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CEACAM1 confers resistance toward oxygen-induced vessel damage in a mouse model of retinopathy of prematurity

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CEACAM1 confers resistance toward oxygen-induced vessel damage in a mouse model of retinopathy of prematurity. / Ludewig, Peter; Flachsbarth, Kai; Wegscheid, Claudia; Tiegs, Gisa; Richard, Gisbert; Wagener, Christoph; Bartsch, Udo; Horst, Andrea Kristina.

In: INVEST OPHTH VIS SCI, Vol. 55, No. 12, 2014, p. 7950-7960.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Ludewig, P, Flachsbarth, K, Wegscheid, C, Tiegs, G, Richard, G, Wagener, C, Bartsch, U & Horst, AK 2014, 'CEACAM1 confers resistance toward oxygen-induced vessel damage in a mouse model of retinopathy of prematurity', INVEST OPHTH VIS SCI, vol. 55, no. 12, pp. 7950-7960. https://doi.org/10.1167/iovs.13-13403

APA

Ludewig, P., Flachsbarth, K., Wegscheid, C., Tiegs, G., Richard, G., Wagener, C., Bartsch, U., & Horst, A. K. (2014). CEACAM1 confers resistance toward oxygen-induced vessel damage in a mouse model of retinopathy of prematurity. INVEST OPHTH VIS SCI, 55(12), 7950-7960. https://doi.org/10.1167/iovs.13-13403

Vancouver

Ludewig P, Flachsbarth K, Wegscheid C, Tiegs G, Richard G, Wagener C et al. CEACAM1 confers resistance toward oxygen-induced vessel damage in a mouse model of retinopathy of prematurity. INVEST OPHTH VIS SCI. 2014;55(12):7950-7960. https://doi.org/10.1167/iovs.13-13403

Bibtex

@article{15fc5ce61ff1415d895bb30cb7430fe7,
title = "CEACAM1 confers resistance toward oxygen-induced vessel damage in a mouse model of retinopathy of prematurity",
abstract = "PURPOSE: To determine a functional role for the carcinoembryonic antigen-related cell-adhesion molecule 1 (CEACAM1) in retinal neovascularization in a mouse model of oxygen-induced retinopathy (OIR).METHODS: In a 21/75/21% OIR mouse model, retinal neovascularization was compared in wild-type and CEACAM1-deficient mice. Animals were housed under normoxic conditions until postnatal day 7, followed by exposure to 75% oxygen for 5 days, and further housing under normoxic conditions. Retinal vascular anatomy, vaso-obliteration, neovascularization, and tuft formation were characterized and quantified in retinal flat-mounts from untreated mice and from experimental mice during and at different time points after exposure to high oxygen levels. The vascular network was stained with fluorescently labeled isolectin B4.RESULTS: Mice deficient in CEACAM1 did not present any apparent abnormalities in their postnatal retinal vascular development under normoxic housing conditions. However, after hyperoxia and under relative hypoxic conditions, retinal neovascularization and tuft formation were aggravated in the mutant. Congruently, revascularization and vessel maturation were delayed in CEACAM1-deficient mice whereas in wild-type mice, tuft regression and vascular remodeling occurred efficiently after exposure to high oxygen levels.CONCLUSIONS: Our report describes a functional role for CEACAM1 in retinal neovascularization in a mouse model of OIR. This is the first study demonstrating that CEACAM1 enhances vascular remodeling and tuft regression by increasing endothelial resistance to alterations in oxygen tension, thus accelerating vascular recovery after systemic hypoxia.",
keywords = "Animals, Antigens, CD, Cell Adhesion Molecules, Disease Models, Animal, Hyperoxia, Mice, Mice, Inbred C57BL, Oxygen, Retinal Neovascularization, Retinal Vessels, Retinopathy of Prematurity",
author = "Peter Ludewig and Kai Flachsbarth and Claudia Wegscheid and Gisa Tiegs and Gisbert Richard and Christoph Wagener and Udo Bartsch and Horst, {Andrea Kristina}",
note = "Copyright 2014 The Association for Research in Vision and Ophthalmology, Inc.",
year = "2014",
doi = "10.1167/iovs.13-13403",
language = "English",
volume = "55",
pages = "7950--7960",
journal = "INVEST OPHTH VIS SCI",
issn = "0146-0404",
publisher = "Association for Research in Vision and Ophthalmology Inc.",
number = "12",

}

RIS

TY - JOUR

T1 - CEACAM1 confers resistance toward oxygen-induced vessel damage in a mouse model of retinopathy of prematurity

AU - Ludewig, Peter

AU - Flachsbarth, Kai

AU - Wegscheid, Claudia

AU - Tiegs, Gisa

AU - Richard, Gisbert

AU - Wagener, Christoph

AU - Bartsch, Udo

AU - Horst, Andrea Kristina

N1 - Copyright 2014 The Association for Research in Vision and Ophthalmology, Inc.

