Decreased outflow facility and Schlemm's canal defects in a mouse model of glaucoma

Timur A. Mavlyutov; Megan S. Kuhn; Samer E. Bilal; Michael L. De Ieso; Anil K. Chauhan; W. Daniel Stamer; Colleen M. McDowell

doi:10.1016/j.exer.2022.109249

Decreased outflow facility and Schlemm's canal defects in a mouse model of glaucoma

Timur A. Mavlyutov, Megan S. Kuhn, Samer E. Bilal, Michael L. De Ieso, Anil K. Chauhan, W. Daniel Stamer, Colleen M. McDowell

Research output: Contribution to journal › Article › peer-review

1 Scopus citations

Abstract

Previously we identified B6.EDA^+/+ mice as a novel mouse model that presents with elevated IOP and trabecular meshwork damage. Here, we expand on our previous findings by measuring aqueous humor outflow facility and analyzing the integrity of the inner wall of Schlemm's canal. As expected, intraocular pressure (IOP) was increased, and outflow facility was decreased compared to C57BL/6J controls. B6.EDA^+/+ mice had significantly increased expression of the adherens junction protein, VE-cadherin by the inner wall endothelium of Schlemm's canal. These data suggest that in addition to trabecular meshwork damage, there are changes in Schlemm's canal in B6.EDA^+/+ mice that lead to aqueous outflow dysfunction and ocular hypertension.

Original language	English (US)
Article number	109249
Journal	Experimental eye research
Volume	225
DOIs	https://doi.org/10.1016/j.exer.2022.109249
State	Published - Dec 2022
Externally published	Yes

Keywords

FN-EDA
IOP
Ocular hypertension
Outflow facility
VE-Cadherin

ASJC Scopus subject areas

Ophthalmology
Sensory Systems
Cellular and Molecular Neuroscience

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10.1016/j.exer.2022.109249

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title = "Decreased outflow facility and Schlemm's canal defects in a mouse model of glaucoma",

abstract = "Previously we identified B6.EDA+/+ mice as a novel mouse model that presents with elevated IOP and trabecular meshwork damage. Here, we expand on our previous findings by measuring aqueous humor outflow facility and analyzing the integrity of the inner wall of Schlemm's canal. As expected, intraocular pressure (IOP) was increased, and outflow facility was decreased compared to C57BL/6J controls. B6.EDA+/+ mice had significantly increased expression of the adherens junction protein, VE-cadherin by the inner wall endothelium of Schlemm's canal. These data suggest that in addition to trabecular meshwork damage, there are changes in Schlemm's canal in B6.EDA+/+ mice that lead to aqueous outflow dysfunction and ocular hypertension.",

keywords = "FN-EDA, IOP, Ocular hypertension, Outflow facility, VE-Cadherin",

author = "Mavlyutov, {Timur A.} and Kuhn, {Megan S.} and Bilal, {Samer E.} and {De Ieso}, {Michael L.} and Chauhan, {Anil K.} and Stamer, {W. Daniel} and McDowell, {Colleen M.}",

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year = "2022",

month = dec,

doi = "10.1016/j.exer.2022.109249",

language = "English (US)",

volume = "225",

journal = "Experimental eye research",

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T1 - Decreased outflow facility and Schlemm's canal defects in a mouse model of glaucoma

AU - Mavlyutov, Timur A.

AU - Kuhn, Megan S.

AU - Bilal, Samer E.

AU - De Ieso, Michael L.

AU - Chauhan, Anil K.

AU - Stamer, W. Daniel

AU - McDowell, Colleen M.

PY - 2022/12

Y1 - 2022/12

N2 - Previously we identified B6.EDA+/+ mice as a novel mouse model that presents with elevated IOP and trabecular meshwork damage. Here, we expand on our previous findings by measuring aqueous humor outflow facility and analyzing the integrity of the inner wall of Schlemm's canal. As expected, intraocular pressure (IOP) was increased, and outflow facility was decreased compared to C57BL/6J controls. B6.EDA+/+ mice had significantly increased expression of the adherens junction protein, VE-cadherin by the inner wall endothelium of Schlemm's canal. These data suggest that in addition to trabecular meshwork damage, there are changes in Schlemm's canal in B6.EDA+/+ mice that lead to aqueous outflow dysfunction and ocular hypertension.

AB - Previously we identified B6.EDA+/+ mice as a novel mouse model that presents with elevated IOP and trabecular meshwork damage. Here, we expand on our previous findings by measuring aqueous humor outflow facility and analyzing the integrity of the inner wall of Schlemm's canal. As expected, intraocular pressure (IOP) was increased, and outflow facility was decreased compared to C57BL/6J controls. B6.EDA+/+ mice had significantly increased expression of the adherens junction protein, VE-cadherin by the inner wall endothelium of Schlemm's canal. These data suggest that in addition to trabecular meshwork damage, there are changes in Schlemm's canal in B6.EDA+/+ mice that lead to aqueous outflow dysfunction and ocular hypertension.

KW - FN-EDA

KW - IOP

KW - Ocular hypertension

KW - Outflow facility

KW - VE-Cadherin

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Decreased outflow facility and Schlemm's canal defects in a mouse model of glaucoma

Abstract

Keywords

ASJC Scopus subject areas

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