Fig. 4: Restoration of ACOT12 ameliorates lipid accumulation and kidney fibrosis in Acot12−/− UUO kidneys.
From: ACOT12, a novel factor in the pathogenesis of kidney fibrosis, modulates ACBD5
a Masson’s trichrome and immunohistochemical staining of αSMA and PLIN2 in Acot12−/− UUO kidneys with or without parenchymal injection of lentivirus containing the Acot12 construct (LV-Acot12) (n = 4 per group). A control lentivirus (LV-control) was used as a negative control. The positive area was determined and the data are presented as a bar graph. Scale bar, 200 μm. b The expression levels of fibrotic genes in Acot12−/− UUO kidneys with or without parenchymal injection of LV-Acot12 (n = 4 per group). c Synthesis and chemical structure of CHI–DHCA. d UV‒Vis spectra of the DHCA monomer, chitosan and CHI–DHCA. e Scanning electron microscope image of the CHI–DHCA patch. f Immunohistochemical staining of αSMA and PLIN2 in Acot12−/− UUO kidneys with or without a chitosan patch conjugated with the Acot12 expression vector (n = 3 per group). The positive area was determined and is represented in a bar graph. Scale bar, 200 μm. g The expression levels of fibrotic and inflammatory genes in Acot12−/− UUO kidneys with or without chitosan patch-conjugation with the Acot12 expression vector (n = 3 per group). *P < 0.05, **P < 0.01 and ***P < 0.001 per control CL. #P < 0.05, ##P < 0.01 and ###P < 0.001 per control UUO.
