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Endothelial cell whole genome expression analysis in a mouse model of early-onset Fuchs' endothelial corneal dystrophy

Standard

Endothelial cell whole genome expression analysis in a mouse model of early-onset Fuchs' endothelial corneal dystrophy. / Matthaei, Mario; Hu, Jianfei; Meng, Huan; Lackner, Eva-Maria; Eberhart, Charles G; Qian, Jiang; Hao, Haiping; Jun, Albert S.

in: INVEST OPHTH VIS SCI, Jahrgang 54, Nr. 3, 01.03.2013, S. 1931-40.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Matthaei, M, Hu, J, Meng, H, Lackner, E-M, Eberhart, CG, Qian, J, Hao, H & Jun, AS 2013, 'Endothelial cell whole genome expression analysis in a mouse model of early-onset Fuchs' endothelial corneal dystrophy', INVEST OPHTH VIS SCI, Jg. 54, Nr. 3, S. 1931-40. https://doi.org/10.1167/iovs.12-10898

APA

Matthaei, M., Hu, J., Meng, H., Lackner, E-M., Eberhart, C. G., Qian, J., Hao, H., & Jun, A. S. (2013). Endothelial cell whole genome expression analysis in a mouse model of early-onset Fuchs' endothelial corneal dystrophy. INVEST OPHTH VIS SCI, 54(3), 1931-40. https://doi.org/10.1167/iovs.12-10898

Vancouver

Matthaei M, Hu J, Meng H, Lackner E-M, Eberhart CG, Qian J et al. Endothelial cell whole genome expression analysis in a mouse model of early-onset Fuchs' endothelial corneal dystrophy. INVEST OPHTH VIS SCI. 2013 Mär 1;54(3):1931-40. https://doi.org/10.1167/iovs.12-10898

Bibtex

@article{1098bdeb314f4628a6634dafdeff5391,
title = "Endothelial cell whole genome expression analysis in a mouse model of early-onset Fuchs' endothelial corneal dystrophy",
abstract = "PURPOSE: To investigate the endothelial gene expression profile in a Col8a2 Q455K mutant knock-in mouse model of early-onset Fuchs' endothelial corneal dystrophy (FECD) and identify potential targets that can be correlated to human late-onset FECD.METHODS: Diseased or normal endothelial phenotypes were verified in 12-month-old homozygous Col8a2(Q455K/Q455K) mutant and wild-type mice by clinical confocal microscopy. An endothelial whole genome expression profile was generated by microarray-based analysis. Result validation was performed by real-time PCR. Endothelial COX2 and JUN expression was further studied in human late-onset FECD compared to normal samples.RESULTS: Microarray analysis demonstrated endothelial expression of 24,538 genes (162 up-regulated and 172 down-regulated targets) and identified affected gene ontology terms including Response to Stress, Protein Metabolic Process, Protein Folding, Regulation of Apoptosis, and Transporter Activity. Real-time PCR assessment confirmed increased Cox2 (P = 0.001) and Jun mRNA (P = 0.03) levels in Col8a2(Q455K/Q455K) mutant compared to wild-type mice. In human FECD samples, real-time PCR demonstrated a statistically significant increase in COX2 mRNA (P < 0.0001) and JUN mRNA (P = 0.002) and tissue microarray analysis showed increased endothelial COX2 (P = 0.02) and JUN protein (P = 0.04).CONCLUSIONS: The present study provides the first endothelial whole genome expression analysis in an animal model of FECD and represents a useful resource for future studies of the disease. In particular endothelial COX2 up-regulation warrants further investigation of its role in FECD.",
keywords = "Aged, Animals, Cyclooxygenase 2, Disease Models, Animal, Endothelium, Corneal, Female, Fuchs' Endothelial Dystrophy, Genes, jun, Genome, Genome-Wide Association Study, Humans, Male, Mice, Mice, Knockout, Microscopy, Confocal, Phenotype, RNA, Messenger, Real-Time Polymerase Chain Reaction, Up-Regulation",
author = "Mario Matthaei and Jianfei Hu and Huan Meng and Eva-Maria Lackner and Eberhart, {Charles G} and Jiang Qian and Haiping Hao and Jun, {Albert S}",
year = "2013",
month = mar,
day = "1",
doi = "10.1167/iovs.12-10898",
language = "English",
volume = "54",
pages = "1931--40",
journal = "INVEST OPHTH VIS SCI",
issn = "0146-0404",
publisher = "Association for Research in Vision and Ophthalmology Inc.",
number = "3",

