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. 2003 May 15;111(10):1475–1486. doi: 10.1172/JCI17295

Figure 5.

Figure 5

p38 signaling regulates NFAT transcriptional responses. (a) Transient transfections in neonatal cardiomyocytes using an NFAT-dependent luciferase reporter plasmid with vectors encoding either NFATc4, activated CnA, dnMKK3, or dnp38α and combinations thereof. The data demonstrate that p38 inhibition activates the NFAT reporter in cardiomyocytes (*P < 0.05 versus vector alone). (b) This p38 inhibitory effect was surveyed against all four NFAT factors in 10T1/2 cells (NFATc1-c4). The data demonstrate that dnp38α cotransfection activates NFATc1, NFATc2, and NFATc4 transcription nearly as well as activated calcineurin. Similar results were observed in two additional, independent experiments (*P < 0.05 versus NFAT alone). (c) Recombinant adenovirus encoding NFATc1-GFP was used to evaluate nuclear translocation in cultured cardiomyocytes. Control coinfection with adenovirus-encoding β-galactosidase (Adβgal) did not induce NFATc1-GFP nuclear translocation, distinct from the effect of CnA adenovirus (AdCnA; activated). The dnp38α-encoding adenovirus (Ad-dnp38α) induced significant NFATc1 nuclear translocation. These results were quantified in approximately 250 infected cardiomyocytes. Arrows, cells with cytoplasmic NFAT-GFP; arrowheads, cells with nuclear NFAT-GFP. Similar results were observed in three independent experiments (*P < 0.05 versus Adβgal).