Key result
Hypoxia decreases and hyperoxia slightly increases proteoglycan secretion in pulmonary artery endothelial cells.
Oxygen tension directly modulates the type and amount of proteoglycans secreted by pulmonary artery endothelial cells in vitro.
Hypoxia may alter endothelial proteoglycan output in vitro; leaves open any role in human pulmonary vascular disease.
Bovine pulmonary artery endothelial cells in culture were used to assess the influence of oxygen tension on proteoglycan synthesis. Cells exposed to 3% O2 (hypoxia) for 72 h and then labeled with [35S]sulfate for 5 h accumulated significantly less [35S]proteoglycan in medium than cells exposed to 20% O2 (control). This decrease was due primarily to a reduction in heparan sulfate. Cells exposed to 80% O2 (hyperoxia) for 72 h secreted slightly more [35S]proteoglycan into medium than controls. Greater accumulation of chondroitin sulfate was responsible for the increase. The amount of cell-associated proteoglycan did not change significantly in cells cultured in 3% or 80% O2 as compared with control cells cultured in 20% O2. Proteoglycans produced by hypoxia- or hyperoxia-treated cells were found to be similar in size to proteoglycans produced by cells cultured at 20% O2. Glycosaminoglycan sulfation, as measured by ion-exchange chromatography, did not appear to change with varying oxygen tensions. Our results demonstrate that production of proteoglycans secreted by endothelial cells in culture is sensitive to oxygen tension.
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Humphries et al. (1986) studied this question. Hypoxia (3% O2) and hyperoxia (80% O2) vs. 20% O2 (control) was evaluated on Proteoglycan synthesis and accumulation in medium. Exposure of bovine pulmonary artery endothelial cells to hypoxia significantly decreased proteoglycan secretion, whereas hyperoxia slightly increased it compared to 20% O2 controls.
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