Fig. 2: Global deletion of ACSS2 suppressed H3K9cr level and alleviated kidney fibrosis in mice. | Nature Communications

Fig. 2: Global deletion of ACSS2 suppressed H3K9cr level and alleviated kidney fibrosis in mice.

From: Inhibition of ACSS2-mediated histone crotonylation alleviates kidney fibrosis via IL-1β-dependent macrophage activation and tubular cell senescence

Fig. 2: Global deletion of ACSS2 suppressed H3K9cr level and alleviated kidney fibrosis in mice.The alternative text for this image may have been generated using AI.

A Schematic overview of process for screening factors influencing H3K9cr in vitro and experimental design in ACSS2-/- mouse. B Protein level and quantitative analysis of H3K9cr, H3K9ac, and H3 in whole kidney lysates of control and UUO of WT and ACSS2-/- mice (n = 3 per group, Control vs. UUO: p = 0.032; UUO vs. ACSS2KO + UUO: p = 0.03). C Representative images of H&E staining in UUO of WT and ACSS2-/- mice (n = 6 per group). Scale bar: 200 μm. D FN1, COL6, α-SMA, and GAPDH immunoblotting in the whole kidney lysates of control and UUO of WT and ACSS2-/- mice (n = 3 per group). E mRNA levels of Fn1, Col1a1 and Acta2 in whole kidney lysates of WT and ACSS2-/- mice treated with UUO (n = 5 per group, Control vs. UUO: p < 0.001 for Fn1, p < 0.001 for Col1a, p < 0.001 for Acta2; UUO vs. ACSS2-/- + UUO: p < 0.001 for Fn1, p = 0.007 for Col1a, p < 0.001 for Acta2). FAN: folic acid nephropathy; UUO: unilateral ureteric obstruction; WT: wild type; ACSS2-/-: ACSS2 knockout; Ctrl: Control. Data shown are means ± SEM. Statistical analysis by one-way ANOVA with Tukey’s post hoc test. *p < 0.05, **p < 0.01 and ***p < 0.001.

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