PY - 2014

Y1 - 2014

N2 - PURPOSE: To determine a functional role for the carcinoembryonic antigen-related cell-adhesion molecule 1 (CEACAM1) in retinal neovascularization in a mouse model of oxygen-induced retinopathy (OIR).METHODS: In a 21/75/21% OIR mouse model, retinal neovascularization was compared in wild-type and CEACAM1-deficient mice. Animals were housed under normoxic conditions until postnatal day 7, followed by exposure to 75% oxygen for 5 days, and further housing under normoxic conditions. Retinal vascular anatomy, vaso-obliteration, neovascularization, and tuft formation were characterized and quantified in retinal flat-mounts from untreated mice and from experimental mice during and at different time points after exposure to high oxygen levels. The vascular network was stained with fluorescently labeled isolectin B4.RESULTS: Mice deficient in CEACAM1 did not present any apparent abnormalities in their postnatal retinal vascular development under normoxic housing conditions. However, after hyperoxia and under relative hypoxic conditions, retinal neovascularization and tuft formation were aggravated in the mutant. Congruently, revascularization and vessel maturation were delayed in CEACAM1-deficient mice whereas in wild-type mice, tuft regression and vascular remodeling occurred efficiently after exposure to high oxygen levels.CONCLUSIONS: Our report describes a functional role for CEACAM1 in retinal neovascularization in a mouse model of OIR. This is the first study demonstrating that CEACAM1 enhances vascular remodeling and tuft regression by increasing endothelial resistance to alterations in oxygen tension, thus accelerating vascular recovery after systemic hypoxia.

AB - PURPOSE: To determine a functional role for the carcinoembryonic antigen-related cell-adhesion molecule 1 (CEACAM1) in retinal neovascularization in a mouse model of oxygen-induced retinopathy (OIR).METHODS: In a 21/75/21% OIR mouse model, retinal neovascularization was compared in wild-type and CEACAM1-deficient mice. Animals were housed under normoxic conditions until postnatal day 7, followed by exposure to 75% oxygen for 5 days, and further housing under normoxic conditions. Retinal vascular anatomy, vaso-obliteration, neovascularization, and tuft formation were characterized and quantified in retinal flat-mounts from untreated mice and from experimental mice during and at different time points after exposure to high oxygen levels. The vascular network was stained with fluorescently labeled isolectin B4.RESULTS: Mice deficient in CEACAM1 did not present any apparent abnormalities in their postnatal retinal vascular development under normoxic housing conditions. However, after hyperoxia and under relative hypoxic conditions, retinal neovascularization and tuft formation were aggravated in the mutant. Congruently, revascularization and vessel maturation were delayed in CEACAM1-deficient mice whereas in wild-type mice, tuft regression and vascular remodeling occurred efficiently after exposure to high oxygen levels.CONCLUSIONS: Our report describes a functional role for CEACAM1 in retinal neovascularization in a mouse model of OIR. This is the first study demonstrating that CEACAM1 enhances vascular remodeling and tuft regression by increasing endothelial resistance to alterations in oxygen tension, thus accelerating vascular recovery after systemic hypoxia.

KW - Animals

KW - Antigens, CD

KW - Cell Adhesion Molecules

KW - Disease Models, Animal

KW - Hyperoxia

KW - Mice

KW - Mice, Inbred C57BL

KW - Oxygen

KW - Retinal Neovascularization

KW - Retinal Vessels

KW - Retinopathy of Prematurity

U2 - 10.1167/iovs.13-13403

DO - 10.1167/iovs.13-13403

M3 - SCORING: Journal article

C2 - 25406283

VL - 55

SP - 7950

EP - 7960

JO - INVEST OPHTH VIS SCI

JF - INVEST OPHTH VIS SCI

SN - 0146-0404

IS - 12

ER -