Relative contributions of apolipoprotein(a) and apolipoprotein-B to the development of fatty lesions in the proximal aorta of mice

F. P. Mancini, D. L. Newland, V. Mooser, J. Murata, S. Marcovina, S. G. Young, Robert E Hammer, D. A. Sanan, Helen H Hobbs

Research output: Contribution to journalArticlepeer-review

42 Scopus citations

Abstract

Transgenic mice expressing transgenes for both human apolipoprotein B-100 (h-apoB) and apolipoprotein(a) [apo(a)] were fed a high-fat, atherogenic diet for 14 weeks to examine the effect of lipoprotein(a) [Lp(a)] on the development of aortic rally lesions. The extent of lesions in the proximal region of the aorta of Lp(a) mice was measured by use of a computer-assisted image analysis of 20 sections per animal and compared with that of nontransgenic mice as well as mice expressing either the apo(a) or h-apoB transgene. The control (n=23) and apo(a) (n=22) transgenic mice had very small mean lesion areas (607 versus 128 μm2 per section). The h-apoB- expressing mice (n=20) had significantly higher mean lesion areas (3288 μm2 per section) than either the control or apo(a) transgenic animals. Coexpression of apo(a) and h-apoB transgenes resulted in only a modest increase in lesion area (4678 μm2 per section, n=19). Thus, the expression of human apo(a) in C57BL/6/SJL hybrid mice fed an atherogenic diet failed to significantly potentiate the development of aortic fatty lesions in the absence or presence of high levels of h-apoB.

Original languageEnglish (US)
Pages (from-to)1911-1916
Number of pages6
JournalArteriosclerosis, thrombosis, and vascular biology
Volume15
Issue number11
DOIs
StatePublished - Nov 1995

Keywords

  • apo(a)
  • atherosclerosis
  • lipoprotein(a)
  • transgenic mice

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Fingerprint Dive into the research topics of 'Relative contributions of apolipoprotein(a) and apolipoprotein-B to the development of fatty lesions in the proximal aorta of mice'. Together they form a unique fingerprint.

Cite this