A transcriptomic study of myogenic differentiation under the overexpression of PPARγ by RNA-Seq

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作者
Kan He
Guoying Wu
Wen-Xing Li
Daogang Guan
Wenwen Lv
Mengting Gong
Shoudong Ye
Aiping Lu
机构
[1] School of Life Sciences,Department of Biostatistics
[2] Anhui University,undefined
[3] School of Chinese Medicine,undefined
[4] Hong Kong Baptist University,undefined
[5] 7 Baptist University Road,undefined
[6] Center for Stem Cell and Translational Medicine,undefined
[7] School of Life Sciences,undefined
[8] Anhui University,undefined
[9] State Key Laboratory of Genetic Resources and Evolution,undefined
[10] Kunming Institute of Zoology,undefined
[11] Chinese Academy of Sciences,undefined
[12] Kunming College of Life Science,undefined
[13] University of Chinese Academy of Sciences,undefined
[14] Hongqiao International Institute of Medicine,undefined
[15] Shanghai Tongren Hospital/Faculty of Public Health,undefined
[16] School of Medicine,undefined
[17] Shanghai Jiao Tong University,undefined
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摘要
To study the cellular and molecular function of peroxisome proliferator-activated receptor γ (PPARγ) in skeletal muscle differentiation, we have generated inducible gain-of-function to overexpress PPARγ in C2C12 myoblasts. In order to identify PPARγ targets, RNA sequencing (RNA-seq) was used to evaluate and quantify the transcriptomes and expression patterns during myogenic differentiation under the overexpression of PPARγ. The formation of myotubes and the expression of muscle-specific myogenic genes such as MyoD and MyoG may be inhibited by PPARγ overexpression. Multiple genes and pathways were significantly involved in this process, including 11 genes such as Fndc9 and Slc14a1 with fundamental change of regulation modes, 9 genes of which were validated by the data of qRT-PCR. Our studies demonstrate that PPARγ would play critical roles on myoblasts differentiation, mediating crosstalk among several pathways and transcription factors. Our data is available in the Gene Expression Omnibus (GEO) database with the accession number as GSE99399.
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