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Jean Mazella - One of the best experts on this subject based on the ideXlab platform.
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neurotensin and the neurotensin receptor 3 in Microglial Cells
Journal of Neuroscience Research, 2005Co-Authors: Stephane Martin, Eleni Dicou, Jeanpierre Vincent, Jean MazellaAbstract:Microglia motility plays a crucial role in response to lesion or exocytotoxic damage of the cerebral tissue. The neuropeptide neurotensin elicited the migration of the human Microglial Cell Line C13NJ by a mechanism dependent on both phosphatidylinositol-3 kinase (PI3 kinase) and mitogen-activated protein (MAP) kinases pathways. The effect of neurotensin on Cell migration was blocked by the neurotensin receptor-3 propeptide, a selective ligand of this receptor. The type I neurotensin receptor-3 was the only known neurotensin receptor expressed in these Microglial Cells, and its activation led to the phosphorylation of both extraCellular signaling-regulated kinases Erk1/2 and Akt. Furthermore, the effect of neurotensin on Cell migration was preceded by a profound modification of the F-actin cytoskeleton, particularly by the rapid formation of numerous Cell filopodia. Both the motility and the filopodia appearance induced by neurotensin were totally blocked by selective inhibitors of MAP kinases or PI3 kinase pathways. In the murine Microglial Cell Line N11, the neurotensin receptor-3 is also the only neurotensin receptor expressed, and its activation by neurotensin leads to the phosphorylation of both Erk1/2 and Akt. In these Cells, neurotensin induces the gene expression of several cytokines/chemokines, including MIP-2, MCP-1, interleukin-1β and tumor necrosis factor-α. This induction is dependent on both protein kinases pathways. We observed that the effect of neurotensin on the cytokine/chemokine expression is also inhibited by the neurotensin receptor-3 propeptide. This is the demonstration that the neurotensin receptor-3 is functional and mediates both the migratory action of neurotensin and its induction of chemokines/cytokines expression. © 2005 Wiley-Liss, Inc.
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Neurotensin receptor-3/sortilin mediates neurotensin-induced cytokine/chemokine expression in a murine Microglial Cell Line.
Journal of neuroscience research, 2004Co-Authors: Eleni Dicou, Jeanpierre Vincent, Jean MazellaAbstract:We show that the type I neurotensin receptor-3 (also called sortilin) is the only known neurotensin receptor expressed in a murine Microglial Cell Line and that its activation leads to phosphorylation of both extraCellular signaling-regulated (Erk1/2) and Akt kinases. Using semiquantitative reverse-transcriptase (RT) PCR, we demonstrate that neurotensin induces gene expression of several cytokines/chemokines including macrophage inflammatory protein (MIP)-2, monocyte chemotactic protein (MCP)-1, interleukin (IL)-1β and tumor necrosis factor (TNF)-α. This induction is dependent on both phosphatidylinositol 3-kinase and mitogen-activated protein kinases pathways. We observe that the effect of neurotensin on cytokine/chemokine expression is inhibited by the neurotensin receptor-3 propeptide, a selective ligand of this receptor. These results demonstrate that the neurotensin receptor-3 is functional in Microglial Cells where it mediates the induction of chemokines/cytokines expression by neurotensin. © 2004 Wiley-Liss, Inc.
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neurotensin receptor 3 sortilin mediates neurotensin induced cytokine chemokine expression in a murine Microglial Cell Line
Journal of Neuroscience Research, 2004Co-Authors: Eleni Dicou, Jeanpierre Vincent, Jean MazellaAbstract:We show that the type I neurotensin receptor-3 (also called sortilin) is the only known neurotensin receptor expressed in a murine Microglial Cell Line and that its activation leads to phosphorylation of both extraCellular signaling-regulated (Erk1/2) and Akt kinases. Using semiquantitative reverse-transcriptase (RT) PCR, we demonstrate that neurotensin induces gene expression of several cytokines/chemokines including macrophage inflammatory protein (MIP)-2, monocyte chemotactic protein (MCP)-1, interleukin (IL)-1β and tumor necrosis factor (TNF)-α. This induction is dependent on both phosphatidylinositol 3-kinase and mitogen-activated protein kinases pathways. We observe that the effect of neurotensin on cytokine/chemokine expression is inhibited by the neurotensin receptor-3 propeptide, a selective ligand of this receptor. These results demonstrate that the neurotensin receptor-3 is functional in Microglial Cells where it mediates the induction of chemokines/cytokines expression by neurotensin. © 2004 Wiley-Liss, Inc.
