Actually not easy to do. Those little guys do not normally have elevated cholesterol levels and their arteries stay unclogged. But with a little genetic engineering you can knockout the gene for the protein apolipoprotein E, which plays a role in clearing bad cholesterol – LDL – from the blood. The result is high levels of blood plasma cholesterol and the development of plaques that block coronary arteries. Why would you want to do this to a mouse? Well, Dr. Jonathan Smith of the Lerner Research Institute of the Cleveland Clinic is using these mice as a model to identify additional genes that are involved in atherosclerosis. He recently visited my Anatomy and Physiology class to tell us about this work. OK, the visit was two weeks ago. I have just been a lazy blogger.
When these mice prone to atherosclerosis are bred to other mouse strains the offspring show different susceptibilities to developing arterial plaques. This suggests that other allelic variants (versions of genes) in these different strains influence plaque development. Quantitative trait locus mapping can then be used to identify variations in regions of the mouse chromosome that are correlated with increased amounts of atherosclerotic lesions. This may sound like genomic mumbo-jumbo, but it is an amazing way to relatively quickly identify putative chromosome regions that influence this disease. Now they have to find the specific genes.
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