Atherogenesis in transgenic mice expressing human apolipoprotein(a)

Richard M. Lawn, David P. Wade, Robert E Hammer, Giulia Chiesa, Judy G. Verstuyft, Edward M. Rubin

Research output: Contribution to journalArticle

239 Citations (Scopus)

Abstract

ELEVATED plasma levels of the lipoprotein Lp(a) are associated with increased risk for atherosclerosis and its manifestations, myocardial infarction, stroke and restenosis (for reviews, see refs 1-3). Lp(a) differs from low-density lipoprotein by the addition of the glycoprotein apolipoprotein(a), a homologue of plasminogen that contains many tandemly repeated units which resemble the fourth kringle domain of plasminogen, and single homologues of its kringle-5 and protease domain4. As plasma Lp(a) concentration is strongly influenced by heritable factors and is refractory to most drug and dietary manipulation, the effects of modulating it are difficult to mimic experimentally. In addition, the absence of apolipoprotein(a) from virtually all species other than primates precludes the use of convenient animal models. Here we show that transgenic mice expressing human apolipoprotein(a) are more susceptible than control mice to the development of lipid-staining lesions in the aorta, and that apolipoprotein(a) co-localizes with lipid deposition in the artery walls.

Original languageEnglish (US)
Pages (from-to)670-672
Number of pages3
JournalNature
Volume360
Issue number6405
StatePublished - Dec 17 1992

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Apoprotein(a)
Transgenic Mice
Atherosclerosis
Kringles
Plasminogen
Lipids
Lipoprotein(a)
LDL Lipoproteins
Primates
Aorta
Glycoproteins
Peptide Hydrolases
Animal Models
Arteries
Stroke
Myocardial Infarction
Staining and Labeling
Pharmaceutical Preparations

ASJC Scopus subject areas

  • General

Cite this

Lawn, R. M., Wade, D. P., Hammer, R. E., Chiesa, G., Verstuyft, J. G., & Rubin, E. M. (1992). Atherogenesis in transgenic mice expressing human apolipoprotein(a). Nature, 360(6405), 670-672.

Atherogenesis in transgenic mice expressing human apolipoprotein(a). / Lawn, Richard M.; Wade, David P.; Hammer, Robert E; Chiesa, Giulia; Verstuyft, Judy G.; Rubin, Edward M.

In: Nature, Vol. 360, No. 6405, 17.12.1992, p. 670-672.

Research output: Contribution to journalArticle

Lawn, RM, Wade, DP, Hammer, RE, Chiesa, G, Verstuyft, JG & Rubin, EM 1992, 'Atherogenesis in transgenic mice expressing human apolipoprotein(a)', Nature, vol. 360, no. 6405, pp. 670-672.
Lawn RM, Wade DP, Hammer RE, Chiesa G, Verstuyft JG, Rubin EM. Atherogenesis in transgenic mice expressing human apolipoprotein(a). Nature. 1992 Dec 17;360(6405):670-672.
Lawn, Richard M. ; Wade, David P. ; Hammer, Robert E ; Chiesa, Giulia ; Verstuyft, Judy G. ; Rubin, Edward M. / Atherogenesis in transgenic mice expressing human apolipoprotein(a). In: Nature. 1992 ; Vol. 360, No. 6405. pp. 670-672.
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AU - Rubin, Edward M.

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N2 - ELEVATED plasma levels of the lipoprotein Lp(a) are associated with increased risk for atherosclerosis and its manifestations, myocardial infarction, stroke and restenosis (for reviews, see refs 1-3). Lp(a) differs from low-density lipoprotein by the addition of the glycoprotein apolipoprotein(a), a homologue of plasminogen that contains many tandemly repeated units which resemble the fourth kringle domain of plasminogen, and single homologues of its kringle-5 and protease domain4. As plasma Lp(a) concentration is strongly influenced by heritable factors and is refractory to most drug and dietary manipulation, the effects of modulating it are difficult to mimic experimentally. In addition, the absence of apolipoprotein(a) from virtually all species other than primates precludes the use of convenient animal models. Here we show that transgenic mice expressing human apolipoprotein(a) are more susceptible than control mice to the development of lipid-staining lesions in the aorta, and that apolipoprotein(a) co-localizes with lipid deposition in the artery walls.

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