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Cited by 113Lipid metabolism and disordersCholesterol and Lipid MetabolismLipoproteins and Cardiovascular Health

The DOI matches its Crossref record; 34 of the 34 references it cites were found in a registry or an index.

Hepatic Lipase Deficiency Increases Plasma Cholesterol but Reduces Susceptibility to Atherosclerosis in Apolipoprotein E-deficient Mice

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Mezdour, Hafid, Jones, Robert, Dengremont, Catherine, Castro, Graciela, Maeda, Nobuyo·1997·Journal of Biological Chemistry
DOI 10.1074/jbc.272.21.13570
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Abstract

The effect of hepatic lipase (HL) deficiency on the susceptibility to atherosclerosis was tested using mice with combined deficiencies in HL and apoE. Mice lacking both HL and apoE (hhee) have a plasma total cholesterol of 917 +/- 252 mg/dl (n = 24), which is 184% that of mice lacking only apoE (HHee; 497 +/- 161 mg/dl, n = 20, p < 0. 001). The increase in cholesterol was mainly in beta-migrating very low density lipoproteins, although high density lipoprotein cholesterol (HDLc) was also increased (53 +/- 37 versus 20 +/- 13 mg/dl, p < 0.01). Despite the increase in plasma cholesterol, we found that HL deficiency significantly decreased aortic plaque sizes in female mice fed normal chow (31 x 10(3) +/- 22 x 10(3) microm2 in hhee versus 115 x 10(3) +/- 69 x 10(3) microm2 in HHee, p < 0.001). Reduction of plaque sizes was also observed in female heterozygous apoE-deficient mice fed an atherogenic diet (2 x 10(3) +/- 2.5 x 10(3) microm2 in hhEe versus 56 x 10(3) +/- 49 x 10(3) microm2 in HHEe, p < 0.01). Changes in aortic lesion size were not apparent in the small number of male mice studied. In HHee females, both HDLc and the capacity of high density lipoprotein (HDL) particles to promote cholesterol efflux from cultured cells were 26% of the wild type. The absence of HL in hhee females partially restored HDLc levels to 57% and cholesterol efflux to 55% of the wild type. Circulating pre-beta1-migrating HDL were present in all mutants, suggesting that there are alternative pathways in the formation of these pre-beta-HDL not involving apoE, HL, or cholesteryl ester transfer protein. The improved capacity to promote cholesterol efflux, together with increased HDL, may explain why these animals can overcome the increase in atherogenic lipoproteins.

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Crossref · 10.1074/jbc.272.21.13570

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Metadata

Authors
Mezdour, H., Jones, R., Dengremont, C., Castro, G., & Maeda, N.
Affiliations
  • University of North Carolina at Chapel Hill (US)
  • Institut Pasteur (FR)
Corresponding author
Maeda, Nobuyo
ORCID
Maeda, Nobuyo
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
1997-05
Volume
272
Issue
21
Pages
13570-13575
ISSN
0021-9258 (ISSN-L)
DOI
10.1074/jbc.272.21.13570
OpenAlex
W2071388690
Cited by
113
References
34
Citations by year
2026: 1 · 2025: 1 · 2022: 2 · 2021: 2 · 2020: 3 · 2019: 1 · 2017: 2 · 2016: 1 · 2015: 5 · 2014: 5 · 2013: 4 · 2012: 3
FWCI
6.00
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Biological Chemistry (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
National Heart, Lung, and Blood Institute (HL 42630)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
Keywords
apolipoprotein E deficiency, atherosclerosis susceptibility, serum cholesterol, HDL cholesterol, cholesterol efflux, aortic plaque, VLDL, prebeta-HDL, atherogenic diet, sex differences, cholesteryl ester transfer protein, lipoprotein metabolism, atheroprotection
MeSH terms
Animals, Apolipoproteins E, Arteries, Arteriosclerosis, Cholesterol, Electrophoresis, Agar Gel, Female, Lipase, Lipids, Lipoproteins, Lipoproteins, HDL, Liver, Male, Mice, Mutant Strains, Mice

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