Glucosamine exposure reduces proteoglycan synthesis in primary human endothelial cells in vitro
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https://hdl.handle.net/10037/10189Date
2016-09-23Type
Journal articleTidsskriftartikkel
Peer reviewed
Abstract
Purpose: Glucosamine (GlcN) supplements are promoted for medical reasons, for example, for patients with
arthritis and other joint-related diseases. Oral intake of GlcN is followed by uptake in the intestine, transport
in the circulation and thereafter delivery to chondrocytes. Here, it is postulated to have an effect on synthesis
and turnover of extracellular matrix constituents expressed by these cells. Following uptake in the intestine,
serum levels are transiently increased, and the endothelium is exposed to increased levels of GlcN.
We investigated the possible effects of GlcN on synthesis of proteoglycans (PGs), an important matrix
component, in primary human endothelial cells.
Methods: Primary human endothelial cells were cultured in vitro in medium with 5 mM glucose and 010 mM GlcN. PGs were recovered and analysed by western blotting, or by SDS-PAGE, gel chromatography or ionexchange chromatography of 35S-PGs after 35S-sulphate labelling of the cells.
Results: The synthesis and secretion of 35S-PGs from cultured endothelial cells were reduced in a dose- and time-dependent manner after exposure to GlcN. PGs are substituted with sulphated glycosaminoglycan (GAG) chains, vital for PG function. The reduction in 35S-PGs was not related to an effect on GAG chain length, number or sulphation, but rather to the total expression of PGs.
Conclusion: Exposure of endothelial cells to GlcN leads to a general decrease in 35S-PG synthesis. These results suggest that exposure to high levels of GlcN can lead to decreased matrix synthesis, contrary to what has been claimed by supporters of such supplements.
Methods: Primary human endothelial cells were cultured in vitro in medium with 5 mM glucose and 010 mM GlcN. PGs were recovered and analysed by western blotting, or by SDS-PAGE, gel chromatography or ionexchange chromatography of 35S-PGs after 35S-sulphate labelling of the cells.
Results: The synthesis and secretion of 35S-PGs from cultured endothelial cells were reduced in a dose- and time-dependent manner after exposure to GlcN. PGs are substituted with sulphated glycosaminoglycan (GAG) chains, vital for PG function. The reduction in 35S-PGs was not related to an effect on GAG chain length, number or sulphation, but rather to the total expression of PGs.
Conclusion: Exposure of endothelial cells to GlcN leads to a general decrease in 35S-PG synthesis. These results suggest that exposure to high levels of GlcN can lead to decreased matrix synthesis, contrary to what has been claimed by supporters of such supplements.
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