Quantification of apolipoprotein B in grossly normal human aorta.

Hoff, Hans; Heideman, Carol L.; Gaubatz, John W.; Gotto, Antonio M.; Erickson, Ethel E.; Jackson, Richard L.

doi:10.1161/01.res.40.1.56

Cited by 50 publications

(23 citation statements)

References 32 publications

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“…Oxidatively truncated phosphatidylcholines (PCs), which are generated through the autoxidation of polyunsaturated diacyl PCs, exhibit diverse and important biological activities. For example, atherosclerosis is a chronic inflammatory disease (1), and mounting evidence suggests that the oxidation of LDL plays a major role throughout the development and progression of the inflammatory process (2)(3)(4)(5). LDL can be oxidatively modified to a form that can be recognized by macrophage scavenger receptors, which are expressed by each of the three major cell Abbreviations: AA, arachidonic acid; A-PAF, 1-O-hexadecyl-2-azeleylsn-glycero-3-phosphatidylcholine; AA-PAF, 1-O-hexadecyl-2-arachidonoylsn-3-phosphatidylcholine; CEP, carboxyethylpyrrole; DHA, docosahexaenoic acid; DHA-PAF, 1-O-hexadecyl-2-docosahexaenoyl-sn-3-phosphatidylcholine; G-PAF, 1-O-hexadecyl-2-glutaroyl-sn-glycero-3-phosphatidylcholine; HDdiA-PAF, 1-O-hexadecyl-2-(11-carboxy-9-hydroxyundec-10-enoyl)-sn-glycero-3-phosphatidylcholine; HHdiA-PAF, 1-O-hexadecyl-2-(7-carboxy-4-hydroxyhex-5-enoyl)-sn-glycero-3-phosphatidylcholine; HODA-PAF, 1-O-hexadecyl-2-(9-hydroxy-12-oxododec-10-enoyl)-sn-glycero-3-phosphatidylcholine; HOdiA-PAF, 1-O-hexadecyl-2-(5-hydroxy-7-carboxyhept-6-enoyl)-sn-glycero-3-phosphatidylcholine; HOHA-PAF, 1-Ohexadecyl-2-(4-hydroxy-7-oxohept-5-enoyl)-sn-glycero-3-phosphatidylcholine; HOOA-PAF, 1-O-hexadecyl-2-(5-hydroxy-8-oxooct-6-enoyl)-snglycero-3-phosphatidylcholine; KDdiA-PAF, 1-O-hexadecyl-2-(11-carboxy-9-oxoundec-10-enoyl)-sn-glycero-3-phosphatidylcholine; KHdiA-PAF, 1-Ohexadecyl-2-(6-carboxy-4-oxohex-5-enoyl)-sn-glycero-3-phosphatidylcholine; KODA-PAF, 1-O -hexadecyl-2-(9-oxo-12-oxododec-10-enoyl)-snglycero-3-phosphatidylcholine; KOdiA-PAF, 1-O-hexadecyl-2-(7-carboxy-5-oxohep-6-enoyl)-sn-glycero-3-phosphatidylcholine; KOHA-PAF, 1-Ohexadecyl-2-(4-oxo-7-oxohept-5-enoyl)-sn-glycero-3-phosphatidylcholine; KOOA-PAF, 1-O-hexadecyl-2-(5-oxo-8-oxooct-6-enoyl)-sn-glycero-3-phosphatidylcholine; LA, linoleic acid; LA-PAF, 1-O-hexadecyl-2-linoleoyl-snglycero-3-phosphatidylcholine; LA-PC, linoleic acid ester of 2-lysophosphatidylcholine; lyso-PAF, 1-alkyl-2-hydroxy-sn-glycero-3-phosphocholine; MPO, myeloperoxidase; MRM, multiple reaction monitoring; OB-PAF, 1-O -hexadecyl-2-(4-oxobutyroyl)-sn-glycero-3-phosphatidylcholine; ON-PAF, 1-O-hexadecyl-2-(9-oxononanoyl)-sn-glycero-3-phosphatidylcholine; OV-PAF, 1-O-hexadecyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphatidylcholine; OxLDL, oxidized low density lipoprotein; OxPAF, oxidatively truncated alkylacylphosphatidylcholine; OxPC, oxidatively truncated diacylphosphatidylcholine; PAF, platelet-activating factor; PAFR, plateletactivating factor receptor; PC, phosphatidylcholine; S-PAF, 1-O-hexadecyl-2-succinoyl-sn-glycero-3-phosphatidylcholine; SUV, small unilamellar vesicle.…”

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confidence: 99%

Polyunsaturated phospholipids promote the oxidation and fragmentation of γ-hydroxyalkenals: formation and reactions of oxidatively truncated ether phospholipids

Chen

Zhang²,

Laird³

et al. 2008

Journal of Lipid Research

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Low density lipoprotein contains traces of biologically active platelet-activating factor (PAF)-like ether phosphatidylcholines (PCs). These oxidatively truncated alkylacylphosphatidylcholines (OxPAFs) are presumably formed through the oxidative truncation of 1-alkyl-2-polyunsaturated fatty acyl PCs. We now report that a diverse structural variety of OxPAFs are generated in small unilamellar vesicles (SUVs) upon myeloperoxidase (MPO)-promoted autoxidation of ether PCs that incorporate linoleoyl, arachidonyl, or docosahexaenoyl groups at the sn-2 position. Total syntheses are reported that confirm the identities of the new OxPAFs and will facilitate the evaluation of their biologically important chemistry and activities. Especially noteworthy is the formation of OxPAFs containing g-hydroxyalkenal functionality. Analogous oxidatively truncated diacylphosphatidylcholines are biologically important because they and their more oxidized derivatives are strong ligands for the scavenger receptor CD36. Furthermore, their covalent adduction with proteins can interfere with protein function or generate biologically active carboxyalkylpyrrole derivatives. We now find a profound influence of membrane composition on the stability of OxPAFs. In the presence of a polyunsaturated diacyl PC, the linoleic acid ester of 2-lysophosphatidylcholine, MPO induces the oxidation of aldehydes to carboxylic acids and the further oxidative truncation of g-hydroxyalkenals. Remarkably, these reactions do not occur readily with MPO in SUVs composed entirely of saturated diacyl-PCs. A mechanistic rationale is presented that can account for this dichotomy.-Chen, X., W. Zhang, J. Laird, S. L. Hazen, and R. G. Salomon. Polyunsaturated phospholipids promote the oxidation and fragmentation of g-hydroxyalkenals: formation and reactions of oxidatively truncated ether phospholipids. J. Lipid Res. 2008. 49: 832-846.

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confidence: 99%

Polyunsaturated phospholipids promote the oxidation and fragmentation of γ-hydroxyalkenals: formation and reactions of oxidatively truncated ether phospholipids

Chen

Zhang²,

Laird³

et al. 2008

Journal of Lipid Research

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“…They were appreciably lower than those found in the intimal lining of grossly normal human aortas. 21 This is perhaps not surprising for a number of reasons: (1) only the intimal lining was used in the aorta" in contrast to the total vessel in intracranial arteries. The tunica media has been shown in grossly normal arteries not to contain apoB, both by histochemical 17 " 20 and quantitative techniques.…”

Section: Discussionmentioning

confidence: 99%

“…16 We have utilized the immunological reactivity of apoB as a marker for these lipoproteins in immunofluorescence studies to determine the apoB localization in both normal and atherosclerotic regions of aortic, coronary, as well as intracranial artery beds."" 20 Since immunofluorescence procedures are only qualitative, we have used an electro-immunoassay or "rocket" technique 21 …”

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confidence: 99%

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Apolipoprotein B (apoB) retention in atherosclerotic intracranial arteries.

Hoff¹,

Heideman²,

Gaubatz³

1977

Stroke

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SUMMARY Low (LDL) and very low (VLDL) density lipoproteins retained in grossly normal and atherosclerotic human intracranial arteries have been quantitated using an electro-immunoassay directed against apolipoprotein B (apoB), the major protein of these two lipoprotein fractions. Buffer-homogenales of grossly normal arteries contained apoB amounts ranging from < 0.04 to 1.58 Mg/mg tissue dry weight, while those of atherosclerotic plaques gave values ranging from 0.80 to 3.9 ng per mg tissue dry weight. These results were consistent with immunofluorescence studies localizing apoB in these arteries. Plaques also contained a remaining fraction of tightly-bound apoB as evidenced by positive immunofluorescence in sections of pellets from buffer homogenates. This was in contrast to the negative results from grossly normal arteries. These results would suggest that retention of apoB by intracranial arteries correlates positively with vessel lesions. Arterial apoB is present in both grossly normal regions and plaques in a loosely-bound form, possibly representing intact lipoprotein. ApoB is also present in a tightlybound form in plaques.

