Modulation of angiogenesis by genetic manipulation of ATF4 in mouse model of oxygen-induced retinopathy [corrected].

ABSTRACT:

Purpose

The activation of the unfolded protein response (UPR) and an increase in activating transcription factor 4 (ATF4) has been previously reported in the diabetic retina. Despite this, a direct link between ATF4 and the degree of proliferative retinopathy has not been demonstrated to date. Therefore, the objective of this study was to determine whether ATF4 deficiency could reduce neovascularization in mice with oxygen-induced retinopathy (OIR).

Methods

We induced OIR in C57BL/6, ATF4(+/-), and endoplasmic reticulum stress-activated indicator (ERAI) mice and used quantitative RT-PCR and Western blot analysis to evaluate relative gene and protein expression. Histology and microscopy were used to calculate the extent of neovascularization in flat-mounted retinas.

Result

SUBMITTER: Wang X 

PROVIDER: S-EPMC3762331 | biostudies-literature | 2013 Sep

REPOSITORIES: biostudies-literature