Figure 2.

Genetic loss of Cxcl4 mitigates organ fibrosis

(A) RT-qPCR analysis for Cxcl4, Fn1, Arg1, and Spp1 in CD11b⁺ monocytes isolated from WT or Cxcl4^−/− PBMCs after stimulation with vehicle or LPS (n = 4). Mono, monocytes.

(B) Design of myocardial infarction experiments.

(C) Picrosirius red stained serial heart sections over seven levels from WT and Cxcl4^−/− mice after MI. ECM is stained red. LV, left ventricle; RV, right ventricle. Scale bar = 1 mm.

(D) Fibrosis of serial heart sections in WT sham, Cxcl4^−/− sham, WT MI, and Cxcl4^−/− MI mice based on quantification of serial heart sections shown in (C). Quantification by spectral thresholding analysis of red ECM (WT Sham = 8; Cxcl4^−/− Sham = 6; WT MI = 8; Cxcl4^−/− MI = 7).

(E) MI scar sizes in WT and Cxcl4^−/− mice based on quantification of serial heart sections shown in (C).

(F) Left ventricular ejection fraction (Simpsons) 2 days before, as well as 28 and 56 days after MI or sham surgery in WT and Cxcl4^−/− mice.

(G) Experimental design of IRI experiments.

(H) Representative images of picrosirius red stained cortical kidney sections from WT and Cxcl4^−/− mice after sham or IRI surgery. Scale bar = 50 μm.

(I) Kidney cortex fibrosis (in % of cortex area) after sham or IRI surgery by quantification of red ECM of scans shown in (H) (WT mice = 8, Cxcl4^−/− mice = 5).

All quantitative data are shown as mean ± SD. For (A), (D), (F), and (I), two-way ANOVA was computed using Tukey corrections. For (E), a two-tailed unpaired t test was performed. ^∗p < 0.05, ^∗∗p < 0.01, ^∗∗∗p < 0.001, ^∗∗∗∗p < 0.0001.