Oxidized lipid-mediated alterations in proteoglycan metabolism in cultured pulmonary endothelial cells

Santhini Ramasamy; David W. Lipke; Gibert A. Boissonneault; Hongtao Guo; Bernhard Hennig

doi:10.1016/0021-9150(95)05702-1

Oxidized lipid-mediated alterations in proteoglycan metabolism in cultured pulmonary endothelial cells

Santhini Ramasamy, David W. Lipke, Gibert A. Boissonneault, Hongtao Guo, Bernhard Hennig

Research output: Contribution to journal › Article › peer-review

12 Scopus citations

Abstract

Compared to cholesterol or linoleic acid (18:2), oxidized lipids such as cholestan-3β,5α,6β-triol (triol) and hydroperoxy linoleic acid (HPODE) markedly impair endothelial barrier function in culture [Hennig and Boissonneault, 1987; Hennig et al. 1986]. Because proteoglycans contribute to vascular permeability properties, the effects of cholesterol and 18:2 and their oxidation products, triol and HPODE, on endothelial proteoglycan metabolism were determined. While cholesterol was without effect, a concentration-dependent decrease in cellular proteoglycans (measured by ³⁵S incorporation) was observed after exposure to triol. Compared to control cultures, cholesterol reduced mRNA levels for the proteoglycans, perlecan and biglycan. Triol had a similar effect on biglycan but not on perlecan mRNA levels. Compared to 18:2, 1, 3 and 5 μM HPODE depressed cellular proteoglycans. Perlecan mRNA levels were reduced more by HPODE when compared to 18:2. Biglycan mRNA levels were reduced by 3 μM, but not by 5 μM HPODE. These data demonstrate that oxidized lipids such as triol and HPODE can decrease cellular proteoglycan metabolism in endothelial monolayers and alter mRNA levels of major specific proteoglycans in a concentration-dependent manner. This may have implications in lipid-mediated disruption of endothelial barrier function and atherosclerosis.

Original language	English
Pages (from-to)	199-208
Number of pages	10
Journal	Atherosclerosis
Volume	120
Issue number	1-2
DOIs	https://doi.org/10.1016/0021-9150(95)05702-1
State	Published - Feb 1996

Bibliographical note

Funding Information:
Supported in part by grant lPO1 HL36552 from the National Institute of Health and the Kentucky Agricultural Experiment Station (article number 94-9 133).

Funding

Supported in part by grant lPO1 HL36552 from the National Institute of Health and the Kentucky Agricultural Experiment Station (article number 94-9 133).

Funders	Funder number
National Institutes of Health (NIH)
National Institute of Environmental Health Sciences (NIEHS)	P42ES007380
Kentucky Agricultural Experiment Station	94-9 133

Keywords

Atherosclerosis
Endothelial cells
Oxidized lipids
Proteoglycans

ASJC Scopus subject areas

Cardiology and Cardiovascular Medicine

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10.1016/0021-9150(95)05702-1

Cite this

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title = "Oxidized lipid-mediated alterations in proteoglycan metabolism in cultured pulmonary endothelial cells",

abstract = "Compared to cholesterol or linoleic acid (18:2), oxidized lipids such as cholestan-3β,5α,6β-triol (triol) and hydroperoxy linoleic acid (HPODE) markedly impair endothelial barrier function in culture [Hennig and Boissonneault, 1987; Hennig et al. 1986]. Because proteoglycans contribute to vascular permeability properties, the effects of cholesterol and 18:2 and their oxidation products, triol and HPODE, on endothelial proteoglycan metabolism were determined. While cholesterol was without effect, a concentration-dependent decrease in cellular proteoglycans (measured by 35S incorporation) was observed after exposure to triol. Compared to control cultures, cholesterol reduced mRNA levels for the proteoglycans, perlecan and biglycan. Triol had a similar effect on biglycan but not on perlecan mRNA levels. Compared to 18:2, 1, 3 and 5 μM HPODE depressed cellular proteoglycans. Perlecan mRNA levels were reduced more by HPODE when compared to 18:2. Biglycan mRNA levels were reduced by 3 μM, but not by 5 μM HPODE. These data demonstrate that oxidized lipids such as triol and HPODE can decrease cellular proteoglycan metabolism in endothelial monolayers and alter mRNA levels of major specific proteoglycans in a concentration-dependent manner. This may have implications in lipid-mediated disruption of endothelial barrier function and atherosclerosis.",

