Atherosclerosis Mouse Model (Gene-editing)

Apoe and Ldlr gene knockout (KO) mice can spontaneously form atherosclerotic plaques and are widely used in atherosclerosis (AS) studies.

1. ApoE Knockout Mice

The Apolipoprotein E-deficient (apoEKO) mice, as a model of spontaneously developed atherosclerosis, are most similar to the human atherosclerosis process. ApoE is a component of very low-density lipoprotein (VLDL) and high-density lipoprotein (HDL), and is involved in the cholesterol transport. Contrary to human lipoprotein profile, mice have higher level of HDL but lower low-density lipoprotein (LDL), and mice carry most of their cholesterol in HDL. Cholesterol of apoEKO mice is largely distributed in VLDL, and high amounts of cholesterol it carries cannot be bound by lipoprotein receptors on the cell surface and degraded, resulting in accumulation and atherosclerosis. Studies have shown that ApoE^-/- mice can spontaneously develop hypercholesterolemia (300-500 mg/dL), and significant atherosclerotic lesions under normal diet conditions. The high-cholesterol/high-fat (HCHF) atherogenic diet will increase the plasma cholesterol level by more than 1000 mg/dL and accelerate the atherosclerosis process. The level of triacylglycerol in the plasma of ApoE^-/- mice is 68% higher than that of normal mice, regardless age and gender, while its high-density lipoprotein (HDL) is only 45% of normal mice. The lesions of ApoE^-/- mice mainly occur in the aortic root, aortic arch, innominate artery, aortic branch and renal artery bifurcation. Under normal diet conditions, early foam cell lesions can occur within 10 weeks, and developed into atherosclerotic lesions after 15 weeks, and advanced fibrosis after 20 weeks. A high-cholesterol/high-fat (HCHF) diet can accelerate the atherosclerosis process., including the formation of cholesterol crystals, necrotic cores, and calcifications.

Health Standard: SPF

2. LDLR Gene Knockout Mice

Low density lipoprotein receptor (LDLR) gene knockout (KO) mice are currently one of the most popular genetically engineered animal models in atherosclerosis (AS) research. LDLR knockout mice can hardly absorb low density lipoprotein (LDL), which leads to chronic high levels of LDL in the plasma, promoting the process of lipid infiltration and inducing atherosclerosis. Researchers discovered infiltration of mast cells is the vital step in the process of atherosclerosis inflammatory reaction by studying Ldlr^-/- mice - as either the removal of mast cells or the degranulation of a mast cells can significantly reduce the formation of atherosclerosis. This research is of great significance to the prevention and treatment of atherosclerosis.

Detection Items: Body weight, food intake, serum biochemical test or ELISA test, morphology of aortic arch pathology (Arterial Tissues H&E staining, oil red, measure the area proportion of plaque in artery intima and Cross Section)

3. Other Genetically Modified Mouse Models Related to Atherosclerosis Research