Fig. 5.

Il-11 signaling limits myofibroblast differentiation and profibrotic ECM remodeling after injury.

(A) Immunostaining for αSMA (white) and MHC (magenta) expression on cryosections from cardiac ventricles (wt siblings, n = 5; mut, n = 6; 7 dpci). (B) Quantification of αSMA⁺ cell density. (C) Immunostaining for αSMA (white), GFP (magenta), and Zns-5 antigen (scleroblasts, green) expression on longitudinal cryosections from Tg(fli1:EGFP) caudal fins (wt, n = 10; mut, n = 10; 14 dpa). (D) GSE analysis plots for Reactome and KEGG pathway terms from il11ra^−/− versus wild-type sibling adult ventricle transcriptomic analyses, 96 hpci. (E and F) RT-qPCR analysis on dissected injured areas from cardiac ventricles (E) (wt siblings, n = 4; mut, n = 5; 96 hpci) and caudal fins (F) (wt siblings, n = 4; mut, n = 4; 48 hpa) for selected profibrotic gene expression levels. (G and H) Immunostaining [(G) Elastin, green; MHC, magenta; (H) GFP, white] on cryosections from cardiac ventricles [(G) wt siblings, n = 11; mut, n = 10; (H) Tg(fli1:EGFP); mut, n = 6; 7 dpci]. Data represent means ± SD (B), and box plots (E and F) show median, interquartile range (IQR; box margins), and 5th and 95th percentiles (whiskers). Student’s t tests (B, E, and F). n, ventricles (A, E, G, and H); n, caudal fins (C); n, pools of two caudal fins (F). Yellow dashed lines demarcate the injured area (A, G, and H); yellow arrowheads point to αSMA⁺ myofibroblasts in il11ra mutant fins (C) and Elastin1 expression associated with endocardial cells in the injured area [inset in (H)]; white arrowheads point to vessel-associated αSMA⁺ smooth muscle cells (C); white arrows point to the amputation plane (C). Ct values are listed in table S5. Scale bars, 50 μm (A, C, G, and H), 20 μm [(C) left inset], and 10 μm [(C) right inset and (H) inset].