Differential expression network analysis for diabetes mellitus type 2 based on expressed level of islet cells
ANNALES D ENDOCRINOLOGIE
Authors: Cui, Ying; Chen, Wen; Chi, Jinfeng; Wang, Lei
Abstract
Objective. - Diabetes mellitus type 2 (T2DM) is a metabolic disease that has become a pressing issue, with potential adverse impact on mental health. We aimed to explore the potential molecular mechanism of T2DM. Material and methods. - GSE38642 microarray data downloaded from gene expression omnibus was used to identify the differentially expressed genes (DEGs). Profiling of complex functionality (ProfCom) was used to analyze the complex function and mine T2DM signature genes. Finally, the differential expression network (DEN) was constructed. Results. - We identified 147 DEGs including 59 up- and 88 down-regulated genes. With increasing of degree, the specificity of functional description of DEGs was higher. GO term of "integral to membrane and immune response (not receptor activity) not regulation of immune response" in degree 4 was enriched by 6 DEGs, while the GO term of "immune response" in degree 1 was enriched by 12 DEGs. Two complex functions of integral to membrane an immune response and response to glucose stimulus were enriched by 11 T2DM signature genes including ARG2, GLP1R, PFKFB2, PTPRN, ACSL5, CCR7, IL2RA, IL7R, IL1R2, IL1RL1 and CHST4. Finally, DEN including 11 signature genes and 491 edges was obtained. Conclusion. - The identified DEGs especially 11 signature genes such as PTPRN, GLP1R, CCR7 and IL2RA may play important roles in the pathogenesis of T2DM. (C) 2015 Elsevier Masson SAS. All rights reserved.
Transcriptome analysis reveals similarities between human blood CD3(-) CD56(bright) cells and mouse CD127(+) innate lymphoid cells
SCIENTIFIC REPORTS
Authors: Allan, David S. J.; Cerdeira, Ana Sofia; Ranjan, Anuisa; Kirkham, Christina L.; Aguilar, Oscar A.; Tanaka, Miho; Childs, Richard W.; Dunbar, Cynthia E.; Strominger, Jack L.; Kopcow, Hernan D.; Carlyle, James R.
Abstract
For many years, human peripheral blood natural killer (NK) cells have been divided into functionally distinct CD3(-)CD56(bright) CD16(-) and CD3(-)CD56(dim) CD16(+) subsets. Recently, several groups of innate lymphoid cells (ILC), distinct from NK cells in development and function, have been defined in mouse. A signature of genes present in mouse ILC except NK cells, defined by Immunological Genome Project studies, is significantly over-represented in human CD56(bright) cells, by gene set enrichment analysis. Conversely, the signature genes of mouse NK cells are enriched in human CD56(dim) cells. Correlations are based upon large differences in expression of a few key genes. CD56bright cells show preferential expression of ILC-associated IL7R (CD127), TNFSF10 (TRAIL), KIT (CD117), IL2RA (CD25), CD27, CXCR3, DPP4 (CD26), GPR183, and MHC class II transcripts and proteins. This could indicate an ontological relationship between human CD56(bright) cells and mouse CD127(+) ILC, or conserved networks of transcriptional regulation. In line with the latter hypothesis, among transcription factors known to impact ILC or NK cell development, GATA3, TCF7 (TCF-1), AHR, SOX4, RUNX2, and ZEB1 transcript levels are higher in CD56(bright) cells, while IKZF3 (AIOLOS), TBX21 (T-bet), NFIL3 (E4BP4), ZEB2, PRDM1 (BLIMP1), and RORA mRNA levels are higher in CD56(dim) cells.