Anti-inflammatory effects of kinins via microglia in the central nervous system
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Mami Noda
Abstract
Kinins are important biologically active peptides that are up-regulated after lesions in both the peripheral and central (CNS) nervous systems. Microglia are immune cells in the CNS and play an important role in the defense of the neuronal parenchyma. In cultured murine microglia, bradykinin (BK) induces mobilization of intracellular Ca2+, microglial migration, and increases the release of nitric oxide and prostaglandin E2. On the other hand, BK attenuates lipopolysaccharide-activated TNF-α and IL-1β release. These results suggest that BK functions as a signal in brain trauma and may have an anti-inflammatory role in the CNS.
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©2006 by Walter de Gruyter Berlin New York
Artikel in diesem Heft
- Exploring the future of local vascular and inflammatory mediators
- Genetically altered animal models in the kallikrein-kinin system
- The kinin system mediates hyperalgesia through the inducible bradykinin B1 receptor subtype: evidence in various experimental animal models of type 1 and type 2 diabetic neuropathy
- Cross-talk of the renin-angiotensin and kallikrein-kinin systems
- Which endothelium-derived factors are really important in humans?
- Kinin- and angiotensin-converting enzyme (ACE) inhibitor-mediated nitric oxide production in endothelial cells
- Anti-inflammatory effects of kinins via microglia in the central nervous system
- Platelets promote coagulation factor XII-mediated proteolytic cascade systems in plasma
- Three-dimensional structure of an AMPA receptor without associated stargazin/TARP proteins
- Dual antagonists of the bradykinin B1 and B2 receptors based on a postulated common pharmacophore from existing non-peptide antagonists
- Generation and characterization of a humanized bradykinin B1 receptor mouse
- The role of bradykinin B1 receptor on cardiac remodeling in stroke-prone spontaneously hypertensive rats (SHR-SP)
- Molecular identification and pharmacological profile of the bovine kinin B1 receptor
- Interplay of human tissue kallikrein 4 (hK4) with the plasminogen activation system: hK4 regulates the structure and functions of the urokinase-type plasminogen activator receptor (uPAR)
- Cathepsin B localizes to plasma membrane caveolae of differentiating myoblasts and is secreted in an active form at physiological pH
Artikel in diesem Heft
- Exploring the future of local vascular and inflammatory mediators
- Genetically altered animal models in the kallikrein-kinin system
- The kinin system mediates hyperalgesia through the inducible bradykinin B1 receptor subtype: evidence in various experimental animal models of type 1 and type 2 diabetic neuropathy
- Cross-talk of the renin-angiotensin and kallikrein-kinin systems
- Which endothelium-derived factors are really important in humans?
- Kinin- and angiotensin-converting enzyme (ACE) inhibitor-mediated nitric oxide production in endothelial cells
- Anti-inflammatory effects of kinins via microglia in the central nervous system
- Platelets promote coagulation factor XII-mediated proteolytic cascade systems in plasma
- Three-dimensional structure of an AMPA receptor without associated stargazin/TARP proteins
- Dual antagonists of the bradykinin B1 and B2 receptors based on a postulated common pharmacophore from existing non-peptide antagonists
- Generation and characterization of a humanized bradykinin B1 receptor mouse
- The role of bradykinin B1 receptor on cardiac remodeling in stroke-prone spontaneously hypertensive rats (SHR-SP)
- Molecular identification and pharmacological profile of the bovine kinin B1 receptor
- Interplay of human tissue kallikrein 4 (hK4) with the plasminogen activation system: hK4 regulates the structure and functions of the urokinase-type plasminogen activator receptor (uPAR)
- Cathepsin B localizes to plasma membrane caveolae of differentiating myoblasts and is secreted in an active form at physiological pH