Premium
Macrophage inflammatory protein 1‐α mRNA expression in an immortalized microglial cell line and cortical astrocyte cultures
Author(s) -
Murphy Greer,
Jia X.C.,
Song Y.,
Ong E.,
Shrivastava R.,
Bocchini V.,
Lee Y. L.,
Eng L. F.
Publication year - 1995
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/jnr.490400607
Subject(s) - astrocyte , microglia , proinflammatory cytokine , macrophage inflammatory protein , cell culture , biology , microbiology and biotechnology , messenger rna , lipopolysaccharide , neuroglia , tumor necrosis factor alpha , cytokine , macrophage , inflammation , immunology , interleukin , in vitro , endocrinology , biochemistry , central nervous system , genetics , gene
Macrophage inflammatory protein 1 (MIP‐1) is a recently characterized inflammatory and chemokinetic cytokine. Proinflammatory stimuli have been shown to induce expression of MIP‐1 by macrophages. We hypothesized that microglia and astrocytes express MIP‐1α because of their many immunologic similarities to macrophages. MIP‐1α mRNA was examined with quantitative reverse transcription and polymerase chain reaction in an immortalized mouse microglial cell line (BV‐2) and in mouse cortical astrocyte cultures. We found that in both the BV‐2 microglial cell line and in astrocyte cultures, MIP‐1α mRNA was strongly induced by lipopolysaccharide and the phorbol ester PMA. MIP‐1α mRNA was reduced by dBcAMP, interferon‐γ, and PGE 1 . Dexamethasone decreased MIP‐1α mRNA levels in astrocyte cultures, but not in BV‐2 microglial cells. Interleukin‐1β, tumor necrosis factor α and MIP‐1α had no effect on MIP‐1α mRNA is expression. These findings demonstrate that MIP‐1α mRNA is expressed by cultured glial cells and is regulated by proinflammatory and anti‐inflammatory stimuli. MIP‐1α may be expressed by microglia and astrocytes in vivo, and may help modulate cerebral inflammation. © 1995 Wiley‐Liss, Inc.