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

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

PROVIDER: PRJNA872521 | ENA |

REPOSITORIES: ENA

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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

JNK Signalling Regulates Self-Renewal of Proliferative Urine-Derived Renal Progenitor Cells via Inhibition of Ferroptosis.

Project description: Not available

| S-EPMC10486975 | biostudies-literature

Targeting JNK Pathway Expands Human Hematopoietic Stem Cells

Project description:The limited number of human hematopoietic stem cells (HSCs) has restrained their widespread clinical application. Despite great efforts in recent years, the in vitro expansion of HSCs remains a challenge due to incomplete understanding of the signaling networks underlying HSC self-renewal. Here we show that culturing human cord blood (CB) CD34+ cells with JNK-IN-8, an inhibitor of the JNK signaling pathway, can enhance the self-renewal of HSCs with a 6-fold increase in number. These expanded CD34+ cells repopulated recipient mice for 20 weeks and can form secondary engraftment that lasted for more than 21 weeks. Knockdown of c-Jun, a major downstream target in the JNK pathway, significantly promoted the expansion of hematopoietic stem and progenitor cells (HSPCs). Our findings demonstrate a critical role of JNK pathway in regulating HSC expansion, provide new insights into HSC self-renewal mechanism, and may lead to improved clinical application of HSCs.

2019-01-17 | GSE114524 | GEO

Expression data from Xenopus laevis embryonic epidermis depleted for Jnk signalling

Project description:St. 14 embryos were incubated in 100mM of a Jnk inhibitor (SP600125)-0,1x MBS until stage 24. Embryonic epidermis was isolated and stored immediately in chilled (4Â°C) Trizol. We sought to uncover all the putative targets of Jnk expresssed in the embryonic epidermis whole embryonic skin was isolated and immediately stored in chilled trizol Xenopus embryos skins were isolated at stage 24 of early development for Trizol RNA extraction and hybridization on Affymetrix microarrays. Each sample contains 20 whole embryonic skins

2016-06-24 | E-GEOD-83672 | biostudies-arrayexpress

Expression data from Xenopus laevis embryonic epidermis depleted for Jnk signalling

2016-06-24 | GSE83672 | GEO

Urine

Project description:Urine Raw sequence reads

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GADD45A loss enhances leukemia-initiating cell self-renewal and ferroptosis resistance in AML

Project description:Loss of GADD45A expression is implicated in poor patient outcomes in acute myeloid leukemia (AML) but its role in leukemia stem cells (LSCs) and disease pathogenesis remains largely unknown. Here we report that GADD45A loss is a critical determinant of high self-renewal potential and knockout of GADD45A supports long-term self-renewal and promotes LSC quiescence, accompanied by the acquisition of an increasingly aggressive phenotype upon serial transplantation in mice. The enhanced LSC characteristics are associated with GADD45A deletion-induced increase in key WNT/self-renewal-related genes. GADD45A knockout promotes engraftment of patient-derived xenograft (PDX) of relapsed AML in mice. Single cell RNA-seq on primary LSCs of AML PDXs and subsequent functional studies show that low expression of GADD45A, an important sensor of oxidative stress, confers ferroptosis resistance through upregulation of genes involved in detoxification of excess iron and reactive oxygen species (ROS), revealing a mechanism of drug resistance in primary AML with unfavorable cytogenetics.

2025-08-29 | E-MTAB-9803 | biostudies-arrayexpress

Escherichia coli strain:urine | isolate:urine

Project description:Escherichia coli strain:urine | isolate:urine Genome sequencing

| PRJNA1501663 | ENA

Kdm6b is Required for Self-Renewal of Normal and Leukemic Stem Cells Under Proliferative Stress

Project description:Kdm6b is Required for Self-Renewal of Normal and Leukemic Stem Cells Under Proliferative Stress

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urine metagenome

Project description:urine metagenome Metagenome

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