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Resilient CD133+CD24+ Kidney Progenitor Cells Drive Hypoxic Injury Recovery via HIF1A, EGFR, and EDN1 Expression

ABSTRACT: Resilient CD133+CD24+ Kidney Progenitor Cells Drive Hypoxic Injury Recovery via HIF1A, EGFR, and EDN1 Expression

PROVIDER: PRJNA1177503 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31110715_1.fastq.gz	Fastqsanger.gz
	SRR31110715_2.fastq.gz	Fastqsanger.gz
	SRR31110716_1.fastq.gz	Fastqsanger.gz
	SRR31110716_2.fastq.gz	Fastqsanger.gz
	SRR31110717_1.fastq.gz	Fastqsanger.gz

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Resilient CD133+CD24+ Kidney Progenitor Cells Drive Hypoxic Injury Recovery via HIF1A, EGFR, and EDN1 Expression

Project description:Kidney progenitor cells play a crucial role in the repair and regeneration of renal tubules following injury. This study investigates the differential responses of human renal tubular precursor TERT (HRTPT) CD133+CD24+ kidney progenitor cells and Human renal epithelial cell 24 TERT (HREC24T) CD133-CD24+ non-progenitor cells to hypoxic conditions, as well as their gene expression profiles. Whole transcriptome sequencing revealed distinct molecular characteristics, with HRTPT cells exhibiting enrichment in pathways associated with human and mouse embryonic stem cell pluripotency and hypoxia response. In vitro experiments demonstrated that HRTPT cells are more resistant to hypoxia, showing minimal cell death and a 100-fold increase in HIF1A protein levels. In contrast, HREC24T cells exhibited significant cell death and only a modest increase in HIF1A protein. Functional network analysis identified a central role for Endothelin-1 (EDN1) in the interaction between HIF1A and epidermal growth factor (EGF) signaling pathways. These results suggest that CD133+CD24+ kidney progenitor cells have enhanced survival mechanisms under hypoxic stress, enabling them to effectively proliferate and replace damaged tubular cells. This study provides novel insights into the protective role of kidney progenitor cells in renal injury and their potential therapeutic applications in kidney regeneration

2025-04-03 | GSE280279 | GEO

Analyze the transcriptional signature of human primary culture of CD133+ CD24+ renal progenitor cells

Project description:Analyze the transcriptional signature of human primary culture of CD133+ CD24+ renal progenitor cells

| PRJNA1142979 | ENA

Notch1 enhances NF-κB activation to promote CD133+ Skin Cancer Stem Cells

Project description:Cancer stem-like cells are hypothesized to be the major tumor initiating cell (TIC) population of human cutaneous squamous cell carcinoma (hcSCC), but the molecular alterations underpinning their cellular phenotype remain undefined. Here, a small CD133+CD31-CD45-CD61-CD24- (CD133+) cell population enriched for self-renewing and TIC features was isolated by sorting from primary hcSCC tumors. CD133+ cells show enhanced spheroid formation in vitro and tumor generation in vivo. Gene expression profiling comparing CD133+ with CD133- cells revealed that CD133+ cells expressed enriched stem cell-like and cancer-related gene signatures. Eighty differentially expressed stem cell-related genes were identified in CD133+ cells, where the top pathways include Notch, Notch1-mediated NF-κB, and WNT signaling. Overexpression of growth factor receptors, PI3K/mTOR, and STAT pathway genes and inactivation of genes regulating epigenetic modification of chromatin implicated in cancer were also identified. Verification of these gene signatures was conducted with Nanostring in an independent tumor set. Pharmacologic or genetic modulation of Notch1, IKKα, RELA and RELB modulated NF-κB transactivation, the CD133+ population, and phenotype. Immunofluorescent staining confirmed co-localization of CD133+ and IKKα expression in SCC tumor specimens. Our data support the linkage and importance of non-canonical Notch1 and IKK-mediated NF-κB activation in promoting CD133+ population and TIC phenotype in hcSCC.

