Regulation of glucose transport by nonsteroidal anti-inflammatory drugs

Ali Mobasheri, Carolyn A. Bondy, Kelle Moley, Alexandrina Ferreira Mendes, Susana Carvalho Rosa, Stephen M. Richardson, Judith A. Hoyland, Richard Barrett-Jolley, Mehdi Shakibaei

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

Abstract

Cartilage destruction in arthritis and OA is linked to aberrant proinflammatory cytokine and growth factor expression in the joint (Chikanza and Fernandes 2000; Malemud et al. 2003). The proinflammatory cytokines TNF-α and IL-β have been found in significantly elevated levels in the synovial fluid of OA joints (Goldring 1999, 2000a; van den Berg 1999). Catabolic pathways are activated by TNF-α and IL-β, which are both upregulated in OA (Malemud et al. 2003). These proinflammatory mediators cause an increase in cartilage matrix degradation through increased MMP and aggrecanase activity in the joint. In addition, TNF-α and IL-β downregulate ECM protein biosynthesis while concomitantly up-regulating matrix MMP gene and protein expression. When MMPs are activated, cartilage ECM degradation ensues apparently because levels of endogenous cartilage MMP inhibitors cannot regulate MMP activity (Malemud et al. 2003).

Original languageEnglish
Title of host publicationFacilitative Glucose Transporters in Articular Chondrocytes
Subtitle of host publicationExpression, Distribution and Functional Regulation of GLUT Isoforms by Hypoxia, Hypoxia Mimetics, Growth Factors and Pro-Inflammatory Cytok
EditorsAli Mobasheri, Carolyn Bondy, Kelle Moley, Alexandrina Ferreira Mendes, Susana Carvalho Rosa, Stephen Richardson, Judith Hoyland, Richard Barrett-Jolley, Mehdi Shakibaei
Pages50-53
Number of pages4
DOIs
StatePublished - 2008

Publication series

NameAdvances in Anatomy Embryology and Cell Biology
Volume200
ISSN (Print)0301-5556

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