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- W2031832049 abstract "Background: Previously we found that abrogating activator protein-1 (AP-1) in neonatal rat ventricular myocytes subjected to pathologic stimuli resulted in reversal of the pathologic/fetal gene profile while maintaining agonist-induced myocyte hypertrophy. We now extend these observations to the adult rat cardiomyocyte (ARVM) and further investigate if reversing the gene program towards a physiologic profile in a pathologic model results in improved myocyte function. Methods and Results: Hypertrophy was induced in cultured ARVMs using norepinephrine with propranolol pretreatment or with phenylephrine. Induction of the pathological gene profile was observed, ie, expression of beta-myosin heavy chain (βMHC), and atrial/brain natriuretic peptides (ANP/BNP) was increased, whereas expression for the alpha-myosin heavy chain (αMHC) was repressed. As with the neonatal cardiomyocyte experiments the role of AP-1 in the hypertrophic phenotype was evaluated with the use of an adenoviral construct expressing a dominant negative mutant of the c-Fos proto-oncogene (AdAFos). Although AdAFos infection did not change the myocyte growth response as assessed by radio-labeled protein incorporation and total protein content, it resulted in the reversal of the gene profile to α-adrenergic stimulation, ie, upregulation of αMHC and repression of βMHC and ANP/BNP. Further, ARVM infected with Ad-AFos showed improved myocyte shortening, contraction and relaxation velocities, and times to reach 50% and 90% baseline length, surrogate markers for contractile function. Conclusion: Abrogation of AP-1 transcription factor in the setting of alpha-adrenergic stimulation results in improved cardiomyocyte function." @default.
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- W2031832049 date "2007-08-01" @default.
- W2031832049 modified "2023-09-23" @default.
- W2031832049 title "Reversing the alpha-Adrenergic Mediated Fetal Gene Program Reverses Cardiomyocyte Dysfunction" @default.
- W2031832049 doi "https://doi.org/10.1016/j.cardfail.2007.06.430" @default.
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