csrp3 expression increases in response to zebrafish heart injury. A The temporal expression profiles of GFP in + /218A hearts (upper) and endogenous csrp3 in wild-type hearts (bottom) after ventricle ablation. Scale bars, 20 μm. B Immunostaining showed the colocalization of GFP fluorescence with MF20-marked myocardium in + /218A larval hearts after ventricle ablation. Scale bar, 20 μm. C Confocal images illuminated a significant increase of GFP fluorescence in TnnT2(CT3)-marked myocardial cells at the border zone of the cryoinjured + /218A adult ventricle. Areas of dashed boxes are magnified. Scale bars, 100 μm. D Immunostaining revealed that GFP fluorescence of + /218A was specifically expressed in myocardial (Actn1+) cells, while absent in the endocardial (Flk+) and epicardial (Pck+) cells. Areas of dashed boxes are magnified. Scale bars, 100 μm. E Fluorescence in situ hybridization (FISH) analysis corroborated a robust upregulation of csrp3 expression at the border zone of cryoinjured ventricle, compared to the faint and dispersive signal in the uninjured adult ventricle. Scale bars, 100 μm
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