Europe PMC
Nothing Special   »   [go: up one dir, main page]

Europe PMC requires Javascript to function effectively.

Either your web browser doesn't support Javascript or it is currently turned off. In the latter case, please turn on Javascript support in your web browser and reload this page.

This website requires cookies, and the limited processing of your personal data in order to function. By using the site you are agreeing to this as outlined in our privacy notice and cookie policy.

Susceptibility to atherosclerosis in mice expressing exclusively apolipoprotein B48 or apolipoprotein B100.

Author information

Affiliations

  • 1. Gladstone Institute of Cardiovascular Disease, San Francisco, California 94141-9100, USA.
      Authors
    • Véniant MM 1
    (1 author)

ORCIDs linked to this article

The Journal of Clinical Investigation, 01 Jul 1997, 100(1):180-188
https://doi.org/10.1172/jci119511 PMID: 9202070 PMCID: PMC508178

Free full text in Europe PMC

Abstract 

All classes of lipoproteins considered to be atherogenic contain apo-B100 or apo-B48. However, there is a distinct paucity of data regarding whether lipoproteins containing apo-B48 or apo-B100 differ in their intrinsic ability to promote the development of atherosclerosis. To address this issue, we compared the extent of atherosclerosis in three groups of animals: apo-E-deficient mice (apo-B+/+apo-E-/-) and apo-E-deficient mice that synthesize exclusively either apo-B48 (apo-B48/48apo-E-/-) or apo-B100 (apo-B100/100apo-E-/-). Mice (n = 25 in each group) were fed a chow diet for 200 days, and plasma lipid levels were assessed throughout the study. Compared with the levels in apo-B+/+apo-E-/- mice, the total plasma cholesterol levels were higher in the apo-B48/48apo-E-/- mice and were lower in the apo-B100/100apo-E-/- mice. However, the ranges of cholesterol levels in the three groups overlapped. Compared with those in the apo-B+/+apo-E-/- mice, atherosclerotic lesions were more extensive in the apo-B48/48apo-E-/- mice and less extensive in the apo-B100/100apo-E-/- mice. Once again, however, there was overlap among the three groups. The extent of atherosclerosis in each group of mice correlated significantly with plasma cholesterol levels. In mice from different groups that had similar cholesterol levels, the extent of atherosclerosis was quite similar. Thus, susceptibility to atherosclerosis was dependent on total cholesterol levels. Whether mice synthesized apo-B48 or apo-B100 did not appear to have an independent effect on susceptibility to atherosclerosis.

Free full text 

Logo of jcinvestThe Journal of Clinical Investigation
J Clin Invest. 1997 Jul 1; 100(1): 180–188.
PMCID: PMC508178
PMID: 9202070

Susceptibility to atherosclerosis in mice expressing exclusively apolipoprotein B48 or apolipoprotein B100.

M M Véniant, V Pierotti, D Newland, C M Cham, D A Sanan, R L Walzem, and S G Young
Author information Copyright and License information Disclaimer

Abstract

All classes of lipoproteins considered to be atherogenic contain apo-B100 or apo-B48. However, there is a distinct paucity of data regarding whether lipoproteins containing apo-B48 or apo-B100 differ in their intrinsic ability to promote the development of atherosclerosis. To address this issue, we compared the extent of atherosclerosis in three groups of animals: apo-E-deficient mice (apo-B+/+apo-E-/-) and apo-E-deficient mice that synthesize exclusively either apo-B48 (apo-B48/48apo-E-/-) or apo-B100 (apo-B100/100apo-E-/-). Mice (n = 25 in each group) were fed a chow diet for 200 days, and plasma lipid levels were assessed throughout the study. Compared with the levels in apo-B+/+apo-E-/- mice, the total plasma cholesterol levels were higher in the apo-B48/48apo-E-/- mice and were lower in the apo-B100/100apo-E-/- mice. However, the ranges of cholesterol levels in the three groups overlapped. Compared with those in the apo-B+/+apo-E-/- mice, atherosclerotic lesions were more extensive in the apo-B48/48apo-E-/- mice and less extensive in the apo-B100/100apo-E-/- mice. Once again, however, there was overlap among the three groups. The extent of atherosclerosis in each group of mice correlated significantly with plasma cholesterol levels. In mice from different groups that had similar cholesterol levels, the extent of atherosclerosis was quite similar. Thus, susceptibility to atherosclerosis was dependent on total cholesterol levels. Whether mice synthesized apo-B48 or apo-B100 did not appear to have an independent effect on susceptibility to atherosclerosis.

Full Text

The Full Text of this article is available as a PDF (329K).

Selected References

These references are in PubMed. This may not be the complete list of references from this article.
  • Young SG. Recent progress in understanding apolipoprotein B. Circulation. 1990 Nov;82(5):1574–1594. [Abstract] [Google Scholar]
  • Nielsen LB, Stender S, Jauhiainen M, Nordestgaard BG. Preferential influx and decreased fractional loss of lipoprotein(a) in atherosclerotic compared with nonlesioned rabbit aorta. J Clin Invest. 1996 Jul 15;98(2):563–571. [Europe PMC free article] [Abstract] [Google Scholar]
  • Steinberg D, Parthasarathy S, Carew TE, Khoo JC, Witztum JL. Beyond cholesterol. Modifications of low-density lipoprotein that increase its atherogenicity. N Engl J Med. 1989 Apr 6;320(14):915–924. [Abstract] [Google Scholar]
  • Henriksen T, Mahoney EM, Steinberg D. Enhanced macrophage degradation of low density lipoprotein previously incubated with cultured endothelial cells: recognition by receptors for acetylated low density lipoproteins. Proc Natl Acad Sci U S A. 1981 Oct;78(10):6499–6503. [Europe PMC free article] [Abstract] [Google Scholar]
  • Quinn MT, Parthasarathy S, Steinberg D. Endothelial cell-derived chemotactic activity for mouse peritoneal macrophages and the effects of modified forms of low density lipoprotein. Proc Natl Acad Sci U S A. 1985 Sep;82(17):5949–5953. [Europe PMC free article] [Abstract] [Google Scholar]
  • Cushing SD, Berliner JA, Valente AJ, Territo MC, Navab M, Parhami F, Gerrity R, Schwartz CJ, Fogelman AM. Minimally modified low density lipoprotein induces monocyte chemotactic protein 1 in human endothelial cells and smooth muscle cells. Proc Natl Acad Sci U S A. 1990 Jul;87(13):5134–5138. [Europe PMC free article] [Abstract] [Google Scholar]
  • Weisgraber KH, Rall SC., Jr Human apolipoprotein B-100 heparin-binding sites. J Biol Chem. 1987 Aug 15;262(23):11097–11103. [Abstract] [Google Scholar]
  • Zilversmit DB. Atherogenesis: a postprandial phenomenon. Circulation. 1979 Sep;60(3):473–485. [Abstract] [Google Scholar]
  • Mahley RW. The role of dietary fat and cholesterol in atherosclerosis and lipoprotein metabolism. West J Med. 1981 Jan;134(1):34–42. [Europe PMC free article] [Abstract] [Google Scholar]
  • Bergeron N, Havel RJ. Prolonged postprandial responses of lipids and apolipoproteins in triglyceride-rich lipoproteins of individuals expressing an apolipoprotein epsilon 4 allele. J Clin Invest. 1996 Jan 1;97(1):65–72. [Europe PMC free article] [Abstract] [Google Scholar]
  • Purcell-Huynh DA, Farese RV, Jr, Johnson DF, Flynn LM, Pierotti V, Newland DL, Linton MF, Sanan DA, Young SG. Transgenic mice expressing high levels of human apolipoprotein B develop severe atherosclerotic lesions in response to a high-fat diet. J Clin Invest. 1995 May;95(5):2246–2257. [Europe PMC free article] [Abstract] [Google Scholar]
  • Callow MJ, Verstuyft J, Tangirala R, Palinski W, Rubin EM. Atherogenesis in transgenic mice with human apolipoprotein B and lipoprotein (a). J Clin Invest. 1995 Sep;96(3):1639–1646. [Europe PMC free article] [Abstract] [Google Scholar]
