| First Author | Zhou Q | Year | 2015 |
| Journal | Sci Rep | Volume | 5 |
| Pages | 17901 | PubMed ID | 26648110 |
| Mgi Jnum | J:356931 | Mgi Id | MGI:6215974 |
| Doi | 10.1038/srep17901 | Citation | Zhou Q, et al. (2015) Identification of Genes Associated with Smad3-dependent Renal Injury by RNA-seq-based Transcriptome Analysis. Sci Rep 5:17901 |
| abstractText | Transforming growth factor-beta/Smad3 signaling plays a critical role in the process of chronic kidney disease (CKD), but targeting Smad3 systematically may cause autoimmune disease by impairing immunity. In this study, we used whole-transcriptome RNA-sequencing to identify the differential gene expression profile, gene ontology, pathways, and alternative splicing related to TGF-beta/Smad3 in CKD. To explore common dysregulation of genes associated with Smad3-dependent renal injury, kidney tissues of Smad3 wild-type and knockout mice with immune (anti-glomerular basement membrane glomerulonephritis) and non-immune (obstructive nephropathy)-mediated CKD were used for RNA-sequencing analysis. Totally 1922 differentially expressed genes (DEGs) were commonly found in these CKD models. The up-regulated genes are inflammatory and immune response associated, while decreased genes are material or electron transportation and metabolism related. Only 9 common DEGs were found to be Smad3-dependent in two models, including 6 immunoglobulin genes (Ighg1, Ighg2c, Igkv12-41, Ighv14-3, Ighv5-6 and Ighg2b) and 3 metabolic genes (Ugt2b37, Slc22a19, and Mfsd2a). Our results identify transcriptomes associated with renal injury may represent a common mechanism for the pathogenesis of CKD and reveal novel Smad3 associated transcriptomes in the development of CKD. |
