LncRNAs Transcriptome Analysis Revealed Potential Mechanisms of Selenium to Mastitis in Dairy Cows.

The trace element selenium (Se) plays an indispensable role in the growth of humans and animals due to its antioxidant function. Mastitis is one of the most important diseases affecting the dairy industry in the world. In recent years, long non-coding RNAs (lncRNAs) have been implicated in a series of cellular processes and disease development processes. RNA-sequencing technology was used to characterize lncRNA profiles and compared transcriptomic dynamics among the control group, the LPS group, and the Se-treated group to highlight the potential roles and functions of lncRNAs in the mammary epithelial cells of dairy cows. We identified 14 specific lncRNAs related to Se and their predicted target genes. KEGG and GO functional annotation was used to elucidate their biological function and the pathways in which they may be involved. The present study provides novel insights for exploring the molecular markers for the protection of Se against mastitis in dairy cows.

Effects of Selenium on MAC-T Cells in Bovine Mastitis: Transcriptome Analysis of Exosomal mRNA Interactions.

Selenium, a micronutrient, is indispensable for maintaining normal metabolic functions in animals and plants. Selenium has shown promise in terms of its effect on the immune function, ability to control inflammation, and ability to improve bovine mammary gland health. Bovine mastitis remains a major threat to dairy herds globally and has economically significant impacts. The exosomes are a new mode of intercellular communication. Exosomal transfer of mRNAs, microRNAs, and proteins between cells affects the protein production of recipient cells. The development of novel high-throughput omics approaches and bioinformatics tools will help us understand the effects of selenium on immunobiology. However, the differential expression of mRNAs in bovine mammary epithelial cell-derived exosomes has rarely been studied. In the present study, differences in the exosomal transcriptome between control and selenium-treated MAC-T cells were identified by RNA sequencing and transcriptome analysis. The results of mRNA profiling revealed 1978 genes in exosomes that were differentially expressed between the selenium-treated and control cells. We selected and analyzed 91 genes that are involved in inflammation, redox reactions, and immune cell function related to mastitis. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses revealed enrichment pathways involved in selenoproteins and the Ras/PI3K/AKT, MAPK, and FOXO signaling pathways. Our results revealed that selenium may play a crucial role in immune and inflammatory regulation by influencing the differential expression of exosomal mRNAs of key genes in bovine mastitis.

Selenium alleviates lipopolysaccharide-induced endometritis via regulating the recruitment of TLR4 into lipid rafts in mice.

Selenium (Se) is an essential trace element for living organisms and plays diverse biological roles. Endometritis is a common reproductive disorder in dairy cows, causing huge economic losses. In this study, we explored the effects of Se on lipopolysaccharide (LPS)-induced endometritis in mice and expounded its underlying mechanism of action. We validated the anti-inflammatory effects of Se in vivo by establishing a mouse model of endometriosis induced by LPS. Se significantly reversed the LPS-induced uterine histopathological changes, MPO activity and inflammatory cytokine levels in vivo. Simultaneously, TLR4 and its downstream signaling pathways, lipid rafts and cholesterol levels in the tissues were also attenuated by Se under LPS stimulation. In addition, the molecular mechanism of the Se anti-inflammatory effect was clarified in mouse endometrial epithelial cells. Se inhibited TLR4-mediated NF-κB and IRF3 signal transduction pathways to reduce the production of inflammatory factors. We found that Se promoted the consumption of cholesterol to suppress the lipid rafts coming into being and inhibited the TLR4 positioning to the lipid raft to prevent the inflammatory response caused by LPS. Meanwhile, Se activated the LxRα-ABCA1 pathway to cause the outflow of cholesterol in cells. The anti-inflammatory effect of Se was disrupted by silencing LxRα. In conclusion, Se exerted anti-inflammatory effects most likely by the LxRα-ABCA1 pathway activation, which inhibited lipid rafts by depleting cholesterol and ultimately impeded the migration of TLR4 to lipid rafts.