keywords = "Atherosclerosis, Endothelial cells, Oxidized lipids, Proteoglycans",

author = "Santhini Ramasamy and Lipke, \{David W.\} and Boissonneault, \{Gibert A.\} and Hongtao Guo and Bernhard Hennig",

note = "Funding Information: Supported in part by grant lPO1 HL36552 from the National Institute of Health and the Kentucky Agricultural Experiment Station (article number 94-9 133).",

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AU - Ramasamy, Santhini

AU - Lipke, David W.

AU - Boissonneault, Gibert A.

AU - Guo, Hongtao

AU - Hennig, Bernhard

N1 - Funding Information: Supported in part by grant lPO1 HL36552 from the National Institute of Health and the Kentucky Agricultural Experiment Station (article number 94-9 133).

PY - 1996/2

Y1 - 1996/2

N2 - Compared to cholesterol or linoleic acid (18:2), oxidized lipids such as cholestan-3β,5α,6β-triol (triol) and hydroperoxy linoleic acid (HPODE) markedly impair endothelial barrier function in culture [Hennig and Boissonneault, 1987; Hennig et al. 1986]. Because proteoglycans contribute to vascular permeability properties, the effects of cholesterol and 18:2 and their oxidation products, triol and HPODE, on endothelial proteoglycan metabolism were determined. While cholesterol was without effect, a concentration-dependent decrease in cellular proteoglycans (measured by 35S incorporation) was observed after exposure to triol. Compared to control cultures, cholesterol reduced mRNA levels for the proteoglycans, perlecan and biglycan. Triol had a similar effect on biglycan but not on perlecan mRNA levels. Compared to 18:2, 1, 3 and 5 μM HPODE depressed cellular proteoglycans. Perlecan mRNA levels were reduced more by HPODE when compared to 18:2. Biglycan mRNA levels were reduced by 3 μM, but not by 5 μM HPODE. These data demonstrate that oxidized lipids such as triol and HPODE can decrease cellular proteoglycan metabolism in endothelial monolayers and alter mRNA levels of major specific proteoglycans in a concentration-dependent manner. This may have implications in lipid-mediated disruption of endothelial barrier function and atherosclerosis.

AB - Compared to cholesterol or linoleic acid (18:2), oxidized lipids such as cholestan-3β,5α,6β-triol (triol) and hydroperoxy linoleic acid (HPODE) markedly impair endothelial barrier function in culture [Hennig and Boissonneault, 1987; Hennig et al. 1986]. Because proteoglycans contribute to vascular permeability properties, the effects of cholesterol and 18:2 and their oxidation products, triol and HPODE, on endothelial proteoglycan metabolism were determined. While cholesterol was without effect, a concentration-dependent decrease in cellular proteoglycans (measured by 35S incorporation) was observed after exposure to triol. Compared to control cultures, cholesterol reduced mRNA levels for the proteoglycans, perlecan and biglycan. Triol had a similar effect on biglycan but not on perlecan mRNA levels. Compared to 18:2, 1, 3 and 5 μM HPODE depressed cellular proteoglycans. Perlecan mRNA levels were reduced more by HPODE when compared to 18:2. Biglycan mRNA levels were reduced by 3 μM, but not by 5 μM HPODE. These data demonstrate that oxidized lipids such as triol and HPODE can decrease cellular proteoglycan metabolism in endothelial monolayers and alter mRNA levels of major specific proteoglycans in a concentration-dependent manner. This may have implications in lipid-mediated disruption of endothelial barrier function and atherosclerosis.

KW - Atherosclerosis

KW - Endothelial cells

KW - Oxidized lipids

KW - Proteoglycans

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Oxidized lipid-mediated alterations in proteoglycan metabolism in cultured pulmonary endothelial cells

Abstract

Bibliographical note

Funding

Keywords

ASJC Scopus subject areas

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