Practical Methods for Plasma Lipoprotein Analysis1 1Work supported in part by the U.S. Atomic Energy Commission and by grants (HE06222 and FR00102) from the U.S. Public Health Service.

Hatch, Frederick T.

doi:10.1016/b978-1-4831-9942-9.50008-5

Cited by 1,097 publications

(34 citation statements)

References 173 publications

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“…LDL (1.019 Ͻ d Ͻ 1.063 g/ml) and lipoprotein-deficient serum (LPDS, d Ͼ 1.215) were prepared from normal human plasma by sequential ultracentrifugation as described (28). Ac-LDL was prepared by chemical modification of the native LDL as described by Basu (29).…”

Section: Methodsmentioning

confidence: 99%

Acquisition of Secretion of Transforming Growth Factor-β1 Leads to Autonomous Suppression of Scavenger Receptor Activity in a Monocyte-Macrophage Cell Line, THP-1

Nishimura

Harada‐Shiba

Tsuji

et al. 1998

Journal of Biological Chemistry

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Section: Methodsmentioning

confidence: 99%

Acquisition of Secretion of Transforming Growth Factor-β1 Leads to Autonomous Suppression of Scavenger Receptor Activity in a Monocyte-Macrophage Cell Line, THP-1

Nishimura

Harada‐Shiba

Tsuji

et al. 1998

Journal of Biological Chemistry

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“…The vessel had previously been evacuated to remove other gasses from solution. Human LDL was isolated from plasma as described previously [18]. Resident peritoneal macrophages were obtained from female Swiss-Webster mice as described previously [19].…”

Section: Methodsmentioning

confidence: 99%

Inhibition of low‐density lipoprotein oxidation by nitric oxide Potential role in atherogenesis

et al. 1993

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The effects of nitric oxide ('NO) and nitrovasodilators on the oxidation of low-density lipoprotein (LDL) have been studied. S-Nitroso-Nacetylpenicillamine (SNAP) and sodium nitroprusside (SNP) inhibited Cu 2÷-and 2,2'-azobis-2-amidinopropane hydrochloride-dependent oxidation of LDL as monitored by oxygen consumption and the formation of thiobarbituric acid-reactive substances, conjugated dienes, and lipid hydroperoxides. In the case of SNP, inhibition of LDL oxidation occurred only when the incubation mixture was irradiated with visible light. SNAP, however, exerted a dose-dependent inhibition of CuZ÷-catalyzed oxidation of LDL even in the dark. Addition of "NO dissolved in deoxygenated buffer also inhibited the progression of LDL oxidation. Mouse peritoneal macrophages were less able to degrade LDL that had been oxidized in the presence of SNAR Using an "NO electrode, it was estimated that a continuous production of'NO (~< 760 nM/min) could retard the progression of LDL oxidation. We propose that "NO can inhibit LDL oxidation by acting as a chain-breaking antioxidant that is capable of scavenging carbon-centered and peroxyl radicals. Biological implications of this novel °NO antioxidant property are discussed in relation to atherogenesis and contrasted to the prooxidant property of "NO when generated in the presence of superoxide.

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“…Free cholesterol-rich phospholipid dispersions and apo-high density lipoprotein/phosphatidylcholine acceptors were prepared as described (25). Lipoproteins were prepared from fresh human plasma by the method of Hatch and Lees (27). LDL were acetylated by the method ofGoldstein et al (28).…”

Section: Methodsmentioning

confidence: 99%

Development of the smooth muscle foam cell: uptake of macrophage lipid inclusions.

Wolfbauer¹,

Glick²,

Minor³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

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A possible mechanism for the formation of smooth muscle foam cells in the atherosclerotic lesion was explored. Cultured macrophages (J774 cell line) were induced to form cytoplasmic cholesteryl ester inclusions by exposure to acetylated low density lpoprotein in the presence of cholesterol-rich phospholipid dispersions. The macrophages were disrupted by brief sonication, and the inclusions were isolated by flotation. When these inclusions were placed in direct contact with cultured smooth muscle cells, cellular uptake of the inclusions in a time-and dose-dependent manner was observed. Light and electron microscopy indicated the presence of lipid inclusions throughout the cytoplasm of the cells. Uptake of inclusion lipid by the smooth muscle cells was inhibited by several metabolic inhibitors, indicating that the process is dependent on metabolic activity. A modest but MATERIALS AND METHODSAnalytic and Preparative Procedures. Protein concentrations were determined by a modification of the Lowry procedure (22) using bovine serum albumin (BSA) as the standard. Lipids were extracted by the method of Bligh and Dyer (23), and mass determinations of free and esterified cholesterol were made using gas-liquid chromatography (24). Estimations of contents of isotopically labeled free and esterified cholesterol were made using TLC (25). Evaluations of the physical state of lipid inclusions were made using polarizing light microscopy (26). Free cholesterol-rich phospholipid dispersions and apo-high density lipoprotein/phosphatidylcholine acceptors were prepared as described (25

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Practical Methods for Plasma Lipoprotein Analysis1 1Work supported in part by the U.S. Atomic Energy Commission and by grants (HE06222 and FR00102) from the U.S. Public Health Service.

Cited by 1,097 publications

References 173 publications

Acquisition of Secretion of Transforming Growth Factor-β1 Leads to Autonomous Suppression of Scavenger Receptor Activity in a Monocyte-Macrophage Cell Line, THP-1

Acquisition of Secretion of Transforming Growth Factor-β1 Leads to Autonomous Suppression of Scavenger Receptor Activity in a Monocyte-Macrophage Cell Line, THP-1

Inhibition of low‐density lipoprotein oxidation by nitric oxide Potential role in atherogenesis

Development of the smooth muscle foam cell: uptake of macrophage lipid inclusions.

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