Gerd Bicker - One of the best experts on this subject based on the ideXlab platform.
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nitric oxide cyclic gmp signaling regulates motility of a Microglial Cell Line and primary microglia in vitro
Brain Research, 2014Co-Authors: Hannah Scheiblich, Frank Roloff, Vikramjeet Singh, Martin Stangel, Michael Stern, Gerd BickerAbstract:Microglia are the resident immune Cells of the brain, which become rapidly activated and migrate to the site of insult in brain infection and disease. Activated microglia generate large amounts of the highly reactive messenger molecule nitric oxide (NO). NO is able to raise cyclic GMP levels via binding to soluble guanylyl cyclase. We investigated potential mechanistic links between inflammation, NO signaling, and Microglial migration. To monitor Cell migration, we used a scratch wound assay and compared results obtained in the BV-2 Microglial Line to primary microglia. Incubation with lipopolysaccharide (LPS) as stimulator of acute inflammatory processes enhanced migration of both Microglial Cell types. LPS activated NO production in BV-2 Cells and application of an NO donor increased BV-2 Cell migration while an NO scavenger reduced motility. Pharmacological inhibition of soluble guanylyl cyclase and the resulting decrease in motility can be rescued by a membrane permeant analog of cGMP. Despite differences in the threshold towards stimulation with the chemical agents, both BV-2 Cells and primary microglia react in a similar way. The important role of NO/cGMP as positive regulator of Microglial migration, the downstream targets of the signaling cascade, and resulting cytoskeletal changes can be conveniently investigated in a Microglial Cell Line.
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Nitric oxide/cyclic GMP signaling regulates motility of a Microglial Cell Line and primary microglia in vitro.
Brain research, 2014Co-Authors: Hannah Scheiblich, Frank Roloff, Vikramjeet Singh, Martin Stangel, Michael Stern, Gerd BickerAbstract:Microglia are the resident immune Cells of the brain, which become rapidly activated and migrate to the site of insult in brain infection and disease. Activated microglia generate large amounts of the highly reactive messenger molecule nitric oxide (NO). NO is able to raise cyclic GMP levels via binding to soluble guanylyl cyclase. We investigated potential mechanistic links between inflammation, NO signaling, and Microglial migration. To monitor Cell migration, we used a scratch wound assay and compared results obtained in the BV-2 Microglial Line to primary microglia. Incubation with lipopolysaccharide (LPS) as stimulator of acute inflammatory processes enhanced migration of both Microglial Cell types. LPS activated NO production in BV-2 Cells and application of an NO donor increased BV-2 Cell migration while an NO scavenger reduced motility. Pharmacological inhibition of soluble guanylyl cyclase and the resulting decrease in motility can be rescued by a membrane permeant analog of cGMP. Despite differences in the threshold towards stimulation with the chemical agents, both BV-2 Cells and primary microglia react in a similar way. The important role of NO/cGMP as positive regulator of Microglial migration, the downstream targets of the signaling cascade, and resulting cytoskeletal changes can be conveniently investigated in a Microglial Cell Line.
Hannah Scheiblich - One of the best experts on this subject based on the ideXlab platform.
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nitric oxide cyclic gmp signaling regulates motility of a Microglial Cell Line and primary microglia in vitro
Brain Research, 2014Co-Authors: Hannah Scheiblich, Frank Roloff, Vikramjeet Singh, Martin Stangel, Michael Stern, Gerd BickerAbstract:Microglia are the resident immune Cells of the brain, which become rapidly activated and migrate to the site of insult in brain infection and disease. Activated microglia generate large amounts of the highly reactive messenger molecule nitric oxide (NO). NO is able to raise cyclic GMP levels via binding to soluble guanylyl cyclase. We investigated potential mechanistic links between inflammation, NO signaling, and Microglial migration. To monitor Cell migration, we used a scratch wound assay and compared results obtained in the BV-2 Microglial Line to primary microglia. Incubation with lipopolysaccharide (LPS) as stimulator of acute inflammatory processes enhanced migration of both Microglial Cell types. LPS activated NO production in BV-2 Cells and application of an NO donor increased BV-2 Cell migration while an NO scavenger reduced motility. Pharmacological inhibition of soluble guanylyl cyclase and the resulting decrease in motility can be rescued by a membrane permeant analog of cGMP. Despite differences in the threshold towards stimulation with the chemical agents, both BV-2 Cells and primary microglia react in a similar way. The important role of NO/cGMP as positive regulator of Microglial migration, the downstream targets of the signaling cascade, and resulting cytoskeletal changes can be conveniently investigated in a Microglial Cell Line.