  • Nakashima Y, Plump AS, Raines EW, Breslow JL, Ross R. ApoE-deficient mice develop lesions of all phases of atherosclerosis throughout the arterial tree. Arterioscler Thromb. 1994 Jan;14(1):133–140. [Abstract] [Google Scholar]
  • Reddick RL, Zhang SH, Maeda N. Atherosclerosis in mice lacking apo E. Evaluation of lesional development and progression. Arterioscler Thromb. 1994 Jan;14(1):141–147. [Abstract] [Google Scholar]
  • Ishibashi S, Goldstein JL, Brown MS, Herz J, Burns DK. Massive xanthomatosis and atherosclerosis in cholesterol-fed low density lipoprotein receptor-negative mice. J Clin Invest. 1994 May;93(5):1885–1893. [Europe PMC free article] [Abstract] [Google Scholar]
  • Purcell-Huynh DA, Weinreb A, Castellani LW, Mehrabian M, Doolittle MH, Lusis AJ. Genetic factors in lipoprotein metabolism. Analysis of a genetic cross between inbred mouse strains NZB/BINJ and SM/J using a complete linkage map approach. J Clin Invest. 1995 Oct;96(4):1845–1858. [Europe PMC free article] [Abstract] [Google Scholar]
  • Farese RV, Jr, Véniant MM, Cham CM, Flynn LM, Pierotti V, Loring JF, Traber M, Ruland S, Stokowski RS, Huszar D, et al. Phenotypic analysis of mice expressing exclusively apolipoprotein B48 or apolipoprotein B100. Proc Natl Acad Sci U S A. 1996 Jun 25;93(13):6393–6398. [Europe PMC free article] [Abstract] [Google Scholar]
  • Piedrahita JA, Zhang SH, Hagaman JR, Oliver PM, Maeda N. Generation of mice carrying a mutant apolipoprotein E gene inactivated by gene targeting in embryonic stem cells. Proc Natl Acad Sci U S A. 1992 May 15;89(10):4471–4475. [Europe PMC free article] [Abstract] [Google Scholar]
  • McCormick SP, Ng JK, Véniant M, Borén J, Pierotti V, Flynn LM, Grass DS, ConnollyA, Young SG. Transgenic mice that overexpress mouse apolipoprotein B. Evidence that the DNA sequences controlling intestinal expression of the apolipoprotein B gene are distant from the structural gene. J Biol Chem. 1996 May 17;271(20):11963–11970. [Abstract] [Google Scholar]
  • Farese RV, Jr, Ruland SL, Flynn LM, Stokowski RP, Young SG. Knockout of the mouse apolipoprotein B gene results in embryonic lethality in homozygotes and protection against diet-induced hypercholesterolemia in heterozygotes. Proc Natl Acad Sci U S A. 1995 Feb 28;92(5):1774–1778. [Europe PMC free article] [Abstract] [Google Scholar]
  • Walzem RL, Davis PA, Hansen RJ. Overfeeding increases very low density lipoprotein diameter and causes the appearance of a unique lipoprotein particle in association with failed yolk deposition. J Lipid Res. 1994 Aug;35(8):1354–1366. [Abstract] [Google Scholar]
  • Forte T, Nichols AV. Application of electron microscopy to the study of plasma lipoprotein structure. Adv Lipid Res. 1972;10:1–41. [Abstract] [Google Scholar]
  • Castle CK, Colca JR, Melchior GW. Lipoprotein profile characterization of the KKA(y) mouse, a rodent model of type II diabetes, before and after treatment with the insulin-sensitizing agent pioglitazone. Arterioscler Thromb. 1993 Feb;13(2):302–309. [Abstract] [Google Scholar]
  • Tangirala RK, Rubin EM, Palinski W. Quantitation of atherosclerosis in murine models: correlation between lesions in the aortic origin and in the entire aorta, and differences in the extent of lesions between sexes in LDL receptor-deficient and apolipoprotein E-deficient mice. J Lipid Res. 1995 Nov;36(11):2320–2328. [Abstract] [Google Scholar]
