Atherosclerosis Induced by Adeno-Associated Virus Encoding Gain-of-Function PCSK9

Induction of atherosclerosis in mice with one or more genetic alterations (e.g., conditional deletion of a gene of interest) has traditionally required crossbreeding with Apoe or Ldlr deficient mice to achieve sufficient hypercholesterolemia. However, this procedure is time consuming and generates a...

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Bibliographic Details
Published inMethods in molecular biology (Clifton, N.J.) Vol. 2419; p. 461
Main Authors Bjørklund, Martin Mæng, Bernal, Juan A, Bentzon, Jacob F
Format Journal Article
LanguageEnglish
Published United States 2022
Subjects
Animals
Atherosclerosis - genetics
Dependovirus - genetics
Gain of Function Mutation
Mice
Mice, Knockout
Proprotein Convertase 9 - genetics
Receptors, LDL - genetics
Adeno-associated virus
Animal models
Hypercholesterolemia
Non-germline
Atherosclerosis
PCSK9
Viral gene transfer
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Summary:Induction of atherosclerosis in mice with one or more genetic alterations (e.g., conditional deletion of a gene of interest) has traditionally required crossbreeding with Apoe or Ldlr deficient mice to achieve sufficient hypercholesterolemia. However, this procedure is time consuming and generates a surplus of mice with genotypes that are irrelevant for experiments. Several alternative methods exist that obviate the need to work in mice with germline-encoded hypercholesterolemia. In this chapter, we detail an efficient and increasingly used method to induce hypercholesterolemia in mice through adeno-associated virus-mediated transfer of the proprotein convertase subtilisin/kexin type 9 (PCSK9) gene.
ISSN:1940-6029
DOI:10.1007/978-1-0716-1924-7_27