}

RIS

TY - JOUR

T1 - Endothelial cell whole genome expression analysis in a mouse model of early-onset Fuchs' endothelial corneal dystrophy

AU - Matthaei, Mario

AU - Hu, Jianfei

AU - Meng, Huan

AU - Lackner, Eva-Maria

AU - Eberhart, Charles G

AU - Qian, Jiang

AU - Hao, Haiping

AU - Jun, Albert S

PY - 2013/3/1

Y1 - 2013/3/1

N2 - PURPOSE: To investigate the endothelial gene expression profile in a Col8a2 Q455K mutant knock-in mouse model of early-onset Fuchs' endothelial corneal dystrophy (FECD) and identify potential targets that can be correlated to human late-onset FECD.METHODS: Diseased or normal endothelial phenotypes were verified in 12-month-old homozygous Col8a2(Q455K/Q455K) mutant and wild-type mice by clinical confocal microscopy. An endothelial whole genome expression profile was generated by microarray-based analysis. Result validation was performed by real-time PCR. Endothelial COX2 and JUN expression was further studied in human late-onset FECD compared to normal samples.RESULTS: Microarray analysis demonstrated endothelial expression of 24,538 genes (162 up-regulated and 172 down-regulated targets) and identified affected gene ontology terms including Response to Stress, Protein Metabolic Process, Protein Folding, Regulation of Apoptosis, and Transporter Activity. Real-time PCR assessment confirmed increased Cox2 (P = 0.001) and Jun mRNA (P = 0.03) levels in Col8a2(Q455K/Q455K) mutant compared to wild-type mice. In human FECD samples, real-time PCR demonstrated a statistically significant increase in COX2 mRNA (P < 0.0001) and JUN mRNA (P = 0.002) and tissue microarray analysis showed increased endothelial COX2 (P = 0.02) and JUN protein (P = 0.04).CONCLUSIONS: The present study provides the first endothelial whole genome expression analysis in an animal model of FECD and represents a useful resource for future studies of the disease. In particular endothelial COX2 up-regulation warrants further investigation of its role in FECD.

AB - PURPOSE: To investigate the endothelial gene expression profile in a Col8a2 Q455K mutant knock-in mouse model of early-onset Fuchs' endothelial corneal dystrophy (FECD) and identify potential targets that can be correlated to human late-onset FECD.METHODS: Diseased or normal endothelial phenotypes were verified in 12-month-old homozygous Col8a2(Q455K/Q455K) mutant and wild-type mice by clinical confocal microscopy. An endothelial whole genome expression profile was generated by microarray-based analysis. Result validation was performed by real-time PCR. Endothelial COX2 and JUN expression was further studied in human late-onset FECD compared to normal samples.RESULTS: Microarray analysis demonstrated endothelial expression of 24,538 genes (162 up-regulated and 172 down-regulated targets) and identified affected gene ontology terms including Response to Stress, Protein Metabolic Process, Protein Folding, Regulation of Apoptosis, and Transporter Activity. Real-time PCR assessment confirmed increased Cox2 (P = 0.001) and Jun mRNA (P = 0.03) levels in Col8a2(Q455K/Q455K) mutant compared to wild-type mice. In human FECD samples, real-time PCR demonstrated a statistically significant increase in COX2 mRNA (P < 0.0001) and JUN mRNA (P = 0.002) and tissue microarray analysis showed increased endothelial COX2 (P = 0.02) and JUN protein (P = 0.04).CONCLUSIONS: The present study provides the first endothelial whole genome expression analysis in an animal model of FECD and represents a useful resource for future studies of the disease. In particular endothelial COX2 up-regulation warrants further investigation of its role in FECD.

KW - Aged

KW - Animals

KW - Cyclooxygenase 2

KW - Disease Models, Animal

KW - Endothelium, Corneal

KW - Female

KW - Fuchs' Endothelial Dystrophy

KW - Genes, jun

KW - Genome

KW - Genome-Wide Association Study

KW - Humans

KW - Male

KW - Mice

KW - Mice, Knockout

KW - Microscopy, Confocal

KW - Phenotype

KW - RNA, Messenger

KW - Real-Time Polymerase Chain Reaction

KW - Up-Regulation

U2 - 10.1167/iovs.12-10898

DO - 10.1167/iovs.12-10898

M3 - SCORING: Journal article

C2 - 23449721

VL - 54

SP - 1931

EP - 1940

JO - INVEST OPHTH VIS SCI

JF - INVEST OPHTH VIS SCI

SN - 0146-0404

IS - 3

ER -