Neuronal adhesion molecule telencephalin induces rapid cell spreading of microglia
| Autor: | Keiko Ohsawa, Shinichi Kohsaka, Kensaku Mori, Yoshinori Imai, Yoshihiro Yoshihara, Takeo Mizuno, Hiroyuki Kagamiyama |
|---|---|
| Rok vydání: | 1999 |
| Předmět: |
Telencephalon
Integrin Central nervous system Mice Inbred Strains Nerve Tissue Proteins Biology Mice Neuroblastoma L Cells Cell–cell interaction Cell Movement Tumor Cells Cultured medicine Animals Diencephalon Neural Cell Adhesion Molecules Molecular Biology Cells Cultured Mice Knockout Membrane Glycoproteins Microglia General Neuroscience Genes p53 Lymphocyte Function-Associated Antigen-1 Recombinant Proteins Cell biology medicine.anatomical_structure Animals Newborn nervous system biology.protein Immunoglobulin superfamily Neuroglia Neurology (clinical) Neuron Tumor Suppressor Protein p53 Lamellipodium Neuroscience Developmental Biology |
| Zdroj: | Brain Research. 849:58-66 |
| ISSN: | 0006-8993 |
| DOI: | 10.1016/s0006-8993(99)01984-8 |
| Popis: | Telencephalin (TLCN) is a neuronal surface glycoprotein whose expression is restricted to the telencephalon, the most rostral segment of the brain. TLCN binds to lymphocyte function-associated antigen-1 (LFA-1) integrin. In the central nervous system, LFA-1 is selectively and constitutively expressed by microglia, suggesting that TLCN/LFA-1 binding may mediate cell–cell interactions between telencephalic neurons and microglia. In the present study, we investigated the effects of recombinant TLCN protein on the morphology of microglia. TLCN induced an intensive spreading of lamellipodia, causing a rapid change in microglial morphology. In contrast, TLCN induced no significant change in morphology of neuroblastoma and fibroblasts. Furthermore, the TLCN-induced spreading of microglia was accompanied by a clustering of LFA-1 on cell surface membrane. These results provide evidence that TLCN binding to the surface of microglia transduces signals into microglia that mediate or accelerate cell spreading and LFA-1 redistribution, implying that neuronal TLCN may control the state and/or function of microglia in both physiological and pathological conditions. |
| Databáze: | OpenAIRE |
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