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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
		Other
	SRR31110715_1.fastq.gz	Fastqsanger.gz
	SRR31110715_2.fastq.gz	Fastqsanger.gz
	SRR31110717_1.fastq.gz	Fastqsanger.gz
	SRR31110717_2.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

Cd24

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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.

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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

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