Fig. 5: Genetic and pharmacological inhibition of EPRS1 suppresses fibroblast activation and proliferation in FA mice.
From: EPRS1-mediated fibroblast activation and mitochondrial dysfunction promote kidney fibrosis
a Representative images of α-SMA, vimentin, Ki67, and proliferating cell nuclear antigen (PCNA) from IHC-stained kidneys examining the effect of genetic Eprs1 inhibition in FA mice. Scale bar = 100 μm (for α-SMA, vimentin, and Ki67), Scale bar = 50 μm (for PCNA). b–e α-SMA- and vimentin-positive areas and Ki67- and PCNA-positive cells were quantified by ImageJ analysis (n = 4‒6). f mRNA levels of fibroblast activation protein (Fap) were analyzed by qPCR and normalized to those of Rpl13a (n = 4–6). g Representative images of α-SMA and PCNA from IHC-stained kidneys used to assess the effect of the EPRS1 inhibitor. Scale bar = 100 μm (α-SMA), Scale bar = 50 μm (PCNA). h The α-SMA-positive area was quantified by ImageJ analysis (n = 7–9). i PCNA-positive cells were quantified by ImageJ analysis (n = 7–9). j mRNA levels of Fap were analyzed by qPCR and normalized to those of Rpl13a (n = 7–9). The data are presented as mean ± standard deviation. Statistical data were analyzed by ANOVA with Tukey’s post hoc test. *P < 0.05, **P < 0.01, and ***P < 0.001.
