12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase

<p dir="ltr">The purpose of the current study was to evaluate the effect of 12/15- lipoxygenase (12/15-LOX) metabolites on retinal endothelial cell (REC) barrier function. FITC-dextran flux across the REC monolayers and electrical cell-substrate impedance sensing (ECIS) were used to...

وصف كامل

محفوظ في:
التفاصيل البيبلوغرافية
المؤلف الرئيسي: Amira Othman (380131) (author)
مؤلفون آخرون: Saif Ahmad (371052) (author), Sylvia Megyerdi (380132) (author), Rene Mussell (380133) (author), Karishma Choksi (380134) (author), Krishna Rao Maddipati (10950942) (author), Ahmed Elmarakby (380136) (author), Nasser Rizk (380137) (author), Mohamed Al-Shabrawey (380138) (author)
منشور في: 2013
الموضوعات:
الوسوم: إضافة وسم
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_version_ 1864513511384678400
author Amira Othman (380131)
author2 Saif Ahmad (371052)
Sylvia Megyerdi (380132)
Rene Mussell (380133)
Karishma Choksi (380134)
Krishna Rao Maddipati (10950942)
Ahmed Elmarakby (380136)
Nasser Rizk (380137)
Mohamed Al-Shabrawey (380138)
author2_role author
author
author
author
author
author
author
author
author_facet Amira Othman (380131)
Saif Ahmad (371052)
Sylvia Megyerdi (380132)
Rene Mussell (380133)
Karishma Choksi (380134)
Krishna Rao Maddipati (10950942)
Ahmed Elmarakby (380136)
Nasser Rizk (380137)
Mohamed Al-Shabrawey (380138)
author_role author
dc.creator.none.fl_str_mv Amira Othman (380131)
Saif Ahmad (371052)
Sylvia Megyerdi (380132)
Rene Mussell (380133)
Karishma Choksi (380134)
Krishna Rao Maddipati (10950942)
Ahmed Elmarakby (380136)
Nasser Rizk (380137)
Mohamed Al-Shabrawey (380138)
dc.date.none.fl_str_mv 2013-02-20T06:00:00Z
dc.identifier.none.fl_str_mv 10.1371/journal.pone.0057254
dc.relation.none.fl_str_mv https://figshare.com/articles/journal_contribution/12_15-Lipoxygenase-Derived_Lipid_Metabolites_Induce_Retinal_Endothelial_Cell_Barrier_Dysfunction_Contribution_of_NADPH_Oxidase/26018509
dc.rights.none.fl_str_mv CC BY 4.0
info:eu-repo/semantics/openAccess
dc.subject.none.fl_str_mv Biomedical and clinical sciences
Medical biochemistry and metabolomics
Ophthalmology and optometry
Diabetes mellitus
Retina
Inflammation
Endothelial cells
Lipid metabolism
Mouse models
Vascular permeability
Metabolites
dc.title.none.fl_str_mv 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase
dc.type.none.fl_str_mv Text
Journal contribution
info:eu-repo/semantics/publishedVersion
text
contribution to journal
description <p dir="ltr">The purpose of the current study was to evaluate the effect of 12/15- lipoxygenase (12/15-LOX) metabolites on retinal endothelial cell (REC) barrier function. FITC-dextran flux across the REC monolayers and electrical cell-substrate impedance sensing (ECIS) were used to evaluate the effect of 12- and 15-hydroxyeicosatetreanoic acids (HETE) on REC permeability and transcellular electrical resistance (TER). Effect of 12- or 15-HETE on the levels of zonula occludens protein 1 (ZO-1), reactive oxygen species (ROS), NOX2, pVEGF-R2 and pSHP1 was examined in the presence or absence of inhibitors of NADPH oxidase. In vivo studies were performed using Ins<sup>2Akita</sup> mice treated with or without the 12/15-LOX inhibitor baicalein. Levels of HETE and inflammatory mediators were examined by LC/MS and Multiplex Immunoassay respectively. ROS generation and NOX2 expression were also measured in mice retinas. 12- and 15- HETE significantly increased permeability and reduced TER and ZO-1expression in REC. VEGF-R2 inhibitor reduced the permeability effect of 12-HETE. Treatment of REC with HETE also increased ROS generation and expression of NOX2 and pVEGF-R2 and decreased pSHP1 expression. Treatment of diabetic mice with baicalein significantly decreased retinal HETE, ICAM-1, VCAM-1, IL-6, ROS generation, and NOX2 expression. Baicalein also reduced pVEGF-R2 while restored pSHP1 levels in diabetic retina. Our findings suggest that 12/15-LOX contributes to vascular hyperpermeability during DR via NADPH oxidase dependent mechanism which involves suppression of protein tyrosine phosphatase and activation of VEGF-R2 signal pathway.</p><h2>Other Information</h2><p dir="ltr">Published in: PLoS ONE<br>License: <a href="http://creativecommons.org/licenses/by/4.0/" target="_blank">http://creativecommons.org/licenses/by/4.0/</a><br>See article on publisher's website: <a href="https://dx.doi.org/10.1371/journal.pone.0057254" target="_blank">https://dx.doi.org/10.1371/journal.pone.0057254</a></p><p dir="ltr">Additional institutions affiliated with: College of Science - QU (1977-2004/2005), College of Arts and Sciences - QU (2004/05-2016).</p>
