Fig. 4: Genetic and pharmacological inhibition of EPRS1 reduces collagen accumulation and hydroxyproline levels.
From: EPRS1-mediated fibroblast activation and mitochondrial dysfunction promote kidney fibrosis
a Hydroxyproline was measured in whole kidney tissue from the three groups to examine the effect of genetic Eprs1 inhibition in FA mice (n = 4–6). b Representative images of COL1A1 from IHC-stained kidneys. Scale bar = 100 μm. c The COL1A1-positive area was quantified by ImageJ analysis (n = 4–6). d, e Representative Western blot and quantitative data showing the protein expression levels of COL1A1, EPRS1, α-SMA, and transforming growth factor β (TGF-β) in kidneys from the three groups. The numbers (1–13) indicate individual animals in a given group. f, g The mRNA levels of Col1a1, Col3, Col4, Fn, Acta2, and Eprs1 were analyzed via quantitative PCR (qPCR) and normalized to those of Rpl13a (n = 4–6). h Hydroxyproline was measured in whole kidney tissue from the five groups to assess the effect of the EPRS1 inhibitor (n = 7–9). i Representative images of COL1A1 from IHC-stained kidneys. Scale bar = 100 μm. j The COL1A1-positive area was quantified by ImageJ analysis (n = 7–9). k, l Representative Western blot and quantitative data of protein (COL1A1, EPRS1, α-SMA, and TGF-β) expression in kidneys from the five groups. The numbers (1–13) indicate individual animals in a given group. 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.
