Fig. 5: ROCK2 deletion improves fatty acid metabolism.
From: ROCK2-induced metabolic rewiring in diabetic podocytopathy
a–c The amounts of ATP (a), the expression of markers of apoptosis (b), the number of TUNEL-positive podocytes (c) treated with vehicle (DMSO) or etomoxir for 24 h. The scale bar on the top left represents 100 μm (n = 3). d The glomerular expression of TGF-β in STZ-injected mice, db/db mice, and mice treated with HFD (n = 6). e FAO was assessed using cell lysates obtained from podocytes treated with siRNA against ROCK2 (n = 3). f Relative mRNA levels of FAO mediators in podocytes treated with siRNA against ROCK2 before stimulation with TGF-β (n = 3). g PPARα mRNA levels in podocytes treated with siRNA against ROCK2 before stimulation with TGF-β (n = 3). h Representative microphotographs and the quantification of TUNEL-positive apoptotic podocytes. Podocytes were pretreated with siRNA against ROCK2 before stimulation with TGF-β. Etomoxir was used in order to inhibit fatty acid oxidation in podocytes treated with ROCK2 siRNA. Fenofibrate was used to investigate the effect of PPARα activation on podocyte apoptosis. The scale bar on the top left represents 50 μm (n = 3). i Glomerular PPARα mRNA levels in WT and PR2KO mice. j A correlation analysis between glomerular transcripts of ROCK2 and PPARα. Hodgin Diabetes Mouse Glom data obtained from the transcriptomic database Nephroseq (https://www.nephroseq.com) were used. The trendline is shown in red. The R value was determined by Pearson correlation analysis; white and gray plots represent non-diabetic mice and diabetic mice, respectively (n = 18–21). *p < 0.05. Data represent the mean ± s.e.m.
