Fig. 3: TEC-specific deletion of ACSS2 suppressed H3K9cr level and alleviated fibrosis in mice. | Nature Communications

Fig. 3: TEC-specific deletion of ACSS2 suppressed H3K9cr level and alleviated fibrosis in mice.

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

Fig. 3: TEC-specific deletion of ACSS2 suppressed H3K9cr level and alleviated fibrosis in mice.The alternative text for this image may have been generated using AI.

A Representative IHC staining of ACSS2 in kidneys of control and mice treated with UUO or injected with FAN (n = 3 per group). Scale bar: upper panels: 50 μm; lower panels:20 μm. B Design strategy of TEC-specific deletion of ACSS2 (ACSS2tecKO) mice. C H3K9cr, H3K9ac and H3 immunoblotting and quantification of these immunoblots in the whole kidney lysates of control and UUO of WT and ACSS2tecKO mice (n = 3 per group, Control vs UUO: p = 0.0212;UUO vs ACSS2CKO + UUO: p = 0.0106). D Representative images of H&E and Masson staining in kidneys of UUO of WT and ACSS2tecKO mice (n = 3 per group). Scale bar: upper panels: 100 μm; lower panels: 50 μm. E FN1, COL1a1, COL6 and GAPDH immunoblotting in the whole kidney lysates of control and UUO of WT and ACSS2tecKO mice (n = 3 per group). F mRNA levels of Fn1, Col1a1, Acta2 or Col6 in whole kidney lysates of WT and ACSS2tecKO mice treated with UUO (n = 6 per group, Control vs. UUO: p < 0.0001 for Fn1, p < 0.0001 for Col1a, p < 0.0001 for Acta2; UUO vs. ACSS2CKO + UUO: p = 0.0055 for Fn1, p = 0.0011 for Col1a, p = 0.0456 for Acta2). UUO unilateral ureteric obstruction, WT wild type, IHC Immunohistochemical, ACSS2 CKO tubular epithelial cell-specific deletion of ACSS2. Triangle: representative positive staining of ACSS2. Data shown are means ± SEM. Statistical analysis by one-way ANOVA with Tukey’s post hoc test. *p < 0.05, **p < 0.01, ***p < 0.001 and ****p < 0.0001.

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