ArticleThe Biochemical journal2001
Targeted overexpression of ornithine decarboxylase enhances beta-adrenergic agonist-induced cardiac hypertrophy.
Article in The Biochemical journal, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 40 citations in OpenAlex.
- Article
- The role of polyamine metabolism in cellular function and physiology.American journal of physiology. Cell physiology · 2024Review
- Mitogen-Activated Protein Kinase and Intracellular Polyamine Signaling Is Involved in TRPV1 Activation-Induced Cardiac Hypertrophy.Journal of the American Heart Association · 2016Article
- Correlation between endogenous polyamines in human cardiac tissues and clinical parameters in patients with heart failure.Journal of cellular and molecular medicine · 2016Article
- Spermine oxidase maintains basal skeletal muscle gene expression and fiber size and is strongly repressed by conditions that cause skeletal muscle atrophy.American journal of physiology. Endocrinology and metabolism · 2015Article
- Article
- Overexpression of ornithine decarboxylase decreases ventricular systolic function during induction of cardiac hypertrophy.Amino acids · 2012Article
- Metformin Inhibits Isoproterenol-induced Cardiac Hypertrophy in Mice.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2010Article
- Article
- Overproduction of cardiac S-adenosylmethionine decarboxylase in transgenic mice.The Biochemical journal · 2006Article
- Tissue-based assay for ornithine decarboxylase to identify patients likely to respond to difluoromethylornithine.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2004Article
- Characterization of transgenic mice with widespread overexpression of spermine synthase.The Biochemical journal · 2004Article
- Ornithine decarboxylase levels in peripheral nerve sheath tumors from NF1 patients.Neuro-oncology advancesArticle
- Sensitivity of cloned muscle, heart and neuronal voltage-gated sodium channels to block by polyamines: a possible basis for modulation of excitability in vivo.Channels (Austin, Tex.)Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
These studies were designed to determine the consequences of constitutive overexpression of ornithine decarboxylase (ODC) in the heart. Induction of ODC is known to occur in response to agents that induce cardiac hypertrophy. However, it is not known whether high ODC levels are sufficient for the development of a hypertrophic phenotype. Transgenic mice were generated with cardiac-specific expression of a stable ODC protein using the alpha-myosin heavy-chain promoter. Founder lines with >1000-fold overexpression of ODC in the heart were established, resulting in a 50-fold overaccumulation of putrescine, 4-fold elevation in spermidine, a slight increase in spermine and accumulation of large amounts of cadaverine compared with littermate controls. Despite these significant alterations in polyamines, myocardial hypertrophy, as measured by ratio of heart to body weight, did not develop, although atrial natriuretic factor RNA was slightly elevated in transgenic ventricles. However, stimulation of beta-adrenergic signalling by isoproterenol resulted in severe hypertrophy and even death in ODC-overexpressing mice without further altering polyamine levels, compared with only a mild hypertrophy in littermates. When beta1-adrenergic stimulation was blocked by simultaneous treatment with isoproterenol and the beta1 antagonist atenolol, a significant, although reduced, hypertrophy was still present in the hearts of transgenic mice, suggesting that both beta1 and beta2 adrenergic receptors contribute to the hypertrophic phenotype. Therefore these mice provide a model to study the in vivo co-operativity between high ODC activity and activation of other pathways leading to hypertrophy in the heart.
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