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Publication
Protective Effect of a GLP-1 Analog on Ischemia-Reperfusion Induced
Blood-Retinal Barrier Breakdown and Inflammation.
Authors
Gonçalves A, Lin CM, Muthusamy A, Fontes-Ribeiro C, Ambrósio AF, Abcouwer SF,
Fernandes R, Antonetti DA
Submitted By
Steven Abcouwer on 6/17/2016
Status
Published
Journal
Investigative ophthalmology & visual science
Year
2016
Date Published
5/1/2016
Volume : Pages
57 : 2584 - 92
PubMed Reference
27163772
Abstract
Inflammation associated with blood-retinal barrier (BRB) breakdown is a common
feature of several retinal diseases. Therefore, the development of novel
nonsteroidal anti-inflammatory approaches may provide important therapeutic
options. Previous studies demonstrated that inhibition of dipeptidyl
peptidase-IV, the enzyme responsible for the degradation of glucagon-like
peptide-1 (GLP-1), led to insulin-independent prevention of diabetes-induced
increases in BRB permeability, suggesting that incretin-based drugs may have
beneficial pleiotropic effects in the retina. In the current study, the barrier
protective and anti-inflammatory properties of exendin-4 (Ex-4), an analog of
GLP-1, after ischemia-reperfusion (IR) injury were examined.,
Ischemia-reperfusion injury was induced in rat retinas by increasing the
intraocular pressure for 45 minutes followed by 48 hours of reperfusion. Rats
were treated with Ex-4 prior to and following IR. Blood-retinal barrier
permeability was assessed by Evans blue dye leakage. Retinal inflammatory gene
expression and leukocytic infiltration were measured by qRT-PCR and
immunofluorescence, respectively. A microglial cell line was used to determine
the effects of Ex-4 on lipopolysaccharide (LPS)-induced inflammatory response.,
Exendin-4 dramatically reduced the BRB permeability induced by IR injury, which
was associated with suppression of inflammatory gene expression. Moreover, in
vitro studies showed that Ex-4 also reduced the inflammatory response to LPS and
inhibited NF-?B activation., The present work suggests that Ex-4 can prevent IR
injury-induced BRB breakdown and inflammation through inhibition of inflammatory
cytokine production by activated microglia and may provide a novel option for
therapeutic intervention in diseases involving retinal inflammation.
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(DiaComp) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
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