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Nitric oxide/cyclic GMP signaling regulates motility of a Microglial Cell Line and primary microglia in vitro.
Brain research, 2014Co-Authors: Hannah Scheiblich, Frank Roloff, Vikramjeet Singh, Martin Stangel, Michael Stern, Gerd BickerAbstract:Microglia are the resident immune Cells of the brain, which become rapidly activated and migrate to the site of insult in brain infection and disease. Activated microglia generate large amounts of the highly reactive messenger molecule nitric oxide (NO). NO is able to raise cyclic GMP levels via binding to soluble guanylyl cyclase. We investigated potential mechanistic links between inflammation, NO signaling, and Microglial migration. To monitor Cell migration, we used a scratch wound assay and compared results obtained in the BV-2 Microglial Line to primary microglia. Incubation with lipopolysaccharide (LPS) as stimulator of acute inflammatory processes enhanced migration of both Microglial Cell types. LPS activated NO production in BV-2 Cells and application of an NO donor increased BV-2 Cell migration while an NO scavenger reduced motility. Pharmacological inhibition of soluble guanylyl cyclase and the resulting decrease in motility can be rescued by a membrane permeant analog of cGMP. Despite differences in the threshold towards stimulation with the chemical agents, both BV-2 Cells and primary microglia react in a similar way. The important role of NO/cGMP as positive regulator of Microglial migration, the downstream targets of the signaling cascade, and resulting cytoskeletal changes can be conveniently investigated in a Microglial Cell Line.
Eleni Dicou - One of the best experts on this subject based on the ideXlab platform.
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neurotensin and the neurotensin receptor 3 in Microglial Cells
Journal of Neuroscience Research, 2005Co-Authors: Stephane Martin, Eleni Dicou, Jeanpierre Vincent, Jean MazellaAbstract:Microglia motility plays a crucial role in response to lesion or exocytotoxic damage of the cerebral tissue. The neuropeptide neurotensin elicited the migration of the human Microglial Cell Line C13NJ by a mechanism dependent on both phosphatidylinositol-3 kinase (PI3 kinase) and mitogen-activated protein (MAP) kinases pathways. The effect of neurotensin on Cell migration was blocked by the neurotensin receptor-3 propeptide, a selective ligand of this receptor. The type I neurotensin receptor-3 was the only known neurotensin receptor expressed in these Microglial Cells, and its activation led to the phosphorylation of both extraCellular signaling-regulated kinases Erk1/2 and Akt. Furthermore, the effect of neurotensin on Cell migration was preceded by a profound modification of the F-actin cytoskeleton, particularly by the rapid formation of numerous Cell filopodia. Both the motility and the filopodia appearance induced by neurotensin were totally blocked by selective inhibitors of MAP kinases or PI3 kinase pathways. In the murine Microglial Cell Line N11, the neurotensin receptor-3 is also the only neurotensin receptor expressed, and its activation by neurotensin leads to the phosphorylation of both Erk1/2 and Akt. In these Cells, neurotensin induces the gene expression of several cytokines/chemokines, including MIP-2, MCP-1, interleukin-1β and tumor necrosis factor-α. This induction is dependent on both protein kinases pathways. We observed that the effect of neurotensin on the cytokine/chemokine expression is also inhibited by the neurotensin receptor-3 propeptide. This is the demonstration that the neurotensin receptor-3 is functional and mediates both the migratory action of neurotensin and its induction of chemokines/cytokines expression. © 2005 Wiley-Liss, Inc.
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Neurotensin receptor-3/sortilin mediates neurotensin-induced cytokine/chemokine expression in a murine Microglial Cell Line.
Journal of neuroscience research, 2004Co-Authors: Eleni Dicou, Jeanpierre Vincent, Jean MazellaAbstract:We show that the type I neurotensin receptor-3 (also called sortilin) is the only known neurotensin receptor expressed in a murine Microglial Cell Line and that its activation leads to phosphorylation of both extraCellular signaling-regulated (Erk1/2) and Akt kinases. Using semiquantitative reverse-transcriptase (RT) PCR, we demonstrate that neurotensin induces gene expression of several cytokines/chemokines including macrophage inflammatory protein (MIP)-2, monocyte chemotactic protein (MCP)-1, interleukin (IL)-1β and tumor necrosis factor (TNF)-α. This induction is dependent on both phosphatidylinositol 3-kinase and mitogen-activated protein kinases pathways. We observe that the effect of neurotensin on cytokine/chemokine expression is inhibited by the neurotensin receptor-3 propeptide, a selective ligand of this receptor. These results demonstrate that the neurotensin receptor-3 is functional in Microglial Cells where it mediates the induction of chemokines/cytokines expression by neurotensin. © 2004 Wiley-Liss, Inc.
