Effect of oxygen tension on 35S-glycosaminoglycan synthesis and UDP-sugar pool size in articular cartilage

Henderson, Gillian E.; Mason, Roger M.

doi:10.1042/bst019364s

Cited by 14 publications

(11 citation statements)

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“…Several studies have demonstrated that proteoglycan synthetic activity is an energy-dependent metabolic process (14,30,31). Within a physiologic range of oxygen tensions, baseline proteoglycan synthesis of articular cartilage is low, whereas the synthetic activity increases with higher oxygen tension (14,30,31). Consistent with the findings of these studies, we found marked upregulation of proteoglycan synthetic activity under normoxic compared with hypoxic conditions.…”

Section: Discussionsupporting

confidence: 92%

“…Apart from its role in the induction of VEGF, HIF-1␣ is also recognized as one of the key regulators of anaerobic glycolytic enzymes and glucose transporters (47,(49)(50)(51). Several studies have demonstrated that proteoglycan synthetic activity is an energy-dependent metabolic process (14,30,31). Within a physiologic range of oxygen tensions, baseline proteoglycan synthesis of articular cartilage is low, whereas the synthetic activity increases with higher oxygen tension (14,30,31).…”

Section: Discussionmentioning

confidence: 97%

“…In healthy articular cartilage, proteoglycan synthetic activity is low, but increases in response to disease, injury, and environmental stress (24)(25)(26)(27)(28). While proteoglycan synthesis has been found to increase with higher oxygen tensions within physiologic ranges of oxygen tension in cultured chondrocytes (29)(30)(31), it is unknown whether HIF-1␣ influences proteoglycan synthesis of articular cartilage.…”

mentioning

confidence: 99%

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Tonic activation of hypoxia‐inducible factor 1α in avascular articular cartilage and implications for metabolic homeostasis

Brucker¹,

Izzo²,

Chu³

2005

Arthritis & Rheumatism

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 97%

mentioning

confidence: 99%

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Tonic activation of hypoxia‐inducible factor 1α in avascular articular cartilage and implications for metabolic homeostasis

Brucker¹,

Izzo²,

Chu³

2005

Arthritis & Rheumatism

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“…Possibly as a result of their low ambient O 2 , chondrocyte metabolism is almost entirely glycolytic. Nevertheless, removal of O 2 has marked effects, depressing both metabolism (reducing adenosine triphosphate (ATP) levels and lactate production-the negative Pasteur effect) almost immediately [17] and inhibiting matrix synthesis [2,7,12,40].…”

Section: Introductionmentioning

confidence: 99%

Rapid effects of hypoxia on H+ homeostasis in articular chondrocytes

Gibson

McCartney²,

Sumpter³

et al. 2009

Pflugers Arch - Eur J Physiol

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Articular chondrocytes experience low oxygen (O(2)) levels compared with many other tissues, and values fall further in disease states. Chondrocyte intracellular pH (pH(i)) is a powerful modulator of matrix synthesis and is principally regulated by Na(+)-H(+) exchange (NHE). In equine chondrocytes, NHE is inhibited when cells are incubated for 3 h at low O(2), leading to intracellular acidosis. O(2)-dependent changes in reactive oxygen species (ROS) levels appear to underlie this effect. The present study examines whether hypoxia can influence chondrocyte NHE activity and pH(i) over shorter timescales using the pH-sensitive fluoroprobe BCECF in cells isolated not only from equine cartilage but also from bovine tissue. O(2) levels in initially oxygenated solutions gassed with N(2) fell to approximately 1% within 2 h. A progressive fall in pH(i) and acid extrusion capacity was observed, with statistically significant effects (P < 0.05) apparent within 3 h. For equine and bovine cell populations subjected to step change in O(2) by resuspension in hypoxic (1%) solutions, a decline in acid extrusion and pH(i) was observed within 10 min and continued throughout the recording period. This effect represented inhibition of the NHE-mediated fraction of acid extrusion. Cells subjected to hypoxic solutions supplemented with CoCl(2) (100 microM) or antimycin A (100 microM) to raise levels of ROS did not acidify. The conserved nature and rapidity of the response to hypoxia has considerable implications for chondrocyte homeostasis and potentially for the maintenance of cartilage integrity.

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“…In other words, at least some O 2 is needed for the basal metabolism of chondrocytes. Studies indicate that both anoxia and hyperoxia are harmful to chondrocytes via impacting glycolysis and matrix production [76–79]. …”

Section: Role Of Oxygen Tension In Chondrocyte Developmentmentioning

confidence: 99%

The Signaling Pathways Involved in Chondrocyte Differentiation and Hypertrophic Differentiation

Dong

2016

Stem Cells International

127

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Chondrocytes communicate with each other mainly via diffusible signals rather than direct cell-to-cell contact. The chondrogenic differentiation of mesenchymal stem cells (MSCs) is well regulated by the interactions of varieties of growth factors, cytokines, and signaling molecules. A number of critical signaling molecules have been identified to regulate the differentiation of chondrocyte from mesenchymal progenitor cells to their terminal maturation of hypertrophic chondrocytes, including bone morphogenetic proteins (BMPs), SRY-related high-mobility group-box gene 9 (Sox9), parathyroid hormone-related peptide (PTHrP), Indian hedgehog (Ihh), fibroblast growth factor receptor 3 (FGFR3), and β-catenin. Except for these molecules, other factors such as adenosine, O2 tension, and reactive oxygen species (ROS) also have a vital role in cartilage formation and chondrocyte maturation. Here, we outlined the complex transcriptional network and the function of key factors in this network that determine and regulate the genetic program of chondrogenesis and chondrocyte differentiation.

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Effect of oxygen tension on 35S-glycosaminoglycan synthesis and UDP-sugar pool size in articular cartilage

Cited by 14 publications

References 0 publications

Tonic activation of hypoxia‐inducible factor 1α in avascular articular cartilage and implications for metabolic homeostasis

Tonic activation of hypoxia‐inducible factor 1α in avascular articular cartilage and implications for metabolic homeostasis

Rapid effects of hypoxia on H+ homeostasis in articular chondrocytes

The Signaling Pathways Involved in Chondrocyte Differentiation and Hypertrophic Differentiation

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