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

ABSTRACT: 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

ORGANISM(S): Homo sapiens

PROVIDER: GSE280279 | GEO | 2025/04/03

REPOSITORIES: GEO

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Project description:Purpose: The aim of the present study was to identify and characterize in tissue samples of clear cell-renal cell carcinoma (ccRCC) a population of CD133+/CD24+ cancer cells (RCC-derived cells-RDCs) and to study the differences with their nonneoplastic counterpart, tubular Adult Renal Progenitor Cells (ARPCs). Materials and methods: CD133+/CD24+ RDCs were isolated from 40 patients. The mesenchymal phenotype and stemness proteomic profile of these RDCs were characterized. The colony-forming efficiency and self-renewal ability were tested with limiting dilution. The tumorigenic properties were evaluated in vitro with Soft Agar Assay. The angiogenic response was evaluated in vivo with the chorioallantoic membrane angiogenic assay. Microarray analysis was performed on 6 tARPCs and 6 RDCs clones. Expression of membrane proteins was evaluated with flowcytometry and immunofluorescence staining. Results: CD133+/CD24+ cells were isolated from normal and tumoral kidney tissue. FACS analysis showed that RDCs did not express the mesenchymal stem cell markers. We showed that CD133+/CD24+ tumor cells were more undifferentiated than tARPCs. RDCs were clonigenic and able to differentiate into adipocytes, epithelial and osteogenic cells. RDCs were able to regenerate tumor cells in vitro and to induce angiogenesis in vivo. The gene expression profile identified CTR2 as a membrane marker for this neoplastic population. Conclusions: Our results indicate the presence, in ccRCC, of a CD133+/CD24+/CTR2+ cancer cells population. These cells possess some stem cell-like features, including in vitro self-maintenance and differentiating capabilities, and are able to induce an angiogenic response in vivo. Study of gene expression profiling of Renal Cancer Cells (RCSCs), tubular Adult Renal Progenitor Cells (tARPCs), Renal Proximal Tubular Cells (RPTEC) and Mesenchymal Stem Cells (MSC). To highlight the similarities and the differences with known renal stem populations and with terminally differentiated renal cells, for each patient, 6 subcultures of tubular ARPCs (tARPCs), 3 subcultures of the MSC and 3 subcultures of the RPTEC were included in the analysis.

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

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