Document Detail

Neurotensin and the neurotensin receptor-3 in microglial cells.
MedLine Citation:
PMID:  15957186     Owner:  NLM     Status:  MEDLINE    
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-1beta and tumor necrosis factor-alpha. 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.
Stéphane Martin; Eleni Dicou; Jean-Pierre Vincent; Jean Mazella
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Journal of neuroscience research     Volume:  81     ISSN:  0360-4012     ISO Abbreviation:  J. Neurosci. Res.     Publication Date:  2005 Aug 
Date Detail:
Created Date:  2005-08-01     Completed Date:  2005-11-07     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  7600111     Medline TA:  J Neurosci Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  322-6     Citation Subset:  IM    
Copyright Information:
(c) 2005 Wiley-Liss, Inc.
Institut de Pharmacologie Moléculaire et Cellulaire, Unité Mixte de Recherche 6097 du Centre National de la Recherche Scientifique, Sophia Antipolis, Valbonne, France.
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MeSH Terms
1-Phosphatidylinositol 3-Kinase / metabolism
Adaptor Proteins, Vesicular Transport
Gene Expression Regulation / drug effects,  physiology
Membrane Glycoproteins / antagonists & inhibitors,  genetics,  metabolism*
Microglia / drug effects*,  metabolism
Mitogen-Activated Protein Kinases / metabolism
Nerve Tissue Proteins / antagonists & inhibitors,  genetics,  metabolism*
Neurotensin / pharmacology*
Signal Transduction / physiology
Time Factors
Reg. No./Substance:
0/Adaptor Proteins, Vesicular Transport; 0/Membrane Glycoproteins; 0/Nerve Tissue Proteins; 0/sortilin; 39379-15-2/Neurotensin; EC 3-Kinase; EC Protein Kinases

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