Facilitative Glucose Transporters in Articular Chondrocytes: by Ali Mobasheri, Carolyn A. Bondy, Kelle Moley, Alexandrina

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

Articular cartilage is a distinct and hugely really good avascular connective tissue during which the supply of oxygen and glucose is considerably less than synovial fluid and plasma. Glucose is a vital resource of strength in the course of embryonic development and fetal improvement and is essential for mesenchymal mobile differentiation, chondrogenesis and skeletal morphogenesis. Glucose is a vital metabolic gas for differentiated chondrocytes in the course of post-natal improvement and in grownup articular cartilage and is a standard structural precursor for the synthesis of extracellular matrix glycosaminoglycans. Glucose metabolism is necessary for progress plate chondrocytes which perform lengthy bone development. Glucose concentrations in articular cartilage can vary looking on age, actual job and endocrine prestige. Chondrocytes are glycolytic cells and has to be in a position to experience the focus of oxygen and glucose within the extracellular matrix and reply competently by means of adjusting mobile metabolism. therefore chondrocytes should have the capability to outlive in an extracellular matrix with constrained foodstuff and coffee oxygen tensions. released info from our laboratories recommend that chondrocytes convey a number of isoforms of the GLUT/SLC2A kin of glucose/polyol transporters. In different tissues GLUT proteins are expressed in a cell-specific demeanour, show special kinetic houses, and are developmentally regulated. a number of GLUTs expressed in chondrocytes are regulated via hypoxia, hypoxia mimetics, metabolic hormones and pro-inflammatory cytokines. during this multidisciplinary article we evaluate the molecular and morphological points of GLUT expression and serve as in chondrocytes and their mesenchymal and embryonic stem phone precursors and suggest key roles for those proteins in glucose sensing and metabolic rules in cartilage.

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Additional info for Facilitative Glucose Transporters in Articular Chondrocytes: Expression, Distribution and Functional Regulation of GLUT Isoforms by Hypoxia, Hypoxia Mimetics

Sample text

2001). GLUT1 has also been shown to be a cytokine inducible glucose transporter in cartilage since it is induced by catabolic, proinflammatory cytokines (Phillips et al. 2005a; Richardson et al. 2003; Shikhman et al. 2004, 2001a) (Fig. 9). 32 Functional Significance of GLUT1 and GLUT3 in Articular Chondrocytes A 1000 500 300 B 1000 C Control β-actin GLUT11 GLUT10 GLUT9 GLUT8 GLUT6 GLUT5 GLUT4 GLUT3 GLUT2 GLUT1 Mw 500 300 1000 GLUT12 Primet set B GLUT12 Primer set A GLUT12 Primet set B GLUT12 Primer set A Mw 500 300 Fig.

In particular we were interested in comparing the effects of human recombinant proinflammatory cytokines on glucose transport in equine chondrocytes and the effects of NSAIDs on glucose transport and metabolism. We were also interested in comparing glucose uptake in chondrocytes isolated from normal and OA joints. Therefore, we used this model to compare 2-deoxy-D-glucose uptake in freshly isolated equine chondrocytes from normal and OA equine joints. We hypothesized that chondrocytes isolated from equine OA joints would exhibit increased glucose transport compared to chondrocytes from normal joints.

In a previous section we discussed the importance of subchondral blood vessels and their physical separation from the articular cartilage making it difficult for them to participate in the provision of nutrients to articular cartilage nutrition. Chondrocytes are glycolytic cells and are able to survive in an ECM with limited nutrients and low oxygen tensions (Henrotin et al. 2005a; Mobasheri et al. 2005b). Consequently, chondrocytes must have the capacity to sense the available levels of nutrients and ATP in the intracellular and extracellular compartments and respond appropriately by adjusting cellular metabolism and ATP production levels (Edwards and Weston 1995).

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