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Fig. 2
The cell-cycle entry and the deposition of ColXII after thoracotomy are dependent on the JAK/STAT3 pathway. a Experimental design. The requirement of different pathways for the increased CM mitotic activity and the ColXII deposition observed after preconditioning was tested at 7 dpt by using specific inhibitors of JAK/STAT (1 µM Ruxolitinib), TGF-β (20 µM SB431542) or FGF (10 µM PD173074) signaling. b, c Transversal sections of hearts treated with different drugs indicated at the left side. Scale bar for the whole section, 500 μm; for the magnified area, 100 μm. b Ventricle of transgenic fish cmlc2:DsRed2-nuc (red) immunostained for the G1/S-phase marker MCM5 (green). Some double positive cells are indicated with arrows. Treatment with Ruxolitinib markedly reduces cells proliferation in the ventricle. c Ventricle of wild type fish immunostained against Tropomyosin (red) and ColXII (green). In the presence of Ruxolitinib, intramyocardial ColXII is reduced. d Proportion of MCM5 + nuclei among cmlc2:DsRed2-nuc + nuclei. e Proportion of MCM5 + cmlc2:DsRed2-nuc-negative nuclei among DAPI + nuclei. f Proportion of the ColXII-positive area within the surface of ventricular section. n ≥ 4 hearts; ≥ 2 sections per heart; ***P < 0.001