Joint profiling of miRNAs and mRNAs reveals miRNA mediated gene regulation in the Göttingen minipig obesity model

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Joint profiling of miRNAs and mRNAs reveals miRNA mediated gene regulation in the Göttingen minipig obesity model. / Mentzel, Caroline M. Junker; Alkan, Ferhat; Keinicke, Helle; Jacobsen, Mette Juul; Gorodkin, Jan; Fredholm, Merete; Cirera Salicio, Susanna.

I: P L o S One, Bind 11, Nr. 11, e0167285, 30.11.2016.

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Harvard

Mentzel, CMJ, Alkan, F, Keinicke, H, Jacobsen, MJ, Gorodkin, J, Fredholm, M & Cirera Salicio, S 2016, 'Joint profiling of miRNAs and mRNAs reveals miRNA mediated gene regulation in the Göttingen minipig obesity model', P L o S One, bind 11, nr. 11, e0167285. https://doi.org/10.1371/journal.pone.0167285

APA

Mentzel, C. M. J., Alkan, F., Keinicke, H., Jacobsen, M. J., Gorodkin, J., Fredholm, M., & Cirera Salicio, S. (2016). Joint profiling of miRNAs and mRNAs reveals miRNA mediated gene regulation in the Göttingen minipig obesity model. P L o S One, 11(11), [e0167285]. https://doi.org/10.1371/journal.pone.0167285

Vancouver

Mentzel CMJ, Alkan F, Keinicke H, Jacobsen MJ, Gorodkin J, Fredholm M o.a. Joint profiling of miRNAs and mRNAs reveals miRNA mediated gene regulation in the Göttingen minipig obesity model. P L o S One. 2016 nov. 30;11(11). e0167285. https://doi.org/10.1371/journal.pone.0167285

Author

Mentzel, Caroline M. Junker ; Alkan, Ferhat ; Keinicke, Helle ; Jacobsen, Mette Juul ; Gorodkin, Jan ; Fredholm, Merete ; Cirera Salicio, Susanna. / Joint profiling of miRNAs and mRNAs reveals miRNA mediated gene regulation in the Göttingen minipig obesity model. I: P L o S One. 2016 ; Bind 11, Nr. 11.

Bibtex

@article{e84188814f2844919b02db895f64faf0,
title = "Joint profiling of miRNAs and mRNAs reveals miRNA mediated gene regulation in the G{\"o}ttingen minipig obesity model",
abstract = "Obesity and its comorbidities are an increasing challenge for both affected individuals and health care systems, worldwide. In obese individuals, perturbation of expression of both protein-coding genes and microRNAs (miRNA) are seen in obesity-relevant tissues (i.e. adipose tissue, liver and skeletal muscle). miRNAs are small non-coding RNA molecules which have important regulatory roles in a wide range of biological processes, including obesity. Rodents are widely used animal models for human diseases including obesity. However, not all research is applicable for human health or diseases. In contrast, pigs are emerging as an excellent animal model for obesity studies, due to their similarities in their metabolism, their digestive tract and their genetics, when compared to humans. The G{\"o}ttingen minipig is a small sized easy-to-handle pig breed which has been extensively used for modeling human obesity, due to its capacity to develop severe obesity when fed ad libitum. The aim of this study was to identify differentially expressed of protein-coding genes and miRNAs in a G{\"o}ttingen minipig obesity model. Liver, skeletal muscle and abdominal adipose tissue were sampled from 7 lean and 7 obese minipigs. Differential gene expression was investigated using high-throughput quantitative real-time PCR (qPCR) on 90 mRNAs and 72 miRNAs. The results revealed de-regulation of several obesity and inflammation-relevant protein-coding genes and miRNAs in all tissues examined. Many genes that are known to be de-regulated in obese humans were confirmed in the obese minipigs and several of these genes have target sites for miRNAs expressed in the opposing direction of the gene, confirming miRNA-mediated regulation in obesity. These results confirm the translational value of the pig for human obesity studies.",
author = "Mentzel, {Caroline M. Junker} and Ferhat Alkan and Helle Keinicke and Jacobsen, {Mette Juul} and Jan Gorodkin and Merete Fredholm and {Cirera Salicio}, Susanna",
year = "2016",
month = nov,
day = "30",
doi = "10.1371/journal.pone.0167285",
language = "English",
volume = "11",
journal = "PLoS ONE",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "11",

