Fig. 8
From: Gucy1α1 specifically marks kidney, heart, lung and liver fibroblasts
Gucy1α1 expression trajectory parallels DDC induced liver fibrosis resolution. (A) Schematic of the biliary fibrosis model. DDC is administered for 14 days, then regular chow (RC) is given. (B and C) Picrosirius Red staining. (B) Representative images, original magnification, ×20, 0.30 μm/px zoom, scale 100 μm. (C) Quantitative Picrosirius Red staining analysis, n = 3 per group, ordinary one-way ANOVA, P ****≤0.0001 compared to the control. (D and E) IF demonstrating the expression of fibrosis markers in the liver over the course of DDC response. (D) Representative IF images demonstrate baseline Gucy1α1 (magenta) expression (red arrows) in the spindle-shaped Pdgfrβ- (yellow) and Vim-positive (green) liver fibroblasts. Baseline αSma (cyan) expression is very low. DDC administration results in dramatic Gucy1α1, Pdgfrβ, αSma and Vim upregulation and colocalization (areas of colocalization pointed with red arrows). 14 days after DDC withdrawal (Day 28) only traces of periductal (Krt8, white) and interstitial fibrosis remain (red arrows). DAPI, blue. Original magnification, ×60, maximal intensity projection from a Z-stack, 0.09 μm/px Nyquist resolution, scale 20 μm. (E) IF quantification, n = 3 per group, ordinary one-way ANOVA, P **≤0.01, ***≤0.001, ****≤0.0001 compared to the control. (F) Correlation analysis between Pdgfrβ, Vim levels and Gucy1α1 at all the timepoints detected by IF. Pearson r correlation analysis, n = 9 per marker (Control, Day 14, 28, n = 3 per group), r values and P as ****≤0.0001 for each pair are shown on the graphs presenting simple linear regression of correlation between Pdgfrβ and Vim vs. Gucy1α1. Data in scatter plots is presented as mean ± SD.