eu_rights_str_mv openAccess
id Manara2_6a583f19dde096a67f0038d4196169fc
identifier_str_mv 10.1371/journal.pone.0057254
network_acronym_str Manara2
network_name_str Manara2
oai_identifier_str oai:figshare.com:article/26018509
publishDate 2013
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spelling 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH OxidaseAmira Othman (380131)Saif Ahmad (371052)Sylvia Megyerdi (380132)Rene Mussell (380133)Karishma Choksi (380134)Krishna Rao Maddipati (10950942)Ahmed Elmarakby (380136)Nasser Rizk (380137)Mohamed Al-Shabrawey (380138)Biomedical and clinical sciencesMedical biochemistry and metabolomicsOphthalmology and optometryDiabetes mellitusRetinaInflammationEndothelial cellsLipid metabolismMouse modelsVascular permeabilityMetabolites<p dir="ltr">The purpose of the current study was to evaluate the effect of 12/15- lipoxygenase (12/15-LOX) metabolites on retinal endothelial cell (REC) barrier function. FITC-dextran flux across the REC monolayers and electrical cell-substrate impedance sensing (ECIS) were used to evaluate the effect of 12- and 15-hydroxyeicosatetreanoic acids (HETE) on REC permeability and transcellular electrical resistance (TER). Effect of 12- or 15-HETE on the levels of zonula occludens protein 1 (ZO-1), reactive oxygen species (ROS), NOX2, pVEGF-R2 and pSHP1 was examined in the presence or absence of inhibitors of NADPH oxidase. In vivo studies were performed using Ins<sup>2Akita</sup> mice treated with or without the 12/15-LOX inhibitor baicalein. Levels of HETE and inflammatory mediators were examined by LC/MS and Multiplex Immunoassay respectively. ROS generation and NOX2 expression were also measured in mice retinas. 12- and 15- HETE significantly increased permeability and reduced TER and ZO-1expression in REC. VEGF-R2 inhibitor reduced the permeability effect of 12-HETE. Treatment of REC with HETE also increased ROS generation and expression of NOX2 and pVEGF-R2 and decreased pSHP1 expression. Treatment of diabetic mice with baicalein significantly decreased retinal HETE, ICAM-1, VCAM-1, IL-6, ROS generation, and NOX2 expression. Baicalein also reduced pVEGF-R2 while restored pSHP1 levels in diabetic retina. Our findings suggest that 12/15-LOX contributes to vascular hyperpermeability during DR via NADPH oxidase dependent mechanism which involves suppression of protein tyrosine phosphatase and activation of VEGF-R2 signal pathway.</p><h2>Other Information</h2><p dir="ltr">Published in: PLoS ONE<br>License: <a href="http://creativecommons.org/licenses/by/4.0/" target="_blank">http://creativecommons.org/licenses/by/4.0/</a><br>See article on publisher's website: <a href="https://dx.doi.org/10.1371/journal.pone.0057254" target="_blank">https://dx.doi.org/10.1371/journal.pone.0057254</a></p><p dir="ltr">Additional institutions affiliated with: College of Science - QU (1977-2004/2005), College of Arts and Sciences - QU (2004/05-2016).</p>2013-02-20T06:00:00ZTextJournal contributioninfo:eu-repo/semantics/publishedVersiontextcontribution to journal10.1371/journal.pone.0057254https://figshare.com/articles/journal_contribution/12_15-Lipoxygenase-Derived_Lipid_Metabolites_Induce_Retinal_Endothelial_Cell_Barrier_Dysfunction_Contribution_of_NADPH_Oxidase/26018509CC BY 4.0info:eu-repo/semantics/openAccessoai:figshare.com:article/260185092013-02-20T06:00:00Z
spellingShingle 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase
Amira Othman (380131)
Biomedical and clinical sciences
Medical biochemistry and metabolomics
Ophthalmology and optometry
Diabetes mellitus
Retina
Inflammation
Endothelial cells
Lipid metabolism
Mouse models
Vascular permeability
Metabolites
status_str publishedVersion
title 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase
title_full 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase
title_fullStr 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase
title_full_unstemmed 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase
title_short 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase
title_sort 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase
topic Biomedical and clinical sciences
Medical biochemistry and metabolomics
Ophthalmology and optometry
Diabetes mellitus
Retina
Inflammation
Endothelial cells
Lipid metabolism
Mouse models
Vascular permeability
Metabolites