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 language | English (US) |
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Pages (from-to) | 1911-1916 |
Number of pages | 6 |
Journal | Arteriosclerosis, thrombosis, and vascular biology |
Volume | 15 |
Issue number | 11 |
DOIs | |
State | Published - Nov 1995 |
Keywords
- apo(a)
- atherosclerosis
- lipoprotein(a)
- transgenic mice
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine