In vivo silencing of the transcription factor IRF5 reprograms the macrophage phenotype and improves infarct healing.

ABSTRACT:

Objectives

The aim of this study was to test whether silencing of the transcription factor interferon regulatory factor 5 (IRF5) in cardiac macrophages improves infarct healing and attenuates post-myocardial infarction (MI) remodeling.

Background

In healing wounds, the M1 toward M2 macrophage phenotype transition supports resolution of inflammation and tissue repair. Persistence of inflammatory M1 macrophages may derail healing and compromise organ functions. The transcription factor IRF5 up-regulates genes associated with M1 macrophages.

Methods

Here we used nanoparticle-delivered small interfering ribonucleic acid (siRNA) to silence IRF5 in macrophages residing in MIs and in surgically-induced skin wounds in mice.

Results

Infarct macrophages expressed high le

SUBMITTER: Courties G 

PROVIDER: S-EPMC3992176 | biostudies-literature | 2014 Apr

REPOSITORIES: biostudies-literature