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. 2009 Mar 16;119(4):976–985. doi: 10.1172/JCI36693

Figure 8. PMCA4b overexpression blunts agonist-induced hypertrophy in cultured neonatal cardiomyocytes.

Figure 8

(A) Cardiomyocyte surface area by immunocytochemistry staining of α-actinin in control (Ad–β-gal) or Ad-PMCA4b–overexpressing conditions (*P < 0.05 versus no stimulation, #P < 0.05 versus Ad–β-gal + ET-1 or PE). (B) Relative [3H]-leucine incorporation in cultured neonatal cardiomyocytes infected with the indicated adenoviruses and co-stimulants (*P < 0.05 versus no stimulation, #P < 0.05 versus Ad–β-gal + PE). (C) DNA amplification from RT-PCR reactions for Anf mRNA, and subsequent quantitation (D) in control (Ad–β-gal) and Ad-PMCA4b–overexpressing cultured cardiomyocytes at baseline or after PE treatment (*P < 0.05 versus no stimulation, #P < 0.05 versus Ad–β-gal + PE). (E) Western blot for PMCA4b from adenoviral-infected neonatal cardiomyocytes expressing the indicated proteins. GAPDH was used as a protein loading control. (F) Fold increase in NFAT-luciferase activity from neonatal cardiomyocytes infected with Ad–NFAT-luciferase and Ad–β-gal, Ad–PMCA4b D672E, or Ad-PMCA4b (*P < 0.05 versus control, #P < 0.05 versus PMCA4b + PE). (G) Relative [3H]-leucine incorporation in cultured neonatal cardiomyocytes infected with the indicated adenoviruses and co-stimulants (*P < 0.05 versus control, #P < 0.05 versus PMCA4b + PE). Data were summed from 4–8 independent experiments.