Cardiac Sympathetic Rejuvenation
| Autor: | Kazuto Yamazaki, Keiichi Fukuda, Masaki Ieda, Makoto Tsunoda, Kenji Yoshimi, Satoshi Ogawa, Kensuke Kimura, Hideki Mochizuki, Takashi Yagi, Shin Ichi Ninomiya, Hideaki Kanazawa, Hiroyuki Kurosawa |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
Male
Sympathetic nervous system medicine.medical_specialty Tyrosine 3-Monooxygenase Physiology Dopamine Heart Ventricles Hypertension Pulmonary Neural Cell Adhesion Molecule L1 Norepinephrine GAP-43 Protein Tubulin Right ventricular hypertrophy Internal medicine Nerve Growth Factor medicine Animals Myocytes Cardiac Rats Wistar Heart Failure Pressure overload Monocrotaline Endothelin-1 Hypertrophy Right Ventricular Tyrosine hydroxylase business.industry medicine.disease Rats Up-Regulation Kinetics Autonomic nervous system medicine.anatomical_structure Cardiac nerve Endocrinology Gene Expression Regulation Sialic Acids Catecholamine Adrenergic Fibers Cardiology and Cardiovascular Medicine business medicine.drug |
| Zdroj: | Circulation Research. 100:1755-1764 |
| ISSN: | 1524-4571 0009-7330 |
| Popis: | Neuronal function and innervation density is regulated by target organ-derived neurotrophic factors. Although cardiac hypertrophy drastically alternates the expression of various growth factors such as endothelin-1, angiotensin II, and leukemia inhibitory factor, little is known about nerve growth factor expression and its effect on the cardiac sympathetic nerves. This study investigated the impact of pressure overload-induced cardiac hypertrophy on the innervation density and cellular function of cardiac sympathetic nerves, including kinetics of norepinephrine synthesis and reuptake, and neuronal gene expression. Right ventricular hypertrophy was induced by monocrotaline treatment in Wistar rats. Newly developed cardiac sympathetic nerves expressing β 3 -tubulin (axonal marker), GAP43 (growth-associated cone marker), and tyrosine hydroxylase were markedly increased only in the right ventricle, in parallel with nerve growth factor upregulation. However, norepinephrine and dopamine content was paradoxically attenuated, and the protein and kinase activity of tyrosine hydroxylase were markedly downregulated in the right ventricle. The reuptake of [ 125 I]-metaiodobenzylguanidine and [ 3 H]-norepinephrine were also significantly diminished in the right ventricle, indicating functional downregulation in cardiac sympathetic nerves. Interestingly, we found cardiac sympathetic nerves in hypertrophic right ventricles strongly expressed highly polysialylated neural cell adhesion molecule (PSA-NCAM) (an immature neuron marker) as well as neonatal heart. Taken together, pressure overload induced anatomical sympathetic hyperinnervation but simultaneously caused deterioration of neuronal cellular function. This phenomenon was explained by the rejuvenation of cardiac sympathetic nerves as well as the hypertrophic cardiomyocytes, which also showed the fetal form gene expression. |
| Databáze: | OpenAIRE |
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