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Neurotrophins regulate the function of cultured microglia
Author(s) -
Nakajima Kazuyuki,
Kikuchi Yoshiaki,
Ikoma Etsuko,
Honda Shizuyo,
Ishikawa Masahiro,
Liu Yongmao,
Kohsaka Shinichi
Publication year - 1998
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/(sici)1098-1136(199811)24:3<272::aid-glia2>3.0.co;2-4
Subject(s) - neurotrophin , trk receptor , biology , microglia , neurotrophic factors , neurotrophin 3 , nerve growth factor , microbiology and biotechnology , tropomyosin receptor kinase a , neuroglia , low affinity nerve growth factor receptor , brain derived neurotrophic factor , receptor , endocrinology , immunology , biochemistry , central nervous system , inflammation
Although the physiological role of neurotrophins in neuronal development and survival has been extensively investigated, their role in glial cell physiology remains to be elucidated. In the present study, we investigated the effects of neurotrophins on cultured microglia from newborn rat brain. All of the neurotrophins tested nerve growth factor (NGF), brain‐derived neurotrophic factor (BDNF), neurotrophin‐3 (NT‐3), and neurotrophin‐4 (NT‐4), increased the secretion of plasminogen and urokinase type‐plasminogen activator and specific activity of acid phosphatase, but suppressed the release of constitutively‐produced and lipopolysaccharide‐stimulated nitric oxide (NO) from microglia. The reverse transcription‐polymerase chain reaction, immunocytochemical staining, and Western blotting revealed that cultured microglia express Trk A, B, and C, and low‐affinity NGF receptor, LNGFRp75. Neurotrophin was found to phosphorylate Trk A and B, and the neurotrophin‐induced enhancement of plasminogen‐secretion was suppressed by protein kinase inhibitor, K252a. Furthermore, neurotrophins caused an activation of transcription factor, NF‐κB. These results indicate that the neurotrophin family regulate the function of microglia through Trk and/or LNGFRp75‐mediated signal transduction. GLIA 24:272–289, 1998. © 1998 Wiley‐Liss, Inc.

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