Peroxisome Proliferator-Activated Receptor α Reduces Endothelin-1-Caused Cardiomyocyte Hypertrophy by Inhibiting Nuclear Factor-κB and Adiponectin

Figure 3

Signaling pathways in ET-1-induced cell hypertrophy and adiponectin expression. In human cardiomyocyte cells, phosphorylation of ERK and p38 was determined by immunoblot assay (a). Assays were performed in triplicate. The role of ERK and p38 and ET-1 in myocardial cell size was determined in cells pretreated with PD98059 (ERK inhibitor) or SB203580 (p38 inhibitor) for 1 h, followed by stimulation with or without ET-1 (50 nM) for 48 h. Cells were fixed and stained with rhodamine-phalloidin (red) and DAPI (blue) followed by cell surface area quantitation (scale bar, 50 μm) (b). Data are expressed as mean ± SEM of values from three independent experiments (c). ³H-leucine incorporation was determined as a measure of relative protein synthesis (d). , compared with 0 min group (a) or untreated control group (c).

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