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neurotensin receptor 3 sortilin mediates neurotensin induced cytokine chemokine expression in a murine Microglial Cell Line
Journal of Neuroscience Research, 2004Co-Authors: Eleni Dicou, Jeanpierre Vincent, Jean MazellaAbstract:We show that the type I neurotensin receptor-3 (also called sortilin) is the only known neurotensin receptor expressed in a murine Microglial Cell Line and that its activation leads to phosphorylation of both extraCellular signaling-regulated (Erk1/2) and Akt kinases. Using semiquantitative reverse-transcriptase (RT) PCR, we demonstrate that neurotensin induces gene expression of several cytokines/chemokines including macrophage inflammatory protein (MIP)-2, monocyte chemotactic protein (MCP)-1, interleukin (IL)-1β and tumor necrosis factor (TNF)-α. This induction is dependent on both phosphatidylinositol 3-kinase and mitogen-activated protein kinases pathways. We observe that the effect of neurotensin on cytokine/chemokine expression is inhibited by the neurotensin receptor-3 propeptide, a selective ligand of this receptor. These results demonstrate that the neurotensin receptor-3 is functional in Microglial Cells where it mediates the induction of chemokines/cytokines expression by neurotensin. © 2004 Wiley-Liss, Inc.
Ju-hee Lee - One of the best experts on this subject based on the ideXlab platform.
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Tryptanthrin Suppresses the Activation of the LPS-Treated BV2 Microglial Cell Line via Nrf2/HO-1 Antioxidant Signaling.
Frontiers in cellular neuroscience, 2017Co-Authors: Young-won Kwon, So Yeong Cheon, Sung Yun Park, Juhyun Song, Ju-hee LeeAbstract:Microglia are the resident macrophages in the central nervous system (CNS) and play essential roles in neuronal homeostasis and neuroinflammatory pathologies. Recently, microglia have been shown to contribute decisively to neuropathologic processes after ischemic stroke. Furthermore, natural compounds have been reported to attenuate inflammation and pathologies associated with neuroinflammation. Tryptanthrin (indolo[2,1-b]quinazoLine-6,12-dione) is a phytoalkaloid with known anti-inflammatory effects in Cells. In present study, the authors confirmed middle cerebral artery occlusion (MCAO) injury triggers the activation of microglia in brain tissue, and investigated whether tryptanthrin influences the function of mouse murine BV2 microglia under LPS-induced inflammatory conditions in vitro. It was found tryptanthrin protected BV2 microglia Cells against LPS-induced inflammation and inhibited the induction of M1 phenotype microglia under inflammatory conditions. In addition, tryptanthrin reduced the production of pro-inflammatory cytokines in BV2 microglia Cells via nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) signaling and NF-κB signaling. The authors suggest that tryptanthrin might alleviate the progress of neuropathologies by controlling Microglial functions under neuroinflammatory conditions.
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tryptanthrin suppresses the activation of the lps treated bv2 Microglial Cell Line via nrf2 ho 1 antioxidant signaling
Frontiers in Cellular Neuroscience, 2017Co-Authors: Young-won Kwon, So Yeong Cheon, Sung Yun Park, Juhyun Song, Ju-hee LeeAbstract:Microglia are the resident macrophages in the central nervous system (CNS) and play essential roles in neuronal homeostasis and neuroinflammatory pathologies. Recently, microglia have been shown to contribute decisively to neuropathologic processes after ischemic stroke. Furthermore, natural compounds have been reported to attenuate inflammation and pathologies associated with neuroinflammation. Tryptanthrin (indolo[2,1-b]quinazoLine-6,12-dione) is a phytoalkaloid with known anti-inflammatory effects in Cells. In present study, the authors confirmed middle cerebral artery occlusion (MCAO) injury triggers the activation of microglia in brain tissue, and investigated whether tryptanthrin influences the function of mouse murine BV2 microglia under LPS-induced inflammatory conditions in vitro. It was found tryptanthrin protected BV2 microglia Cells against LPS-induced inflammation and inhibited the induction of M1 phenotype microglia under inflammatory conditions. In addition, tryptanthrin reduced the production of pro-inflammatory cytokines in BV2 microglia Cells via nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) signaling and NF-κB signaling. The authors suggest that tryptanthrin might alleviate the progress of neuropathologies by controlling Microglial functions under neuroinflammatory conditions.