Novel targets in renal fibrosis based on bioinformatic analysis II
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ABSTRACT:
PROVIDER: PRJNA899899 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22247629.fastq.gz | Fastqsanger.gz | |||
| SRR22247630.fastq.gz | Fastqsanger.gz | |||
| SRR22247631.fastq.gz | Fastqsanger.gz | |||
| SRR22247632.fastq.gz | Fastqsanger.gz | |||
| SRR22247633.fastq.gz | Fastqsanger.gz |
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Project description:Novel targets in renal fibrosis based on bioinformatic analysis I
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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.
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Project description:miR-132 mediates renal fibrosis
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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.
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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
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Project description:Renal fibrosis as the final outcome of many renal diseases, has always been paid more attention to by the researchers. To better understand whether lncRNAs could be a player in this process or be a biomarker for renal fibrosis diagnosis, we compared transcriptome sequencing data on renal tissues and urine respectively between UUO and shamed (Sham) rat model. Numerous genes including lncRNAs with significant changes in their expression were identified. 24 lncRNAs were up-regulated and 79 lncRNAs were down-regulated in the renal tissues of the UUO rats. 625 lncRNAs were up-regulated and 177 lncRNAs were down-regulated in urines of the UUO rats. Among the lncRNAs upregulated in renal tissue of UUO rats, 19 lncRNAs were predicted containing several conserved Smad3 binding motifs in the promoter. Among them, lncRNAs with putative promoter containing more than 4 conserved Smad3 binding motifs were demonstrated to be induced by TGF-β significantly in NRK-52E cells. We further confirmed that lncRNA TCONS_00088786 and TCONS_01496394 were regulated by TGF-β stimulation and also can influence the expression of some fibrosis-related genes through a feedback loop. Based on transcriptome sequencing data, bioinformatics analysis and qRT-PCR detection, we also demonstrated lncRNA in Urine are detectable and might be a novel biomarker of renal fibrosis. These data provide new information about the involvement of lncRNAs in renal fibrosis, indicating that they may serve as candidate biomarkers or therapeutic targets in the future.
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