B6J-Apoe KO Mouse

Apolipoprotein E (ApoE) is a lipid particle-associated polymorphic carrier protein encoded by the APOE gene. It is a core component of plasma lipoproteins, participating in the production, transport, and clearance of lipoproteins. ApoE is associated with chylomicrons, chylomicron remnants, high-density lipoprotein (HDL), very low-density lipoprotein (VLDL), and intermediate-density lipoprotein (IDL), especially showing preferential binding to HDL ^[1]. ApoE is the most important lipid transport protein in the body, having a profound impact on lipid metabolism. The interaction of ApoE with the low-density lipoprotein receptor (LDLR) is essential for the normal processing (catabolism) of triglyceride-rich lipoproteins ^[2]. In peripheral tissues, ApoE is primarily produced by the liver and macrophages and mediates cholesterol metabolism. In the central nervous system, ApoE is produced mainly by astrocytes and is the major cholesterol carrier in the brain. ApoE is essential for transporting cholesterol from astrocytes to neurons ^[1-4]. In addition, ApoE forms a complex with activated C1q, becoming a checkpoint inhibitor target of the classical complement pathway ^[5]. Polymorphisms of the APOE are associated with Alzheimer's disease and lipid accumulation, hyperlipidemia, atherosclerosis, high cholesterolemia, etc., and are related to the risk of various cardiovascular diseases.

The B6J-Apoe KO mouse is a model of ApoE deficiency. It was generated by gene editing technology to knock out the Apoe gene in mice. ApoE protein synthesis is blocked in these mice, leading to elevated cholesterol levels and spontaneous atherosclerosis. Cholesterol levels and atherosclerosis in mice fed a high-fat diet (HFD) are further exacerbated. The B6J-Apoe KO mice are viable and can be used for research in hypercholesterolemia, atherosclerosis, and Alzheimer's disease.