Abstract
Certain fatty acids induce changes in endothelial barrier function which may be mediated by alterations in normal proteoglycan synthesis/metabolism. To test this hypothesis, pulmonary artery derived endothelial cells were treated with media supplemented with linoleic acid (18:2), and/or a known proteoglycan synthesis inhibitor, β-d-xyloside. Independent exposure to 1 MM β-d-xyloside or 90 μM 18:2 increased albumin transfer, i.e., decreased barrier function, when compared with control cultures. 18:2 and β-d-xyloside increased albumin transfer additively, suggesting that the mechanisms by which 18:2 and β-d-xyloside alter the proteoglycan metabolism are different. Compared with the control group, treatment with 18:2 inhibited proteoglycan synthesis, decreased anionic properties of heparan sulfate proteoglycans in the cell monolayers and caused the release of a unique chondroitin sulfate proteoglycan into the culture media. Treatment with β-d-xyloside caused an increased incorporation of radioactive sulfate into glycosaminoglycans but inhibited proteoglycan synthesis. These results suggest that the fatty acid- and β-d-xyloside-induced impairment in endothelial barrier function may involve changes in the synthesis, release and physicochemical properties of proteoglycans.
Original language | English |
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Pages (from-to) | 279-290 |
Number of pages | 12 |
Journal | Atherosclerosis |
Volume | 103 |
Issue number | 2 |
DOIs | |
State | Published - Nov 1993 |
Bibliographical note
Funding Information:Supported in part by grants lPO1 HL36552 from the National Institute of Health, grants from the National Live Stock and Meat Board and Kentucky Beef Cattle Association, National Dairy Council, and the Kentucky Agricultural Experiment Station (article number 92-9-21). The
Keywords
- Endothelial barrier function
- Linoleic acid
- Proteoglycans
- β-d-Xyloside
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine