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J. Biol. Chem., Vol. 277, Issue 34, 30778-30783, August 23, 2002
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From the Hormone and Metabolic Research Unit, University of Louvain
Medical School and Christian de Duve International Institute of
Cellular and Molecular Pathology, B-1200 Brussels, Belgium
The activation of monocytes involves a
stimulation of glycolysis, release of potent inflammatory mediators,
and alterations in gene expression. All of these processes are known to
be further increased under hypoxic conditions. The activated monocytes
express inducible 6-phosphofructo-2-kinase (iPFK-2), which synthesizes fructose 2,6-bisphosphate, a stimulator of glycolysis. During ischemia,
AMP-activated protein kinase (AMPK) activates the homologous heart
6-phosphofructo-2-kinase isoform by phosphorylating its Ser-466.
Here, we studied the involvement of AMPK and iPFK-2 in the stimulation
of glycolysis in activated monocytes under hypoxia. iPFK-2 was
phosphorylated on the homologous serine (Ser-461) and activated by AMPK
in vitro. The activation of human monocytes by
lipopolysaccharide induced iPFK-2 expression and increased fructose
2,6-bisphosphate content and glycolysis. The incubation of activated
monocytes with oligomycin, an inhibitor of oxidative phosphorylation,
or under hypoxic conditions activated AMPK and further increased iPFK-2
activity, fructose 2,6-bisphosphate content, and glycolysis. In
cultured human embryonic kidney 293 cells, the expression of a
dominant-negative AMPK prevented both the activation and
phosphorylation of co-transfected iPFK-2 by oligomycin. It is concluded
that the stimulation of glycolysis by hypoxia in activated monocytes
requires the phosphorylation and activation of iPFK-2 by
AMPK.
The Stimulation of Glycolysis by Hypoxia in Activated Monocytes
Is Mediated by AMP-activated Protein Kinase and Inducible
6-Phosphofructo-2-kinase*
,
*
This work was supported by the Belgian Federal Program
Interuniversity Poles of attraction (P4/23), the Directorate General Higher Education and Scientific Program, French Community of Belgium, The Fund for Medical Scientific Research (Belgium), and by European Union contract QLG1-CT-2001-01488 (AMPDIAMET).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.
Research fellow of the National Fund for Scientific Research (Belgium).
§
Supported by the Fund for Scientific Research in Industry and
Agriculture (Belgium).
¶
Supported by the French Community of Belgium.
To whom correspondence should be addressed: HORM Unit, ICP-UCL
7529, Avenue Hippocrate, 75, B-1200 Brussels, Belgium. Tel.: 32-2-764-74-85; Fax: 32-2-764-75-07; E-mail: hue@horm.ucl.ac.be.
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