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Department of Cell Biology, University of Alabama, Birmingham, AL 35294
Chemokines constitute a superfamily of proteins that function as
chemoattractants and activators of leukocytes. Astrocytes, the major
glial cell type in the CNS, are a source of chemokines within the
diseased brain. Specifically, we have shown that primary human
astrocytes and human astroglioma cell lines produce the CXC chemokines
IFN-
-inducible protein-10 and IL-8 and the CC chemokines monocyte
chemoattractant protein-1 and RANTES in response to stimuli such as
TNF-
, IL-1
, and IFN-. In this study, we investigated chemokine
receptor expression and function on human astroglioma cells.
Enhancement of CXC chemokine receptor 4 (CXCR4) mRNA expression was
observed upon treatment with the cytokines TNF- and IL-1. The
peak of CXCR4 expression in response to TNF- and IL-1 was 8 and
4 h, respectively. CXCR4 protein expression was also enhanced upon
treatment with TNF- and IL-1 (2- to 3-fold). To study the
functional relevance of CXCR4 expression, stable astroglioma
transfectants expressing high levels of CXCR4 were generated.
Stimulation of cells with the ligand for CXCR4, stromal cell-derived
factor-1 (SDF-1), resulted in an elevation in intracellular
Ca2+ concentration and activation of the mitogen-activated
protein kinase cascade, specifically, extracellular signal-regulated
kinase 2 (ERK2) mitogen-activated protein kinase. Of most interest,
SDF-1 treatment induced expression of the chemokines monocyte
chemoattractant protein-1, IL-8, and IFN--inducible protein-10.
SDF-1-induced chemokine expression was abrogated upon inclusion of
U0126, a pharmacological inhibitor of ERK1/2, indicating that the ERK
signaling cascade is involved in this response. Collectively, these
data suggest that CXCR4-mediated signaling pathways in astroglioma
cells may be another mechanism for these cells to express chemokines
involved in angiogenesis and inflammation.
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