  • Paigen B, Morrow A, Brandon C, Mitchell D, Holmes P. Variation in susceptibility to atherosclerosis among inbred strains of mice. Atherosclerosis. 1985 Oct;57(1):65–73. [Abstract] [Google Scholar]
  • Paigen B, Ishida BY, Verstuyft J, Winters RB, Albee D. Atherosclerosis susceptibility differences among progenitors of recombinant inbred strains of mice. Arteriosclerosis. 1990 Mar-Apr;10(2):316–323. [Abstract] [Google Scholar]
  • Krul ES, Tikkanen MJ, Cole TG, Davie JM, Schonfeld G. Roles of apolipoproteins B and E in the cellular binding of very low density lipoproteins. J Clin Invest. 1985 Feb;75(2):361–369. [Europe PMC free article] [Abstract] [Google Scholar]
  • Ishibashi S, Brown MS, Goldstein JL, Gerard RD, Hammer RE, Herz J. Hypercholesterolemia in low density lipoprotein receptor knockout mice and its reversal by adenovirus-mediated gene delivery. J Clin Invest. 1993 Aug;92(2):883–893. [Europe PMC free article] [Abstract] [Google Scholar]
  • Ishibashi S, Herz J, Maeda N, Goldstein JL, Brown MS. The two-receptor model of lipoprotein clearance: tests of the hypothesis in "knockout" mice lacking the low density lipoprotein receptor, apolipoprotein E, or both proteins. Proc Natl Acad Sci U S A. 1994 May 10;91(10):4431–4435. [Europe PMC free article] [Abstract] [Google Scholar]
  • Hirano K, Young SG, Farese RV, Jr, Ng J, Sande E, Warburton C, Powell-Braxton LM, Davidson NO. Targeted disruption of the mouse apobec-1 gene abolishes apolipoprotein B mRNA editing and eliminates apolipoprotein B48. J Biol Chem. 1996 Apr 26;271(17):9887–9890. [Abstract] [Google Scholar]
Articles from The Journal of Clinical Investigation are provided here courtesy of American Society for Clinical Investigation

Full text links 

Read article at publisher's site: https://doi.org/10.1172/jci119511

Read article for free, from open access legal sources, via Unpaywall: http://www.jci.org/articles/view/119511/files/pdfUnpaywall

Citations & impact 

Impact metrics

66
Citations
Jump to Citations
12
Data citations
Jump to Data

Citations of article over time

Alternative metrics

Altmetric item for https://www.altmetric.com/details/36915494
Altmetric
Discover the attention surrounding your research
https://www.altmetric.com/details/36915494

Smart citations by scite.ai
Smart citations by scite.ai include citation statements extracted from the full text of the citing article. The number of the statements may be higher than the number of citations provided by EuropePMC if one paper cites another multiple times or lower if scite has not yet processed some of the citing articles.
Explore citation contexts and check if this article has been supported or disputed.
https://scite.ai/reports/10.1172/jci119511

Supporting
Mentioning
Contrasting
3
80
1

Article citations

Go to all (66) article citations

Data 

Similar Articles 

To arrive at the top five similar articles we use a word-weighted algorithm to compare words from the Title and Abstract of each citation.

Funding 

Funders who supported this work.

NHLBI NIH HHS (1)