Figure 3. Renal tubular specific G9a deletion alleviated cisplatin‐induced kidney injury by enhancing lipolysis and fatty acid oxidation.

• A
  Experimental design for cisplatin‐induced AKI model.
• B
  Representative immunoblots (left) with quantitative results (right) of G9a and H3K9me1/2 in cisplatin‐injured mouse kidneys.
• C
  Representative H&E images (left) with quantitative pathological scores (right) of indicated groups. Scale bar = 100 μm.
• D
  Serum creatine (Crea) and blood urea nitrogen (BUN) levels of indicated groups.
• E
  mRNA levels of Kim1 and Ngal of indicated groups.
• F, G
  Representative Oil Red O staining with quantification (F, scale bar = 100 μm), and renal TG (triglyceride) and TC (cholesterol) levels (G) of indicated groups.
• H
  mRNA levels of fatty acid oxidation related genes of indicated groups.
• I
  Representative Cpt1a immunostaining (up) with quantitative analysis (bottom) in the kidneys of indicated groups. Scale bar = 50 μm. IOD, integral optical density.
• J–L
  mRNA level of Ces1 (J), representative immunoblots with quantitative results of Ces1 (K), and carboxylesterase enzymatic activity (L) of indicated groups.
• M
  Representative immunostaining for F4/80 and quantitative results of indicated groups. Scale bar = 50 μm.
• N
  Representative immunoblots (left) with quantitative results (right) of p‐Mlkl of indicated groups.

Data information: Six mice per group. Cis, cisplatin; in (B–N), data were presented as means ± SD. Panels B (G9a), C, D, E (Kim1), F, I, H (except Acadm), J–N were analyzed with 2‐tailed, unpaired Student's t test. Panels B (H3K9me2), E (Ngal), G and H (Acadm) were analyzed by Mann–Whitney U test. *P < 0.05; **P < 0.01.

Source data are available online for this figure.