作者: Andrés J. López-Contreras , Maria Eugenia de la Morena , Bruno Ramos-Molina , Ana Lambertos , Asunción Cremades
DOI: 10.1002/JCB.24540
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摘要: The role that the induction of cardiac ornithine decarboxylase (ODC), a key enzyme in polyamine biosynthesis, by beta-adrenergic agents may have heart hypertrophy is controversial issue. Besides, signaling pathways related to ODC regulation not been fully elucidated. Here we show Balb C mice stimulation activity adrenergic was mainly mediated β2-adrenergic receptors, and this lower hypertrophic heart. Interestingly, abolished L-calcium channel antagonists verapamil nifedipine. In addition, whereas treatment with associated both increases ODC, ODC-antizyme inhibitor 1 (AZIN1), c-fos c-myc mRNA levels phosphorylation CREB MAP kinases ERK1 ERK2 (ERK1/2), co-treatment blockers differentially prevented most these changes. These results suggest activation through participation channels, itself p-CREB does appear be sufficient for transcriptional ODC. post-translational mechanisms AZIN1 increase activity. J. Cell. Biochem. 114: 1978–1986, 2013. © 2013 Wiley Periodicals, Inc.