Human FGFBP1 ELISA Kit

An alternative control for gastrointestinal nematode (GIN) infection in goats can be achieved by genetic improvement of the host resistance through identification of genes controlling the resistance mechanisms and their use in breeding programs under a marker-assisted selection or gene introgression frameworks. In this context, we aimed to develop genome wide association studies (GWAS) for resistance to H. contortus in Creole goats from Guadeloupe to identify possible candidate genes associated with GIN resistance in this population. Resistance was characterized by the fecal egg counting (FEC). A total of 182 Creole goats were phenotyped for FEC and genotyped through Illumina Goat SNP50 BeadChip. After SNP quality control analysis, 46,643 SNP markers were used for GWAS. The significant associations were identified by fitting a linear mixed model. A total of seven QTL (on the chromosomes 4, 6, 11, and 17) associated to FEC were reported and candidate genes recording was performed at these positions. The identified genes were related to the intestine damage (PROM1), inflammation process (FGFBP1), immune response (LIMCH1), hemorrhage control (ADAMTS3), and muscle weakness (SUCLG1). Network analysis provided annotation results linking all identified candidate genes, which are biologically related to resistance mechanisms approaching H. contortus infections.

Epithelial-mesenchymal transition (EMT) is implicated in bronchial remodeling and loss of lung function in chronic inflammatory airway diseases. Previous studies showed the involvement of the high mobility group box 1 (HMGB1) protein in the pathology of chronic pulmonary inflammatory diseases. However, the role of HMGB1 in EMT of human airway epithelial cells is still unclear. In this study, we used RNA sequencing to show that HMGB1 treatment regulated EMT-related gene expression in human primary-airway epithelial cells. The top five upregulated genes were SNAI2, FGFBP1, VIM, SPARC (osteonectin), and SERPINE1, while the downregulated genes included OCLN, TJP1 (ZO-1), FZD7, CDH1 (E-cadherin), and LAMA5. We found that HMGB1 induced downregulation of E-cadherin and ZO-1, and upregulation of vimentin mRNA transcription and protein translation in a dose-dependent manner. Additionally, we observed that HMGB1 induced AKT phosphorylation, resulting in SK3 beta inactivation, cytoplasmic accumulation, and nuclear translocation of beta-catenin to induce EMT in human airway epithelial cells. Treatment with PI3K inhibitor (LY294006) and beta-catenin shRNA reversed HMGB1-induced EMT. Moreover, HMGB1 induced expression of receptor for advanced glycation products (RAGE), but not that of Toll-like receptor (TLR) 2 or TLR4, and RAGE shRNA inhibited HMGB1-induced EMT in human airway epithelial cells. In conclusion, we found that HMGB1 induced EMT through RAGE and the PI3K/AKT/GSK3 beta/beta-catenin signaling pathway.