Abstract
Selenium deficiency may induce exudative diathesis (ED) in broiler chick, and this damage is closely related to oxidative damage. Long noncoding RNA (LncRNA) can regulate the redox state in vivo. The aim of the present study was to clarify the LncRNA expression profile in broiler veins and filter and verify the LncRNAs related to oxidative damage of ED. This study established an ED model induced by selenium deficiency and presented the expression and characterization of LncRNAs in normal and ED samples. A total of 15412 LncRNAs (including 8052 novel LncRNAs) were generated in six cDNA libraries using the Illumina Hi-Seq 4000 platform. 635 distinct changes in LncRNAs (up-regulated fold change > 1.5, down-regulated fold change < 0.67 and differentially expressed LncRNAs) were filtered. Gene ontology enrichment on LncRNAs target genes showed that the oxidative reduction process was important. This study also defined and verified 19 target mRNAs of 23 LncRNAs related to the oxidative reduction process. The in vivo and vitro experiments also demonstrated these 23 LncRNAs can participate in the oxidative reduction process. This study presents LncRNAs expression profile in broiler chick veins for the first time and confirmed 23 LncRNAs involving in the vein oxidative damage in ED.
Highlights
Long noncoding RNAs (LncRNAs) are a course of transcripts longer than 200 nucleotides that do not encode proteins
This study presents LncRNAs expression profile in broiler chick veins for the first time and confirmed 23 LncRNAs involving in the vein oxidative damage in exudative diathesis (ED)
Studies have shown the important role of LncRNA in regulating growth and development; and the function of LncRNA in regulating vascular health, vein endothelial cell (VEC) and VSMC has been noticed [26,27,28]
Summary
Long noncoding RNAs (LncRNAs) are a course of transcripts longer than 200 nucleotides that do not encode proteins. Increasing evidence demonstrates the important roles of LncRNAs in regulating many biological processes including transcription regulation [1], post-transcriptional processing [2], and subcellular trafficking [3] by mechanisms that are not yet fully understood. Studies have found the transcripts of LncRNAs in humans, pigs and mice [4,5,6]. LncRNAs are emerging as regulators of vascular function in health and disease. It is increasingly important to rapidly identify LncRNAs that are implicated in vascular disease [7]. LncRNAs can regulate redox state in vivo. Sun reported SCAL1 is an LncRNA that shows increased levels as a part of the oxidative stress response in lung carcinogenesis [8], Puthanveetil reported MALAT1 is an initiator of oxidative stress [9]
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