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Division of Arthritis Research, The Scripps Research Institute, La Jolla, CA 92037; and
Division of Rheumatology, Scripps Clinic, La Jolla, CA 92037
Glucose serves as the major energy substrate and the main precursor
for the synthesis of glycosaminoglycans in chondrocytes. Facilitated
glucose transport represents the first rate-limiting step in glucose
metabolism. This study examines molecular regulation of facilitated
glucose transport in normal human articular chondrocytes by
proinflammatory cytokines. IL-1
and TNF-
, and to a lesser degree
IL-6, accelerate facilitated glucose transport as measured by
[3H]2-deoxyglucose uptake. IL-1 induces an increased
expression of glucose transporter (GLUT) 1 mRNA and protein, and GLUT9
mRNA. GLUT3 and GLUT8 mRNA are constitutively expressed in chondrocytes
and are not regulated by IL-1. GLUT2 and GLUT4 mRNA are not detected
in chondrocytes. IL-1 stimulates GLUT1 protein glycosylation and
plasma membrane incorporation. IL-1 regulation of glucose transport
in chondrocytes depends on protein kinase C and p38 signal transduction
pathways, and does not require phosphoinositide 3-kinase, extracellular
signal-related kinase, or c-Jun N-terminal kinase activation.
IL-1-accelerated glucose transport in chondrocytes is not mediated
by endogenous NO or eicosanoids. These results demonstrate that
stimulation of glucose transport represents a component of the
chondrocyte response to IL-1. Two classes of GLUTs are identified in
chondrocytes, constitutively expressed GLUT3 and GLUT8, and the
inducible GLUT1 and GLUT9.
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