Project description:This study investigates the role of endothelial cell (EC) gene expression in the focal origin of atherosclerosis. The EC transcriptome was profiled in multiple arterial regions of normal swine. Specifically, small amounts of EC RNA were isolated from 7 athero-susceptible and 6 athero-protected regions. The number of replicates for each site varied between 4 and 8. A total of 98 samples from 76 animals were used. For each sample, linearly amplified RNA (labeled with Cy5) was co-hybridized with pooled arterial reference RNA (labeled with Cy3) onto a custom-printed porcine oligo microarray (70-mers).
Project description:In recent years, the roles of microRNAs playing in the regulation of influenza viruses replication caused researchers' much attenion. However, much work focused on the interactions between human, mice or chicken microRNAs with human or avian influenza viruses rather than the interactions of swine microRNAs and swine influenza viruses. To investigate the roles of swine microRNAs playing in the regulation of swine influenza A virus replication, the microRNA microarray was performed to identify which swine microRNAs were involved in swine H1N1/2009 influenza A virus infection.
2017-03-24 | GSE96953 | GEO
Project description:Integral approach in the resistome characterization on Spanish swine farms.
Project description:Comparison of gene expression in dendritic cells (DCs) isolated from tumors of C57BL/6 obtained from Taconic farms vs DCs isolated from tumor of C57BL/6 mice obtained from Jackson Labortaory vs DCs isolated from tumors of C57BL/6 obtained from Taconic farms and orally gavaged with Bifidobacterium prior to tumor implantation
Project description:Endothelial dysfunction is a hallmark of LPS-induced acute kidney injury (AKI). Endothelial cells (EC) acquired a fibroblast-like phenotype and contributed to myofibroblasts generation through Endothelial to Mesenchymal Transition (EndMT) process. Noteworthy, ARPCs enhance tubular regenerative mechanism during AKI, but little is known about their effects on EC. Here we investigated whether ARPCs could prevent sepsis-induced EndMT and the related mechanism. When activated by LPS, Human endothelial cells (EC) proliferated and decreased specific EC markers such as CD31 and VE-cadherin and up-regulated myofibroblast markers such as Collagen I and Vimentin. The co-culture with ARPCs normalized EC proliferation rate and abrogated the LPS-induced EndMT by restoring the high expression of EC markers and the low expression of myofibroblast markers. Gene set enrichment analysis showed that most of genes modulated in LPS-stimulated ARPCs belongs to cell activation and defense response pathways. In particular, among most up-regulated genes we found BPIFA2, SAA2, SAA4 and CXCL6. BPIFA2 is recently described as an early biomarker of AKI but little is known about its function in the kidney. The other genes are frequently involved in the response to bacterial infection and kidney injury. Finally, in a swine model of LPS-induced AKI, we observed an increase of CD133+ARPCs that expressed BPIFA2 respect to healthy pigs. Taken together, these results suggest an underestimate role of ARPCS in preventing endothelial dysfuncton by the production of several proteins. The identification of these molecules may offer novel strategies to protect endothelial compartment and promote kidney repair.