Overexpression of constitutively active p38γ and p38δ leads to morphological changes, fibrosis, and predisposes to a worse cardiac prognosis after MI.

Mice were IV injected at PD1 with AAV-cTnT-GFP-Luc (TnTGFP) or AAV-cTnT-p38γ/δ_act (TnTp38γ/δ^act) and analyzed at PD14. (A) Representative H&E staining of transverse heart sections (scale bar: 1 mm). (B) H&E staining of heart sections. Scale bar: 50 μm. (C) Masson’s trichrome staining quantification from heart sections (corresponds to the representative images in Fig 1K). (D) TnTGFP control mice or TnTp38γ/δ^act mice (with AAV injection at PD1) were subjected to MI at PD7 and evaluated after 4 weeks. Echocardiography measurements. Data are mean ± SEM (n = 4–10). **p < 0.01; ***p < 0.001 by Student t test. Raw data are given in S14 Fig. AAV, adeno-associated virus; FS, fractional shortening; H&E, hematoxylin and eosin; IVS;d, interventricular septum thickness in diastole; LVID;d, left ventricular internal diameter in diastole; LVPW;d, left ventricle posterior wall thickness in diastole; MI, myocardial infarction; WT, wild-type.

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