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“…The intimal lining of each aortic specimen was stripped from the underlying tunica media, and the intima was used for preparation of extracts as previously described. 16 ' 17 All operations were carried out at 4°C. Tissues were finely minced, and aliquots were weighed and placed in 1:1 or 1:2 (v/w) cold homogenization buffer (0.13 M Tris-HCI, 0.1% sodium EDTA, and 0.01% sodium azide at pH 7.4).…”

Section: Tissue Extractsmentioning

confidence: 99%

Stimulation of cholesteryl ester synthesis in macrophages by extracts of atherosclerotic human aortas and complexes of albumin/cholesteryl esters.

Goldstein¹,

Hoff²,

Ho³

et al. 1981

Arteriosclerosis

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100

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This research was supported by research Grants HL 20948 and NS 09287 from the National Institutes of Health. Dr. Hoff was an Established Investigator of the American Heart Association.Address This sequence of uptake, hydrolysis, and reesterification occurs when macrophages are incubated with LDL that has been rendered polyanionic by chemical derivitization, such as by maleylation 57 or by reaction with malondialdehyde, 7 " 9 in addition to acetylation. 5 ' 9 A similar uptake can be triggered by allowing LDL to form complexes with certain sulfated polysaccharides, such as dextran sulfate, which bind to the macrophage surface. 10 The only unmodified plasma lipoproteins known to be recognized directly by mouse peritoneal macrophages are the ^-migrating very low density lipoproteins (fr-VLDL) that accumulate in the plasma of cholesterol-fed animals."• 12 The /8-VLDL bind to a discrete class of macrophage receptors that are distinct from the ones that bind polyanions. The intracellular metabolism of /3-VLDL is the same as that of acetyl-LDL, i.e., lysosomal hydrolysis followed by cytoplasmic re-esterification. These studies raise the question as to whether any of the cholesteryl ester present in human atherosclerotic plaque is in a form recognized and taken up by macrophages. Hoff et al. 13 and Hollander et al.14 have shown that cholesterol-rich particles can be extracted from human atherosclerotic plaque after vigorous homogenization. Some of this extracted cholesterol is found in the form of large lipid/protein complexes that appear in the void volume of a Bio-Gel A-150 m column. Another portion of the cholesterol is found in particles in the molecular weight range of 3 X 10 6 as determined by gel filtration and electron microscopy (Gaubatz and Hoff, unpublished data). 13 These particles, which are about the same size as plasma LDL, are reactive with an antibody directed against apoprotein B (apo-B), the major protein component of plasma LDL. By sodium dodecyl sulfate polyacrylamide gel electrophoresis, the protein component of these aortic LDL-like particles migrates similarly to apo-B.13 In contrast to plasma LDL, these aortic particles have an enhanced mobility on agarose gel electrophoresis, suggesting an increased negative charge (Gaubatz and Hoff, unpublished data). '14 Woodard et al. 18 and Srinivasan et al. 19have isolated lipoprotein/glycosaminoglycan complexes from human atheroma. These complexes are excluded in the void volume of a BioGel A-50 m column and float in the ultracentrifuge in the density range of 1.006-1.063 g/ml. 19Our current studies were undertaken to determine whether any of the cholesteryl ester/protein complexes extracted from human aortas are taken up efficiently by mouse peritoneal macrophages. As an index of uptake, we measured the ability of the aortic extracts to increase the rate at which the macrophages incorporate [ 11 ' 12 The current results show that the cholesteryl ester of aortic extracts is in a form that is susceptible to rapid uptake by macrophages. Rapid uptake is obse...

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Quantification of apolipoprotein B in grossly normal human aorta.

Cited by 50 publications

References 32 publications

Polyunsaturated phospholipids promote the oxidation and fragmentation of γ-hydroxyalkenals: formation and reactions of oxidatively truncated ether phospholipids

Polyunsaturated phospholipids promote the oxidation and fragmentation of γ-hydroxyalkenals: formation and reactions of oxidatively truncated ether phospholipids

Apolipoprotein B (apoB) retention in atherosclerotic intracranial arteries.

Stimulation of cholesteryl ester synthesis in macrophages by extracts of atherosclerotic human aortas and complexes of albumin/cholesteryl esters.

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