}

RIS

TY - JOUR

T1 - Joint profiling of miRNAs and mRNAs reveals miRNA mediated gene regulation in the Göttingen minipig obesity model

AU - Mentzel, Caroline M. Junker

AU - Alkan, Ferhat

AU - Keinicke, Helle

AU - Jacobsen, Mette Juul

AU - Gorodkin, Jan

AU - Fredholm, Merete

AU - Cirera Salicio, Susanna

PY - 2016/11/30

Y1 - 2016/11/30

N2 - Obesity and its comorbidities are an increasing challenge for both affected individuals and health care systems, worldwide. In obese individuals, perturbation of expression of both protein-coding genes and microRNAs (miRNA) are seen in obesity-relevant tissues (i.e. adipose tissue, liver and skeletal muscle). miRNAs are small non-coding RNA molecules which have important regulatory roles in a wide range of biological processes, including obesity. Rodents are widely used animal models for human diseases including obesity. However, not all research is applicable for human health or diseases. In contrast, pigs are emerging as an excellent animal model for obesity studies, due to their similarities in their metabolism, their digestive tract and their genetics, when compared to humans. The Göttingen minipig is a small sized easy-to-handle pig breed which has been extensively used for modeling human obesity, due to its capacity to develop severe obesity when fed ad libitum. The aim of this study was to identify differentially expressed of protein-coding genes and miRNAs in a Göttingen minipig obesity model. Liver, skeletal muscle and abdominal adipose tissue were sampled from 7 lean and 7 obese minipigs. Differential gene expression was investigated using high-throughput quantitative real-time PCR (qPCR) on 90 mRNAs and 72 miRNAs. The results revealed de-regulation of several obesity and inflammation-relevant protein-coding genes and miRNAs in all tissues examined. Many genes that are known to be de-regulated in obese humans were confirmed in the obese minipigs and several of these genes have target sites for miRNAs expressed in the opposing direction of the gene, confirming miRNA-mediated regulation in obesity. These results confirm the translational value of the pig for human obesity studies.

AB - Obesity and its comorbidities are an increasing challenge for both affected individuals and health care systems, worldwide. In obese individuals, perturbation of expression of both protein-coding genes and microRNAs (miRNA) are seen in obesity-relevant tissues (i.e. adipose tissue, liver and skeletal muscle). miRNAs are small non-coding RNA molecules which have important regulatory roles in a wide range of biological processes, including obesity. Rodents are widely used animal models for human diseases including obesity. However, not all research is applicable for human health or diseases. In contrast, pigs are emerging as an excellent animal model for obesity studies, due to their similarities in their metabolism, their digestive tract and their genetics, when compared to humans. The Göttingen minipig is a small sized easy-to-handle pig breed which has been extensively used for modeling human obesity, due to its capacity to develop severe obesity when fed ad libitum. The aim of this study was to identify differentially expressed of protein-coding genes and miRNAs in a Göttingen minipig obesity model. Liver, skeletal muscle and abdominal adipose tissue were sampled from 7 lean and 7 obese minipigs. Differential gene expression was investigated using high-throughput quantitative real-time PCR (qPCR) on 90 mRNAs and 72 miRNAs. The results revealed de-regulation of several obesity and inflammation-relevant protein-coding genes and miRNAs in all tissues examined. Many genes that are known to be de-regulated in obese humans were confirmed in the obese minipigs and several of these genes have target sites for miRNAs expressed in the opposing direction of the gene, confirming miRNA-mediated regulation in obesity. These results confirm the translational value of the pig for human obesity studies.

U2 - 10.1371/journal.pone.0167285

DO - 10.1371/journal.pone.0167285

M3 - Journal article

C2 - 27902747

VL - 11

JO - PLoS ONE

JF - PLoS ONE

SN - 1932-6203

IS - 11

M1 - e0167285

ER -

ID: 171797121