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J. Biol. Chem., Vol. 277, Issue 42, 39801-39808, October 18, 2002
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From the The chemokine stromal cell-derived factor-1
(SDF-1) and its receptor CXCR4 control the migration of neurons and
microglial cells in the central nervous system. Although functional
CXCR4 is also expressed by astroglia, recent studies have failed to observe a chemotactic response of these cells to SDF-1. Here, we
demonstrate that SDF-1-dependent chemotaxis can be induced by treating cultured cortical astroglia with either dibutyryl cyclic
AMP (dbcAMP; 10
Interleukin-6 and cAMP Induce Stromal
Cell-derived Factor-1 Chemotaxis in Astroglia by Up-regulating
CXCR4 Cell Surface Expression
IMPLICATIONS FOR BRAIN INFLAMMATION*
§,§
Abteilung Anatomie und Zellbiologie,
¶ Abteilung Pharmakologie und Toxikologie, Universität Ulm,
89069 Ulm, Germany
4 M) or interleukin-6
(IL-6; 10 ng/ml). Flow cytometric analysis revealed that both the
dbcAMP- and IL-6-induced onset of SDF-1-dependent chemotaxis of astroglia are due to the increased cell surface expression of CXCR4. In addition, dbcAMP and IL-6 also increased CXCR4
transcript levels, further suggesting that both treatments primarily
affect CXCR4 surface expression in astroglia by stimulation of gene
expression. Moreover, unlike the case with IL-6 and dbcAMP, which
allowed for an optimal chemotactic response to SDF-1 only after 48 h, a similar chemotactic response, associated with an increase in CXCR4
cell surface expression, already occurred after 24 h when
astroglial cultures were maintained with medium conditioned by IL-6- or
dbcAMP-pretreated astrocytes, indicating that the stimulatory effects
of IL-6 and cAMP on CXCR4 cell surface expression involve a secondary
mechanism. The findings that elevated extracellular levels of IL-6 or
factors positively coupled to cAMP result in increased CXCR4 cell
surface expression levels and subsequent SDF-1-dependent
chemotaxis in central nervous system astrocytes point to a crucial role
of this chemokine during reactive gliosis and human immunodeficiency
virus-mediated dementia.
*
This work was supported by Deutsche Forschungsgemeinschaft
Grant SFB497.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed:
Universität Leipzig, Institut für Anatomie, Liebigstr. 13, 04103 Leipzig, Germany. Tel.: 49-341-97-22071; Fax: 49-341-97-22009;
E-mail: engj@medizin.uni-leipzig.de.
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