Cytokine Regulation of Facilitated Glucose Transport in Human Articular Chondrocytes

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 norma...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2001-12, Vol.167 (12), p.7001-7008
Main Authors: Shikhman, Alexander R, Brinson, Diana C, Valbracht, Jean, Lotz, Martin K
Format: Article
Language:English
Subjects:
Biological Transport, Active
Cartilage, Articular - cytology
Cell Membrane - metabolism
Cells, Cultured
Chondrocytes - drug effects
Chondrocytes - metabolism
Cytokines - pharmacology
Deoxyglucose - metabolism
Eicosanoids - physiology
Glucose - metabolism
Glucose Transporter Type 1
GLUT1 protein
GLUT3 protein
GLUT8 protein
GLUT9 protein
glycosaminoglycans
Glycosylation
Humans
interleukin 1^b
Interleukin-1 - pharmacology
Interleukin-6 - pharmacology
Monosaccharide Transport Proteins - genetics
Monosaccharide Transport Proteins - physiology
Nitric Oxide - physiology
RNA, Messenger - biosynthesis
Signal Transduction
Tumor Necrosis Factor-alpha - pharmacology
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Summary: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-1beta and TNF-alpha, and to a lesser degree IL-6, accelerate facilitated glucose transport as measured by [(3)H]2-deoxyglucose uptake. IL-1beta 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-1beta. GLUT2 and GLUT4 mRNA are not detected in chondrocytes. IL-1beta stimulates GLUT1 protein glycosylation and plasma membrane incorporation. IL-1beta 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-1beta-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-1beta. Two classes of GLUTs are identified in chondrocytes, constitutively expressed GLUT3 and GLUT8, and the inducible GLUT1 and GLUT9.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.167.12.7001