Enhanced Phosphorylation of MAPKs by NE Promotes TNF-α Production by Macrophage Through α Adrenergic Receptor
| Autor: | Qian Ma, Chun-Lei Jiang, Jun-Long Huang, Xing-hua Shen, Xia Wang, You-Lei Zhang, Zhou Jiangrui, Cheng-Cai Wang |
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| Rok vydání: | 2011 |
| Předmět: |
Lipopolysaccharides
Male MAPK/ERK pathway medicine.medical_specialty MAP Kinase Signaling System Pyridines p38 mitogen-activated protein kinases Immunology p38 Mitogen-Activated Protein Kinases Mice Norepinephrine Internal medicine Nitriles Butadienes medicine Animals Immunology and Allergy Macrophage Secretion Phosphorylation Extracellular Signal-Regulated MAP Kinases Phentolamine Receptor Adrenergic alpha-Antagonists Cells Cultured Anthracenes Mice Inbred BALB C Tumor Necrosis Factor-alpha Chemistry Kinase Macrophages Imidazoles JNK Mitogen-Activated Protein Kinases Macrophage Activation Receptors Adrenergic alpha Cell biology Endocrinology Tumor necrosis factor alpha Mitogen-Activated Protein Kinases |
| Zdroj: | Inflammation. 35:527-534 |
| ISSN: | 1573-2576 0360-3997 |
| DOI: | 10.1007/s10753-011-9342-4 |
| Popis: | The aim of this study was to investigate whether norepinephrine (NE) could regulate macrophage production of tumor necrosis factor alpha (TNF-α) by influencing the phosphorylation of mitogen-activated protein kinases (MAPKs). Primary macrophages from male BALB/c mice were applied to explore the mechanism by which NE influences the the secretion of TNF-α when macrophages were activated by lipopolysaccharides (LPS). We found that NE could increase crophage production of TNF-α when macrophages were activated by LPS, and this effect could be inhibited by α adrenergic antagonist phentolamine. Also, NE could increase the phosphorylation of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinases (ERK), and p38, through α receptor. Furthermore, JNK inhibitor SP600125, ERK inhibitor U0126, and p38 inhibitor SB203580 could all partially counteract NE's effect on the phosphorylation of MAPKs, as well as TNF-α production by macrophages. This study revealed that as macrophages were activated by LPS, NE promoted the secretion of inflammatory factors by increasing the phosphorylation of MAPKs through an α receptor-dependent pathway. Our results provide the evidence of a relationship between stress and diseases, as well as the mechanism by which stress induces or affects the inflammation-related diseases. |
| Databáze: | OpenAIRE |
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