Deletion of the murine ortholog of human 9p21.3 locus promotes atherosclerosis by increasing macrophage proinflammatory activity.

ABSTRACT:

Background

Several genome-wide association studies have reported a risk locus for coronary artery disease (CAD) in the 9p21. 3 chromosomal region. This region encodes a lncRNA in the INK4 locus (ANRIL) and its genetic variance has a strong association with CAD, but its mechanisms in atherogenesis remain unclear.

Objectives

This study aimed to investigate the role of the murine ortholog of human 9p21.3 locus in atherogenesis in hypercholesterolemic mice.

Methods

Murine 9p21.3 ortholog knockout mice (Chr4^{Δ70kb/Δ70kb} ) were crossbred with Ldlr ^-/- ApoB ^100/100 mice, and atherosclerotic plaque size and morphology were analyzed on a standard or a high-fat diet (HFD). The hematopoietic cell-specific effect

SUBMITTER: Kettunen S 

PROVIDER: S-EPMC10025322 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature