Hypoxic retinal Müller cells promote vascular permeability by HIF-1–dependent up-regulation of angiopoietin-like 4
0301 basic medicine
0303 health sciences
Diabetic Retinopathy
Reverse Transcriptase Polymerase Chain Reaction
Gene Expression Profiling
Blotting, Western
Hypoxia-Inducible Factor 1, alpha Subunit
Immunohistochemistry
Cell Hypoxia
Up-Regulation
3. Good health
Capillary Permeability
Mice, Inbred C57BL
Mice
03 medical and health sciences
Ischemia
Angiopoietin-Like Protein 4
Animals
Humans
Female
Angiopoietins
Cells, Cultured
Oligonucleotide Array Sequence Analysis
Retinal Neurons
DOI:
10.1073/pnas.1217091110
Publication Date:
2013-08-20T01:59:24Z
AUTHORS (17)
ABSTRACT
Significance
Ischemic retinopathies include a diverse group of diseases in which immature retinal vasculature or damage to mature retinal vessels leads to retinal ischemia. The anticipated rise in the worldwide prevalence of diabetes will result in a concurrent increase in the number of patients with vision impairment from diabetic eye disease, the most common cause of ischemic retinopathy. We set out to identify novel hypoxia-inducible genes that promote vascular permeability and may therefore play a role in the pathogenesis of diabetic eye disease. We demonstrate that angiopoietin-like 4 (ANGPTL4) is up-regulated by the transcriptional enhancer, hypoxia-inducible factor-1 in hypoxic retinal Müller cells, and can promote vascular permeability. Our findings suggest that ANGPTL4 may be a potential therapeutic target for ischemic retinopathies.
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