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Published on: January 13, 2016
Expression profile of long non-coding RNAs in rat models of OSA-induced cardiovascular disease: new insight into
Qingshi Chen1,2, Guofu Lin1,3,4, Jiefeng Huang1,3,4
1Department of Respiratory Disease, The First Affiliated Hospital of Fujian Medical University, No.20 Chazhong Road, Fuzhou, 350005, Taijiang District, China.
Purpose:
Long non-coding RNAs (lncRNAs) are a recently identified class of regulatory molecules involved in the regulation of numerous biological processes, but their functions in a rat model of chronic intermittent hypoxia (CIH) remain largely unknown. Therefore, for further investigation, we aimed to explore lncRNA expression profiles and reveal their potential functional roles in rat models of CIH.
Methods:
We used a well-established CIH rat model and conducted lncRNA microarray experiments on the heart samples of rats with CIH and under normoxia control. Differentially expressed lncRNAs and mRNAs were identified via fold-change filtering and verified by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Bioinformatics analyses were applied to reveal the potential roles of key lncRNAs. Co-expression analysis was conducted to determine the transcriptional regulatory relationship of lncRNAs and mRNAs between the two groups.
Results:
Our data indicated that 157 lncRNAs and 319 mRNAs were upregulated, while 132 lncRNAs and 428 mRNAs were downregulated in the rat model of CIH compared with sham control. Pathway analyses showed that 31 pathways involved in upregulated transcripts and 28 pathways involved in downregulated transcripts. Co-expression networks were also constructed to explore the potential roles of differentially expressed lncRNAs on mRNAs. LncRNAs, namely, XR_596701, XR_344474, XR_600374, ENSRNOT00000065561, XR_590196, and XR_597099, were validated by the use of qRT-PCR.
Conclusions:
The present study first revealed lncRNAs expression profiles in a rat model of CIH, providing new insight into the pathogenesis of obstructive sleep apnea-induced cardiovascular disease.
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