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Modulation of microglia by stem cell factor
Author(s) -
Zhang SuChun,
Fedoroff Sergey
Publication year - 1998
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19980701)53:1<29::aid-jnr4>3.0.co;2-l
Subject(s) - microglia , stem cell factor , neurotrophic factors , microbiology and biotechnology , tumor necrosis factor alpha , cytokine , neurotrophin , nerve growth factor , ciliary neurotrophic factor , biology , neuroglia , brain derived neurotrophic factor , chemistry , inflammation , stem cell , receptor , immunology , neuroscience , central nervous system , biochemistry , progenitor cell
We reported previously that stem cell factor (SCF) is produced mainly by neurons and that its receptor (c‐kitR), encoded by the protooncogene c‐kit, is expressed in microglia, suggesting that SCF/c‐kitR signaling may be involved in neuron‐microglia interactions. We now report that SCF supports microglial survival in cultures, maintains them in process‐bearing morphology, and inhibits microglial proliferation induced by colony stimulating factor‐1. SCF potentiates microglial expression of the mRNAs of nerve growth factor, brain‐derived neurotrophic factor and ciliary neurotrophic factor, and downregulates microglial expression of the inflammation‐associated cytokines, tumor necrosis factor‐a (TNF‐α), and interleukin‐1β (IL‐1β). SCF potentiates lipopolysaccharide‐stimulated, but attenuates interferon‐γ TFNα mediated expression of the mRNAs of IL‐1β and TNF‐α. The SCF‐induced expression of neurotrophin mRNAs is enhanced by the addition of lipopolysaccharide (LPS) but is reduced by IFNγ. The interactions between SCF and LPS or IFNγ in the regulation of inflammation‐associated cytokine gene expression are accompanied by the differential regulation of c‐kitR in microglia. These observations suggest that SCF/c‐kitR signaling modulates microglial activity. J. Neurosci. Res. 53:29–37, 1998. © 1998 Wiley‐Liss, Inc.