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A Comprehensive Molecular Portrait of Human Urine-derived Renal Progenitor Cells

ABSTRACT: A Comprehensive Molecular Portrait of Human Urine-derived Renal Progenitor Cells

PROVIDER: PRJNA527028 | ENA |

REPOSITORIES: ENA

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A Comprehensive Molecular Portrait of Human Urine-derived Renal Progenitor Cells

Project description:Human urine is now recognized as a non-invasive source of stem cells with regeneration potential. These cells are mesenchymal stem cells but their detailed molecular and cellular identities are poorly defined. Furthermore, unlike the mouse, the gene regulatory network driving stemness and differentiation into functional renal cells in vitro remain unresolved. In this study, we isolated urine mesenchymal stem cells from 10 individuals of both genders and distinct ages, these cells express pluripotency- associated proteins- TRA-1-160, TRA-1-181, SSEA4, C-KIT and CD133. Expression of pluripotency-associated proteins enabled rapid reprogramming into iPSCs using episomal-based plasmids without pathway purtabations. Transcriptome analysis revealed expression of a plethora of nephrogenesis-related genes such as SIX2, OSR1, CITED1, NPHS2, NPHS1, PAX2, SALL1, AQP2, EYA1, SLC12A1 and UMOD. As expected the cells transport Albumin by endocytosis. Based on this we refer to these cells as urine derived renal progenitor cells- UdRPCs. Associated GO-term analysis of UdRPCs and UdRPC-iPSCs underlined their renal identity and functionality. Upon differentiation by WNT activation using the GSK3β inhibitor (CHIR99021), transcriptome and KEGG pathway analysis revealed upregulation of WNT-associated genes-AXIN2, JUN and NKD1. Protein interaction network identified JUN,- a downstream target of the WNT pathway in association with STAT3, ATF2 and MAPK1 as a putative key regulator of self-renewal and differentiation in UdRPCs. Furthermore, like pluripotent stem cells, self-renewal is maintained by FGF2-driven TGFβ-SMAD2/3 pathway. Ultimately, our in vitro model and the data presented in this study should lay the foundation for studying nephrogenesis in man.

2020-02-03 | GSE128281 | GEO

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Epigenome and transcriptome profiling of urine progenitor renal cells

Project description:We characterized the transcriptome and methylome of renal progenitor cells in the urine of a cohort of stable kidney transplant recipients to elucidate whether the origin of the donor (living or deceased donor) was associated with a specific molecular reprogramming.

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Epigenome and transcriptome profiling of urine progenitor renal cells

Project description:Epigenome and transcriptome profiling of urine progenitor renal cells

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DNA methylation of Human Urine Renal Progenitors after kidney transplantation

Project description:The Illumina Infinium MethylationEPIC Beadchip was used to obtain genomewide methylation profiles from Human Urine Renal Progenitors obtained after kidney transplantation from lived donors or dead donors

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JNK signalling regulates self-renewal of proliferative urine-derived renal progenitor cells via inhibition of ferroptosis.

Project description:With a global increase in chronic kidney disease patients, alternatives to dialysis and organ transplantation are needed. Stem cell-based therapies could be one possibility to treat chronic kidney disease. Here, we used multipotent urine-derived renal progenitor cells (UdRPCs) to study nephrogenesis. UdRPCs treated with the JNK inhibitor- AEG3482, displayed decreased proliferation and downregulated transcription of cell cycle-associated genes as well as the kidney progenitor markers -SIX2, CITED1, and SALL1. In addition, levels of activated SMAD2/3, which is associated with the maintenance of self-renewal in UdRPCs, were decreased. JNK inhibition resulted in less efficient oxidative phosphorylation and more lipid peroxidation via ferroptosis- an iron-dependent non-apoptotic cell death pathway linked to various forms of kidney disease. Our study reveals the importance of JNK signalling in maintaining self-renewal as well as protection against ferroptosis in SIX2-positive UdRPCs. We propose that UdRPCs can be used for modelling ferroptosis-induced kidney diseases.

2024-08-13 | GSE211892 | GEO

Generation of induced nephron progenitor-like cells from human urine-derived cells

Project description:Analysis of induced nephron progenitor cells from female/male urine cells (iNPC-F/INPC-M) by defined transcription factors vs. ESC derived nephron progenitor cell (ESC-NPC_H9/ESC-NPC_BG01) and female/male urine cells (UC-F/UC-M). Results provide insight into molecular similarities between induced nephron progenitor cells and human ESC derived nephron progenitor cell

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A comprehensive urine proteome database generated from patients with various renal conditions and prostate cancer

Project description:A total of 45 urine samples from 5 prostate cancer (PC) patients, 10 renal transplant patients with proven acute rejection (AR), 10 renal transplant patients with stable graft (STA), 10 non-specific proteinuria patients (NS), and 10 healthy individuals (HI), were utilized for global urine proteome profiling using 2D-LC-MS/MS. Peptides were digested with trypsin then analyzed by LC-MS/MS. Data was searched with MS-GF+ using PNNL's DMS Processing pipeline.

2020-11-19 | MSV000086484 | MassIVE

JNK signalling regulates self-renewal of proliferative urine-derived renal progenitor cells via inhibition of ferroptosis.

Project description:JNK signalling regulates self-renewal of proliferative urine-derived renal progenitor cells via inhibition of ferroptosis.

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Transcriptome sequencing identified RNAs associated with renal fibrosis in UUO rat model (urine)

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.

2017-08-12 | GSE100632 | GEO

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