Apo E knockout atherosclerotic mice
The Apolipoprotein E knockout mouse model is one of the most widely used experimental model of atherosclerosis. These mice rapidly develop atherosclerotic lesions that resemble human lesions evolving over time from initial fatty streaks to complex lesions.
- Apolipoprotein E deficiency directly results in the increase of plasma levels of LDL and VLDL.
Spontaneous development of atherosclerotic lesions throughout the arterial tree appearing first in the aortic arch in young mice and progressing in the thoracic and abdominal aorta in older mice, which can be further accelerated by a lipid-rich diet or type I diabetes induction by streptozotocin (cf. Links to applicable therapeutic areas / targeted disorders: Streptozotocin-induced diabetic rats/mice (STZ) (figure 1).
- Vascular endothelial dysfunction
|Figure 1: En face preparations of oil red O stained aortas from C57BL6/J and ApoE KO mice at 26 weeks of age (from Behr-Roussel et. Al, 2006).|
Erectile function features
- Erectile dysfunction from 26 weeks of age in ApoE KO mice fed a lipid-rich diet from 4 weeks of age (figure 2).
In ApoE KO mice, the development of atherosclerosis can be accelerated by a lipid-enriched Western-diet. Age-matched C57BL6/J mice fed with standard mouse chow are used as control mice.
J Sex Med (2006) : 3(4):596-603
Links to applicable Experimental skills