Origins and consequences of hyperosmolar stress in retinal pigmented epithelial cells

The retinal pigmented epithelium (RPE) is, composed of retinal pigmented epithelial cells joined by tight junctions and, represents the outer blood-retinal barrier (BRB). The inner BRB is made of the endothelial cells joined by tight junctions and glial extensions surrounding all the retinal blood v...

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Main Authors: François eWillermain, Sarah eLibert, Elie eMotulsky, Dany eSalik, Laure eCaspers, Jason ePerret, Christine eDelporte
Format: Article
Language:English
Published: Frontiers Media S.A. 2014-05-01
Series:Frontiers in Physiology
Subjects:
Online Access:http://journal.frontiersin.org/Journal/10.3389/fphys.2014.00199/full
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author François eWillermain
François eWillermain
Sarah eLibert
Sarah eLibert
Elie eMotulsky
Elie eMotulsky
Dany eSalik
Dany eSalik
Laure eCaspers
Jason ePerret
Christine eDelporte
author_facet François eWillermain
François eWillermain
Sarah eLibert
Sarah eLibert
Elie eMotulsky
Elie eMotulsky
Dany eSalik
Dany eSalik
Laure eCaspers
Jason ePerret
Christine eDelporte
author_sort François eWillermain
collection DOAJ
description The retinal pigmented epithelium (RPE) is, composed of retinal pigmented epithelial cells joined by tight junctions and, represents the outer blood-retinal barrier (BRB). The inner BRB is made of the endothelial cells joined by tight junctions and glial extensions surrounding all the retinal blood vessels. One of the functions of the RPE is to maintain an osmotic transepithelial gradient created by ionic pumps and channels, and avoiding paracellular flux. Under such physiological conditions, transcellular water movement follows theis osmotic gradient and is flowingflows normally from the retina to the choroid through the RPE. Several diseases, such as diabetic retinopathy, are characterized by the BRB breakdown leading to leakage of solutes, proteins and fluid from the retina and the choroid. The prevailing hypothesis explaining macular edema formation during diabetic retinopathy relies onincriminates the inner BRB breakdown resulting in increased osmotic pressure leading in turn to massive water accumulation that can affect vision. Under these conditions, it has been hypothesized that RPE is likely to be exposed to hyperosmolar stress at its apical side. This review summarizes the origins and consequences of osmotic stress in the RPE. Ongoing and further research advances will clarify the mechanisms, at the molecular level, involved in the response of the RPE to osmotic stress and delineate potential novel therapeutic targets and tools.
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spelling doaj.art-6a77561b02a240b1957ba7fb4dd9aed82022-12-21T22:07:53ZengFrontiers Media S.A.Frontiers in Physiology1664-042X2014-05-01510.3389/fphys.2014.0019992841Origins and consequences of hyperosmolar stress in retinal pigmented epithelial cellsFrançois eWillermain0François eWillermain1Sarah eLibert2Sarah eLibert3Elie eMotulsky4Elie eMotulsky5Dany eSalik6Dany eSalik7Laure eCaspers8Jason ePerret9Christine eDelporte10CHU Saint Pierre and BrugmannUniversité Libre de BruxellesUniversité Libre de BruxellesCHU Saint Pierre and BrugmannUniversité Libre de BruxellesCHU Saint Pierre and BrugmannUniversité Libre de BruxellesCHU Saint Pierre and BrugmannCHU Saint Pierre and BrugmannUniversité Libre de BruxellesUniversité Libre de BruxellesThe retinal pigmented epithelium (RPE) is, composed of retinal pigmented epithelial cells joined by tight junctions and, represents the outer blood-retinal barrier (BRB). The inner BRB is made of the endothelial cells joined by tight junctions and glial extensions surrounding all the retinal blood vessels. One of the functions of the RPE is to maintain an osmotic transepithelial gradient created by ionic pumps and channels, and avoiding paracellular flux. Under such physiological conditions, transcellular water movement follows theis osmotic gradient and is flowingflows normally from the retina to the choroid through the RPE. Several diseases, such as diabetic retinopathy, are characterized by the BRB breakdown leading to leakage of solutes, proteins and fluid from the retina and the choroid. The prevailing hypothesis explaining macular edema formation during diabetic retinopathy relies onincriminates the inner BRB breakdown resulting in increased osmotic pressure leading in turn to massive water accumulation that can affect vision. Under these conditions, it has been hypothesized that RPE is likely to be exposed to hyperosmolar stress at its apical side. This review summarizes the origins and consequences of osmotic stress in the RPE. Ongoing and further research advances will clarify the mechanisms, at the molecular level, involved in the response of the RPE to osmotic stress and delineate potential novel therapeutic targets and tools.http://journal.frontiersin.org/Journal/10.3389/fphys.2014.00199/fullBlood-Retinal BarrierEdemaUveitisdiabetesage-related macular degenerationretinal pigmented epithelium
spellingShingle François eWillermain
François eWillermain
Sarah eLibert
Sarah eLibert
Elie eMotulsky
Elie eMotulsky
Dany eSalik
Dany eSalik
Laure eCaspers
Jason ePerret
Christine eDelporte
Origins and consequences of hyperosmolar stress in retinal pigmented epithelial cells
Frontiers in Physiology
Blood-Retinal Barrier
Edema
Uveitis
diabetes
age-related macular degeneration
retinal pigmented epithelium
title Origins and consequences of hyperosmolar stress in retinal pigmented epithelial cells
title_full Origins and consequences of hyperosmolar stress in retinal pigmented epithelial cells
title_fullStr Origins and consequences of hyperosmolar stress in retinal pigmented epithelial cells
title_full_unstemmed Origins and consequences of hyperosmolar stress in retinal pigmented epithelial cells
title_short Origins and consequences of hyperosmolar stress in retinal pigmented epithelial cells
title_sort origins and consequences of hyperosmolar stress in retinal pigmented epithelial cells
topic Blood-Retinal Barrier
Edema
Uveitis
diabetes
age-related macular degeneration
retinal pigmented epithelium
url http://journal.frontiersin.org/Journal/10.3389/fphys.2014.00199/full
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