CRISPR-Cas9 Targeting of PCSK9 in Human Hepatocytes In Vivo-Brief Report

Arterioscler Thromb Vasc Biol. 2016 May;36(5):783-6. doi: 10.1161/ATVBAHA.116.307227. Epub 2016 Mar 3.

Abstract

Objective: Although early proof-of-concept studies of somatic in vivo genome editing of the mouse ortholog of proprotein convertase subtilisin/kexin type 9 (Pcsk9) in mice have established its therapeutic potential for the prevention of cardiovascular disease, the unique nature of genome-editing technology-permanent alteration of genomic DNA sequences-mandates that it be tested in vivo against human genes in normal human cells with human genomes to give reliable preclinical insights into the efficacy (on-target mutagenesis) and safety (lack of off-target mutagenesis) of genome-editing therapy before it can be used in patients.

Approach and results: We used a clustered regularly interspaced short palindromic repeats (CRISPR)-CRISPR-associated (Cas) 9 genome-editing system to target the human PCSK9 gene in chimeric liver-humanized mice bearing human hepatocytes. We demonstrated high on-target mutagenesis (approaching 50%), greatly reduced blood levels of human PCSK9 protein, and minimal off-target mutagenesis.

Conclusions: This work yields important information on the efficacy and safety of CRISPR-Cas9 therapy targeting the human PCSK9 gene in human hepatocytes in vivo, and it establishes humanized mice as a useful platform for the preclinical assessment of applications of somatic in vivo genome editing.

Keywords: gene therapy; liver; molecular biology; mutagenesis; subtilisins.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • CRISPR-Associated Proteins / genetics*
  • CRISPR-Associated Proteins / metabolism
  • CRISPR-Cas Systems*
  • Clustered Regularly Interspaced Short Palindromic Repeats*
  • DNA-Binding Proteins / deficiency
  • DNA-Binding Proteins / genetics
  • Down-Regulation
  • Gene Editing / methods*
  • Gene Targeting / methods*
  • Genotype
  • Hepatocytes / enzymology*
  • Hepatocytes / transplantation
  • Humans
  • Hydrolases / deficiency
  • Hydrolases / genetics
  • Interleukin Receptor Common gamma Subunit / deficiency
  • Interleukin Receptor Common gamma Subunit / genetics
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mutation
  • Proprotein Convertase 9 / biosynthesis
  • Proprotein Convertase 9 / blood
  • Proprotein Convertase 9 / genetics*

Substances

  • CRISPR-Associated Proteins
  • DNA-Binding Proteins
  • Il2rg protein, mouse
  • Interleukin Receptor Common gamma Subunit
  • Rag2 protein, mouse
  • Hydrolases
  • PCSK9 protein, human
  • Proprotein Convertase 9
  • fumarylacetoacetase