Regulation of catecholamine release and tyrosine hydroxylase in human adrenal chromaffin cells by interleukin-1β: role of neuropeptide Y and nitric oxide
| Autor: | Joana Rosmaninho-Salgado, Alfredo Mota, Ana Rita Álvaro, Alexandrina Ferreira Mendes, Inês M. Araújo, Eric Grouzmann, Lígia Ferreira, Emília P. Duarte, Cláudia Cavadas |
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| Rok vydání: | 2009 |
| Předmět: |
medicine.medical_specialty
Time Factors Tyrosine 3-Monooxygenase Chromaffin Cells Interleukin-1beta Gene Expression Enzyme-Linked Immunosorbent Assay Biology Nitric Oxide Biochemistry Antibodies Nitric oxide Cellular and Molecular Neuroscience Norepinephrine chemistry.chemical_compound Catecholamines Internal medicine Adrenal Glands medicine Humans Neuropeptide Y Enzyme Inhibitors Tyrosine Cells Cultured Analysis of Variance Dose-Response Relationship Drug Tyrosine hydroxylase Nitric oxide synthase Interleukin 1 Receptor Antagonist Protein NG-Nitroarginine Methyl Ester medicine.anatomical_structure Endocrinology chemistry Chromaffin cell Catecholamine biology.protein Adrenal medulla Signal Transduction medicine.drug |
| Zdroj: | Journal of Neurochemistry. 109:911-922 |
| ISSN: | 1471-4159 0022-3042 |
| Popis: | Adrenal chromaffin cells synthesize and secrete catecholamines and neuropeptides that may regulate hormonal and paracrine signaling in stress and also during inflammation. The aim of our work was to study the role of the cytokine interleukin-1beta (IL-1beta) on catecholamine release and synthesis from primary cell cultures of human adrenal chromaffin cells. The effect of IL-1beta on neuropeptide Y (NPY) release and the intracellular pathways involved in catecholamine release evoked by IL-1beta and NPY were also investigated. We observed that IL-1beta increases the release of NPY, norepinephrine (NE), and epinephrine (EP) from human chromaffin cells. Moreover, the immunoneutralization of released NPY inhibits catecholamine release evoked by IL-1beta. Moreover, IL-1beta regulates catecholamine synthesis as the inhibition of tyrosine hydroxylase decreases IL-1beta-evoked catecholamine release and the cytokine induces tyrosine hydroxylase Ser40 phosphorylation. Moreover, IL-1beta induces catecholamine release by a mitogen-activated protein kinase (MAPK)-dependent mechanism, and by nitric oxide synthase activation. Furthermore, MAPK, protein kinase C (PKC), protein kinase A (PKA), and nitric oxide (NO) production are involved in catecholamine release evoked by NPY. Using human chromaffin cells, our data suggest that IL-1beta, NPY, and nitric oxide (NO) may contribute to a regulatory loop between the immune and the adrenal systems, and this is relevant in pathological conditions such as infection, trauma, stress, or in hypertension. |
| Databáze: | OpenAIRE |
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