Please use this identifier to cite or link to this item:
https://hdl.handle.net/10316/108638
DC Field | Value | Language |
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dc.contributor.author | Gonçalves, Andreia | - |
dc.contributor.author | Lin, Cheng-Mao | - |
dc.contributor.author | Muthusamy, Arivalagan | - |
dc.contributor.author | Fontes-Ribeiro, Carlos A. | - |
dc.contributor.author | Ambrósio, António F. | - |
dc.contributor.author | Abcouwer, Steven F | - |
dc.contributor.author | Fernandes, Rosa | - |
dc.contributor.author | Antonetti, David A. | - |
dc.date.accessioned | 2023-09-06T09:34:53Z | - |
dc.date.available | 2023-09-06T09:34:53Z | - |
dc.date.issued | 2016-05-01 | - |
dc.identifier.issn | 1552-5783 | pt |
dc.identifier.uri | https://hdl.handle.net/10316/108638 | - |
dc.description.abstract | PURPOSE. Inflammation associated with blood–retinal barrier (BRB) breakdown is a common feature of several retinal diseases. Therefore, the development of novel nonsteroidal antiinflammatory 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 antiinflammatory properties of exendin-4 (Ex-4), an analog of GLP-1, after ischemia-reperfusion (IR) injury were examined. METHODS. 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. RESULTS. 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-jB activation. CONCLUSIONS. 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. | pt |
dc.language.iso | eng | pt |
dc.publisher | Association for Research in Vision and Ophthalmology | pt |
dc.relation | Supported by NIH R01 EY012021 (DAA); Research to Prevent Blindness Jules and Doris Stein Professorship (DAA); NIH R01 EY007739 (SFA); the Core Center for Vision Research at the Kellogg Eye Center P30 EY007003; European Foundation for the Study of Diabetes (EFSD)/Glaxo Smith Kline Programme (RF); GIFT/Portuguese Society of Diabetes (RF); Foundation for Science and Technology (FCT Portugal, Strategic Project UID/NEU/04539/ 2013, Project PTDC/NEU-OSD/1113/2012-FCOMP-0124-FEDER- 029665 (AFA); PhD fellowship SFRH/BD/103936/2014 (AG); COMPETE-FEDER; and a Fulbright Research Fellowship (AG). | pt |
dc.rights | openAccess | pt |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | pt |
dc.subject | blood–brain barrier | pt |
dc.subject | inflammation | pt |
dc.subject | ischemia-reperfusion injury | pt |
dc.subject | microglia | pt |
dc.subject | vascular biology | pt |
dc.subject.mesh | Animals | pt |
dc.subject.mesh | Blood-Retinal Barrier | pt |
dc.subject.mesh | Cattle | pt |
dc.subject.mesh | Cells, Cultured | pt |
dc.subject.mesh | Disease Models, Animal | pt |
dc.subject.mesh | Exenatide | pt |
dc.subject.mesh | Glucagon-Like Peptide 1 | pt |
dc.subject.mesh | Immunoblotting | pt |
dc.subject.mesh | Immunohistochemistry | pt |
dc.subject.mesh | Incretins | pt |
dc.subject.mesh | Inflammation | pt |
dc.subject.mesh | Ischemia | pt |
dc.subject.mesh | Male | pt |
dc.subject.mesh | Peptides | pt |
dc.subject.mesh | Rats | pt |
dc.subject.mesh | Rats, Long-Evans | pt |
dc.subject.mesh | Reperfusion Injury | pt |
dc.subject.mesh | Retinal Diseases | pt |
dc.subject.mesh | Venoms | pt |
dc.title | Protective Effect of a GLP-1 Analog on Ischemia-Reperfusion Induced Blood-Retinal Barrier Breakdown and Inflammation | pt |
dc.type | article | - |
degois.publication.firstPage | 2584 | pt |
degois.publication.lastPage | 2592 | pt |
degois.publication.issue | 6 | pt |
degois.publication.title | Investigative Ophthalmology and Visual Science | pt |
dc.peerreviewed | yes | pt |
dc.identifier.doi | 10.1167/iovs.15-19006 | pt |
degois.publication.volume | 57 | pt |
dc.date.embargo | 2016-05-01 | * |
uc.date.periodoEmbargo | 0 | pt |
item.grantfulltext | open | - |
item.cerifentitytype | Publications | - |
item.languageiso639-1 | en | - |
item.openairetype | article | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.fulltext | Com Texto completo | - |
crisitem.author.researchunit | CNC - Center for Neuroscience and Cell Biology | - |
crisitem.author.researchunit | CNC - Center for Neuroscience and Cell Biology | - |
crisitem.author.orcid | 0000-0002-0477-1641 | - |
crisitem.author.orcid | 0000-0001-7828-2296 | - |
Appears in Collections: | FMUC Medicina - Artigos em Revistas Internacionais |
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Protective effect of a GLP-1 analog on ischemia-reperfusion induced blood–retinal barrier breakdown and inflammation.pdf | 1.28 MB | Adobe PDF | View/Open |
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