Novel targets in renal fibrosis based on bioinformatic analysis I
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA899890 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22247534.fastq.gz | Fastqsanger.gz | |||
| SRR22247535.fastq.gz | Fastqsanger.gz | |||
| SRR22247536.fastq.gz | Fastqsanger.gz | |||
| SRR22247537.fastq.gz | Fastqsanger.gz | |||
| SRR22247538.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 10 |
Similar Datasets
Project description:Novel targets in renal fibrosis based on bioinformatic analysis II
| PRJNA899899 | ENA
Project description:Renal fibrosis is a widely used pathological indicator of progressive chronic kidney disease (CKD), and renal fibrosis mediates most progressive renal diseases as a final pathway. Nevertheless, the key genes related to the host response are still unclear. In this study, the potential gene network, signaling pathways, and key genes under UUO model in mouse kidneys were investigated by integrating two transcriptional data profiles.
2023-01-06 | GSE217654 | GEO
Project description:Renal fibrosis is a widely used pathological indicator of progressive chronic kidney disease (CKD), and renal fibrosis mediates most progressive renal diseases as a final pathway. Nevertheless, the key genes related to the host response are still unclear. In this study, the potential gene network, signaling pathways, and key genes under UUO model in mouse kidneys were investigated by integrating two transcriptional data profiles.
2023-01-06 | GSE217650 | GEO
Project description:Background: Renal fibrosis is a widely used pathological indicator of progressive chronic kidney disease (CKD), and renal fibrosis mediates most progressive renal diseases as a final pathway. Nevertheless, the key genes related to the host response are still unclear. In this study, the potential gene network, signaling pathways, and key genes under unilateral ureteral obstruction (UUO) model in mouse kidneys were investigated by integrating two transcriptional data profiles. Methods: The mice were exposed to UUO surgery in two independent experiments. After 7 days, two datasets were sequenced from mice kidney tissues, respectively, and the transcriptome data were analyzed to identify the differentially expressed genes (DEGs). Then, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were executed. A Protein-Protein Interaction (PPI) network was constructed based on an online database STRING. Additionally, hub genes were identified and shown, and their expression levels were investigated in a public dataset and confirmed by quantitative real time-PCR (qRT-PCR) in vivo. Results: A total of 537 DEGs were shared by the two datasets. GO and the KEGG analysis showed that DEGs were typically enriched in seven pathways. Specifically, five hub genes (Bmp1, CD74, Fcer1g, Icam1, H2-Eb1) were identified by performing the 12 scoring methods in cytoHubba, and the receiver operating characteristic (ROC) curve indicated that the hub genes could be served as biomarkers. Conclusion: A gene network reflecting the transcriptome signature in CKD was established. The five hub genes identified in this study are potentially useful for the treatment and/or diagnosis CKD as biomarkers.
| S-EPMC9745177 | biostudies-literature
Project description:miR-132 mediates renal fibrosis
| PRJNA307696 | ENA
Project description:Tubular epithelial cells (TECs) play a major role in potentiating renal fibrosis. While TGF-β1 is a key inducer of the pro-fibrotic phenotype in TECs, inhibition of TGF-β1 also blocks its protective effects, making this an unsuccessful strategy for treating renal fibrosis. Molecules induced by TGF-β1 to regulate TEC phenotype would serve as more specific and effective targets. To uncover such molecules, we performed high throughput analyses on TGF-β1 treated renal tubular epithelial cells (HKC). RNA sequencing identified 3565 genes and proteomics identified 74 proteins differentially regulated by TGF-β1 in HKC. We then selected 47 genes that were most upregulated in our in vitro datasets and that do not have well-characterized roles in renal fibrosis based on our review of the literature. We searched 8 publicly available datasets containing transcriptomic data from diseased human kidneys for gene expression patterns of the selected genes and found that MARCKS and DOCK2 were amongst the most consistently upregulated in the human datasets. In HKC, MARCKS knockdown decreased TGF-β1 mediated upregulation of pro-fibrotic markers, while DOCK2 knockdown had the opposite effect. Our data suggests novel roles for these proteins in renal TECs as potential promoters the pro-fibrotic phenotype.
2022-07-06 | GSE207291 | GEO
Project description:Renal transplantation is the preferred treatment of end stage renal disease, but allograft survival is limited by development of interstitial fibrosis and tubular atrophy in response to various stimuli. Much effort has been put into identifying new protein markers of fibrosis to support the diagnosis. In present work, we performed an in-depth quantitative proteomics analysis of allograft biopsies from 31 prevalent renal transplant patients and identified correlated the quantified proteins with the volume fraction of fibrosis as determined by a morphometric method. Linear regression analysis identified four proteins that were highly associated with the degree of interstitial fibrosis, namely Coagulation Factor XIII A chain (estimate 18.7, adjusted p<0.03), Uridine Phosphorylase 1 (estimate 19.4, adjusted p<0.001), Actin-related protein 2/3 subunit 2 (estimate 34.2, adjusted p<0.05) and Cytochrome C Oxidase Assembly Factor 6 homolog (estimate -44.9, adjusted p<0.002) even after multiple testing. Proteins that were negatively associated with fibrosis (p < 0.005) were primarily related to normal metabolic processes and respiration, whereas proteins that were positively associated with fibrosis (p < 0.005) were involved in catabolic processes, cytoskeleton organization and immune response. The identified proteins may be candidates for further validation with regards to renal fibrosis. The results support the notion that cytoskeleton organization and immune responses are prevalent processes in renal allograft fibrosis.
2020-05-26 | PXD017867 | Pride
Project description:RNA modification play vital roles in renal fibrosis. However, whether ac4C modification functions in renal fibrogenesis remains unknown. Here, we found that NAT10-ac4C axis plays pro—fibrotic role in kidney. ac4C RIP sequencing demonstrated NAT10-ac4C axis functions via regulating multiple master genes of exosome secretion in tubular epithelial cells. In summary, targeting NAT10-ac4C axis is a promising strategy for renal fibrosis.
2024-11-30 | GSE248203 | GEO
Project description:Renal fibrosis is an important pathological change in the development of progressive kidney diseases. Ubiquitination is a post-translational modification of proteins involved in the regulation of various pathophysiological processes. In this study, we found that the deubiquitinating enzyme YOD1 is significantly upregulated in the kidney tissues of Ang II-challenged mice and Ang II upregulates YOD1 expression in renal tubular epithelial cells. YOD1 deficiency significantly alleviated renal injury and fibrosis induced by Ang II infusion in mice. Mechanistically, RNA-seq and co-immunoprecipitation analysis showed a pro-fibrotic protein, JAK2, as a YOD1-binding protein. We identify that JAK2 interacts with the C-terminal Znf domain of YOD1. YOD1 removed K48-linked ubiquitination of JAK2 at residue K970 via its active site C155, which stabilizes JAK2 and then maintains JAK2/STAT3 signaling pathway activation to induce pro-fibrotic gene expression in renal tubular epithelial cells. JAK2 inhibitors reversed the renal fibrosis promoted by YOD1 in mice. We also show increased levels of YOD1 and JAK2 in the kidney tissues of patients with renal fibrosis. In addition, YOD1 knockout significantly prevents unilateral ureteral ligation (UUO)-induced renal fibrosis in mice. Collectively, these findings identify YOD1 as a novel regulator in renal fibrosis via deubiquitinating JAK2.
2024-01-06 | GSE234355 | GEO
Project description:NAT10-ac4C axis promote renal fibrosis
| PRJNA1042804 | ENA