Genomic responses in mouse models greatly mimic human inflammatory diseases

Keizo Takao, Tsuyoshi Miyakawa

Research output: Contribution to journalArticle

236 Citations (Scopus)

Abstract

The use of mice as animal models has long been considered essential in modern biomedical research, but the role of mouse models in research was challenged by a recent report that genomic responses in mouse models poorly mimic human inflammatory diseases. Here we reevaluated the same gene expression datasets used in the previous study by focusing on genes whose expression levels were significantly changed in both humans and mice. Contrary to the previous findings, the gene expression levels in the mouse models showed extraordinarily significant correlations with those of the human conditions (Spearman's rank correlation coefficient: 0.43-0.68; genes changed in the same direction: 77-93%; P = 6.5 × 10-11 to 1.2 × 10-35). Moreover, meta-analysis of those datasets revealed a number of pathways/biogroups commonly regulated by multiple conditions in humans and mice. These findings demonstrate that gene expression patterns in mouse models closely recapitulate those in human inflammatory conditions and strongly argue for the utility of mice as animal models of human disorders.

Original languageEnglish
Pages (from-to)1167-1172
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume112
Issue number4
DOIs
Publication statusPublished - 27-01-2015

Fingerprint

Gene Expression
Animal Models
Nonparametric Statistics
Meta-Analysis
Biomedical Research
Research
Genes
Datasets
Direction compound

All Science Journal Classification (ASJC) codes

  • General

Cite this

@article{a41b1c07c9364125bbba30d2dab0f447,
title = "Genomic responses in mouse models greatly mimic human inflammatory diseases",
abstract = "The use of mice as animal models has long been considered essential in modern biomedical research, but the role of mouse models in research was challenged by a recent report that genomic responses in mouse models poorly mimic human inflammatory diseases. Here we reevaluated the same gene expression datasets used in the previous study by focusing on genes whose expression levels were significantly changed in both humans and mice. Contrary to the previous findings, the gene expression levels in the mouse models showed extraordinarily significant correlations with those of the human conditions (Spearman's rank correlation coefficient: 0.43-0.68; genes changed in the same direction: 77-93{\%}; P = 6.5 × 10-11 to 1.2 × 10-35). Moreover, meta-analysis of those datasets revealed a number of pathways/biogroups commonly regulated by multiple conditions in humans and mice. These findings demonstrate that gene expression patterns in mouse models closely recapitulate those in human inflammatory conditions and strongly argue for the utility of mice as animal models of human disorders.",
author = "Keizo Takao and Tsuyoshi Miyakawa",
year = "2015",
month = "1",
day = "27",
doi = "10.1073/pnas.1401965111",
language = "English",
volume = "112",
pages = "1167--1172",
journal = "Proceedings of the National Academy of Sciences of the United States of America",
issn = "0027-8424",
number = "4",

}

Genomic responses in mouse models greatly mimic human inflammatory diseases. / Takao, Keizo; Miyakawa, Tsuyoshi.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 112, No. 4, 27.01.2015, p. 1167-1172.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Genomic responses in mouse models greatly mimic human inflammatory diseases

AU - Takao, Keizo

AU - Miyakawa, Tsuyoshi

PY - 2015/1/27

Y1 - 2015/1/27

N2 - The use of mice as animal models has long been considered essential in modern biomedical research, but the role of mouse models in research was challenged by a recent report that genomic responses in mouse models poorly mimic human inflammatory diseases. Here we reevaluated the same gene expression datasets used in the previous study by focusing on genes whose expression levels were significantly changed in both humans and mice. Contrary to the previous findings, the gene expression levels in the mouse models showed extraordinarily significant correlations with those of the human conditions (Spearman's rank correlation coefficient: 0.43-0.68; genes changed in the same direction: 77-93%; P = 6.5 × 10-11 to 1.2 × 10-35). Moreover, meta-analysis of those datasets revealed a number of pathways/biogroups commonly regulated by multiple conditions in humans and mice. These findings demonstrate that gene expression patterns in mouse models closely recapitulate those in human inflammatory conditions and strongly argue for the utility of mice as animal models of human disorders.

AB - The use of mice as animal models has long been considered essential in modern biomedical research, but the role of mouse models in research was challenged by a recent report that genomic responses in mouse models poorly mimic human inflammatory diseases. Here we reevaluated the same gene expression datasets used in the previous study by focusing on genes whose expression levels were significantly changed in both humans and mice. Contrary to the previous findings, the gene expression levels in the mouse models showed extraordinarily significant correlations with those of the human conditions (Spearman's rank correlation coefficient: 0.43-0.68; genes changed in the same direction: 77-93%; P = 6.5 × 10-11 to 1.2 × 10-35). Moreover, meta-analysis of those datasets revealed a number of pathways/biogroups commonly regulated by multiple conditions in humans and mice. These findings demonstrate that gene expression patterns in mouse models closely recapitulate those in human inflammatory conditions and strongly argue for the utility of mice as animal models of human disorders.

UR - http://www.scopus.com/inward/record.url?scp=84921727957&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84921727957&partnerID=8YFLogxK

U2 - 10.1073/pnas.1401965111

DO - 10.1073/pnas.1401965111

M3 - Article

C2 - 25092317

AN - SCOPUS:84921727957

VL - 112

SP - 1167

EP - 1172

JO - Proceedings of the National Academy of Sciences of the United States of America

JF - Proceedings of the National Academy of Sciences of the United States of America

SN - 0027-8424

IS - 4

ER -