mProX™ Human CXCR1 Stable Cell Line

Zhuang Y, et al. "Circ_0026579 knockdown ameliorates lipopolysaccharide-induced human lung ." Clinical and experimental pharmacology & physiology, 2023.
Pneumonia is a respiratory disease characterized by inflammation in the lower respiratory tract and is known to involve the dysregulation of various RNA species. Among these RNA groups, circular RNAs have been identified as key players in the progression of pneumonia. However, the specific role of circular RNA circ_0026579 in regulating the occurrence of pneumonia remains unclear. Therefore, this study aimed to investigate the role of circ_0026579 in lipopolysaccharide-induced injury in human lung fibroblast cells and its underlying molecular mechanism. The expression levels of circ_0026579, miR-370-3p, and C-X-C motif chemokine receptor 1 (CXCR1) were measured through quantitative real-time polymerase chain reaction and western blotting. Furthermore, the production of pro-inflammatory cytokines and oxidative stress markers were evaluated through enzyme-linked immunosorbent assays, while cell viability, proliferation, and apoptosis were assessed using cell counting kit-8 assay, 5-Ethynyl-2'-deoxyuridine assay, and flow cytometry analysis, respectively. Through various experimental techniques, the study revealed that circ_0026579 was significantly upregulated, whereas miR-370-3p was downregulated in the serum of pneumonia patients. Upon lipopolysaccharide treatment, cells showed increased inflammation, oxidative stress, and apoptosis, while cell proliferation was inhibited. However, these effects were reversed after the depletion of circ_0026579. Furthermore, the study also demonstrated that circ_0026579 acted as a sponge for miR-370-3p and interacted with CXCR1, thus modulating its expression. Additionally, miR-370-3p was found to regulate CXCR1 expression, and its overexpression alleviated the effects of lipopolysaccharide-induced injury in lung fibroblast cells. Overall, the findings suggested that circ_0026579 played a crucial role in regulating the miR-370-3p/CXCR1 axis in pneumonia, and its absence ameliorated LPS-induced cellular dysfunction through this mechanism.
Pubmed: 37786235   DOI: 10.1111/1440-1681.13826

Lu Z, et al. "Bioinformatics analysis of copper death gene in diabetic immune infiltration.." Medicine, 2023.
Copper has been shown to have a significant impact on the human body and may be linked to the development of diabetes. However, the mechanisms through which copper death genes regulate immune infiltration in diabetes have not been thoroughly investigated. For this study, microarray data from healthy individuals and patients with diabetes was obtained from the GEO database. Through gene enrichment analysis, differentially expressed genes (DEGs) were identified and a protein interaction network was constructed using String online database and Cytoscape software. Further analysis using Wilcox was also conducted, revealing a correlation between copper death genes and diabetes. In addition, immune infiltration cells and their functions were compared between the two groups, resulting in the identification of several DEGs associated with copper death and prediction of potential microRNA through use of Funrich software. Results showed that out of the 328 DEGs identified in the GSE25724 and GSE95849 datasets, 190 were up-regulated and 138 were down-regulated with significant up-regulation observed in neurodegeneration-multiple disease pathways followed by Huntington disease according to KEGG analysis. Furthermore, down-regulated genes including HCK, FPR1, MNDA, AQP9, TLR8, CXCR1, CSF3R, VNN2, TLR4, and CCR5 were mostly enriched in neutrophils as shown by Cytohubba analysis. Immunoinfiltration heat maps indicated a strong positive correlation between Macrophage and Activated dendritic cell, Mast cell, Neutrophil, and Regulatory T cell. Significantly increased immune infiltration cells in the diabetic group included Neutroph, Mast cell, Activated B cell, Macrophage and Eosinophil while Central memory CD4 T cell, Plasmacytoid dendritic cell, Immature dendritic cell, and Central memory CD8 T cell, etal were significantly decreased. The study also revealed that DBT, SLC31A1, ATP7A, LIAS, ATP7B, PDHA1, DLST, PDHB, GCSH, LIPT1, DLD, FDX1, and DLAT genes were significantly linked to immune invasion cells and their functions. Ultimately, 41 miRNA were associated with copper death genes and their potential role in the development of diabetes. In conclusion, it is evident that copper death is closely tied to the occurrence of diabetes and copper death genes may play a crucial role in
Pubmed: 37773841   DOI: 10.1097/MD.0000000000035241