24 h. b, c qPCR and representative western blot analysis of IRF1 expression in H9c2 cells treated with control or various doses of HP for 24 h. d–g qPCR and representative western blot analysis of IRF1 expression in heart lysates from sham, CKD, and HPD-fed CKD mice for 12 weeks (d, e) or in H9c2 cells incubated with the serum of healthy donors or CKD patients for 24 h (f, g). h–l H9c2 cells were transfected with two pairs of siRNA against IRF1, and then treated with control or HP for 24 h. Cells were collected for detection of IRF1 and PGC1α protein expressions (h), PGC1α mRNA expression (i), ROS production (j), relative ATP level (k), and mRNA expression of the metabolic genes (l). m qPCR analysis of IRF1 and PGC1α expressions in H9c2 cells transfected with control plasmids (pCtrl) or IRF1 overexpression plasmids (pIRF1). n Representative western blot analysis of IRF1 and PGC1α expressions in H9c2 cells transfected with pCtrl, pIRF1, control siRNA (siCtrl), and two pairs of siRNA against IRF1 (siIRF1), separately. n = 3 biologically independent experiments (a–n). Data are shown as mean ± SD and were analyzed by a two-tailed unpaired t-test (a, f, g) or one-way ANOVA (b–e, h–n). *P < 0.05, **P < 0.01, ***P < 0.001 versus control. #P < 0.05, ##P < 0.01, ###P < 0.001 versus HP.
