Impact of exudative diathesis induced by selenium deficiency on LncRNAs and their roles in the oxidative reduction process in broiler chick veins

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.

Long-term neurocognitive dysfunction in offspring via NGF/ ERK/CREB signaling pathway caused by ketamine exposure during the second trimester of pregnancy in rats

“…Nissl bodies are characteristic neuronal structures in the cytoplasm of dendritic cells and neurons, and they have been reported to be involved in protein production and are sensitive indicators of neuronal function [ 47 ]. Our results showed ketamine induced neuronal cell loss in the hippocampal CA1 and CA3 regions of offspring, which is consistent with previously published results [ 49 ], it might be related to vascular injury in brain [ 50 , 51 ]. Furthermore, long-term neurocognitive function requires functional integrity of dendritic spines [ 52 ].…”

Regulation of lipid peroxidation and ferroptosis in diverse species

“…As noted above, the selenium-containing enzyme GPX4 (Brigelius-Flohe and Maiorino 2013) acts by reducing lipid hydroperoxides (Yang et al 2014). Lack of protection from lipid peroxidation, such as in selenium deficiency, causes exudative diathesis in broiler birds (Cao et al 2017). Depletion of GPX4 may be the cause of this selenium deficiency disease (Yao et al 2014).…”

WITHDRAWN: Selenium supplementation inhibits lipopolysaccharide-induced endometritis by decreasing the cholesterol content of lipid rafts

“…Selenium (Se), one of the nutritionally necessary trace elements for a large range of species, exerts a variety of biological effects including immune protection [8] and alleviation of tissue injuries [9,10], and regulates muscle metabolism and apoptosis [11,12], brain function and neuropathology [13], and reproduction [14]. Accordingly, Se deficiency can lead to pathological conditions, including reproductive disorders and inflammatory diseases.…”