TRPA1 Promotes Cardiac Myofibroblast Transdifferentiation after Myocardial Infarction Injury via the Calcineurin-NFAT-DYRK1A Signaling Pathway

Figure 7

DYRK1A inhibits CaN-mediated NFATc3 nuclear localization in CMF transdifferentiation. (a) Western blot analysis and quantification of DYRK1A protein expression in neonatal WT mouse cultured primary CFs treated with TGF-β or transfected with negative control (NC) adenoviral vector (not shown), Ad-TRPA1 (Ad), negative control (NC) siRNA (not shown), or si-TRPA1 (si) and treated 48 hr later with TGF-β. Molecular weights in kDa are shown to the right of the blots. per group. (b and c) Immunofluorescence staining (b) and quantification (c) of α-SMA-positive (red) stress fibers and DAPI (blue) in CFs treated with TGF-β or transfected with Ad-TRPA1 and stimulated 48 hr later with TGF-β, with and without harmin (Harm) treatment. (d) α-SMA-luciferase promoter activity in CFs treated as described above (scale  μm). per group. (e and f) Western blot analysis and quantification of NFATc3 protein expression in the cytosolic and nuclear fractions of CFs treated as described above. Molecular weights in kDa are shown to the right of the blots. per group. The error bars represent the and . The data are representative of the results of three or more independent experiments.

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