2019-07-14 | GSE84588 | GEO

Benign Uncultured CD133+ vs CD133-

Project description:6 benign TURP samples taken directly from patients were subjected to collagen digestion overnight. Epithelial cells isolated were adhered to collagen for 15 minutes. Adherent cells were passed through a magnetic bead column and cells positive for CD133 antibody were double selected. RNA was extracted from CD133+ and CD133- cells from each patient and amplified using the RiboAmp HS RNA amplification system. CD133+ (Cy5) and CD133- (Cy5) cDNA was hybridised to 30K cDNA array (CRUK facility) using the Invitrogen post labelling system. In each case that RNA was co-hybridised to a human pooled universal reference cDNA (Cy3). Keywords: repeat sample

2008-03-01 | GSE9935 | GEO

CD24+ and CD24- myeloma-derived cancer stem cell lines

Project description:Expression profiling of CD24+ and CD24- population cells from myeloma cell lines. Results provide insight into the role of CD24+ cells in myeloma development. Keywords: multiple myeloma, cancer stem cell, CD24

2020-10-31 | GSE109650 | GEO

CD24+ and CD24- myeloma-derived cancer stem cell lines

Project description:CD24+ and CD24- myeloma-derived cancer stem cell lines

| PRJNA431593 | ENA

Identification of CD24 interaction partners in urologic tumor cell lines

Project description:Being involved in adhesion, migration, and invasion, the highly glycosylated signal transducer CD24 (cluster of differentiation 24) has been implicated to play an essential role during carcinogenesis. Previously, the molecular and (epi)genetic regulation of CD24 has been characterized in testicular germ cell tumors (GCT). Here, CD24 was exclusively found in embryonal carcinoma (EC), which represents the stem cell like population of GCT (see project PXD025110). For a better understanding of the molecular function of CD24, this study aimed at the identification of the direct interaction partners of CD24 not only in GCTs, but also in other urologic malignancies, such as urothelial- (UC), prostate- (PC), and renal cell carcinoma (RCC). For this purpose, co-immunoprecipitations of CD24 were performed in GCT, UC, PC, and RCC cell lines, while CD24-deficient EC cells as well as IgG2a controls were included for high validity. Extracted proteome was measured by liquid-chromatography coupled with mass spectrometry (LS-MS).

2023-05-10 | PXD039063 | Pride

Real-time quantitative PCR analysis of microRNAs expressed in adult mouse ventricular-subventricular zone cell populations

Project description:Total RNA was isolated from GFAP::GFP+CD133+EGFR-CD24- (quiescent neural stem cells, qNSCs), GFAP::GFP+CD133+EGFR+CD24- (activated neural stem cells, aNSCs) and GFAP::GFP+CD133- EGFR+CD24- (transit amplifying cells, TACs) cells from the adult mouse ventricular-subventricular zone (V-SVZ) (GFAP::GFP mice, Jackson Mice Stock number 003257).

2022-12-05 | GSE217425 | GEO

Hepatic BMAL1 and HIF1a regulate a time-dependent hypoxic response and their absence leads to Hepatopulmonary Syndrome

Project description:The transcriptional response to hypoxia is temporally regulated yet the molecular underpinnings and physiological implications are unknown. We examined herein the roles of hepatic Bmal1 and Hif1a in the circadian response to hypoxia in mice. We found that the majority of the transcriptional response to hypoxia is dependent on Bmal1 or Hif1a, through shared and distinct roles that are daytime determined. We further show that HIF1a accumulation upon hypoxia is temporally regulated and Bmal1-dependent. Unexpectedly, mice lacking both hepatic Bmal1 and Hif1a are hypoxemic and exhibit increased mortality upon hypoxic exposure in a daytime-dependent manner. These mice display mild liver dysfunction with pulmonary vasodilation likely due to ERK activation, endothelial nitric oxide synthase and nitric oxide accumulation in lungs, suggestive of hepatopulmonary syndrome. Our findings indicate that hepatic BMAL1 and HIF1a are key time-dependent regulators of the response to hypoxia and provide molecular insight on the pathophysiology of hepatopulmonary syndrome.

2024-05-08 | GSE254219 | GEO

CD133+ and CD133- expression profiles of benign and HRPC cells

Project description:Epithelial cell cultures derived from benign and HRPC tissue biopsies were expanded in culture for 2-3 weeks. CD133+ and CD133- cells were isolated using the miltenyi magnetic bead system after adherence to collagen. CD133+ and CD133- RNA was isolated and amplified using the RiboAmp HS kit and expression profiling performed using the CRUK WGA gene set. Keywords: Tumour vs normal comparison

2008-03-01 | GSE9962 | GEO

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