ArticleStem cell research & therapy2025
Modelling APOL1-mediated kidney inflammation and fibrosis using a partially reprogrammed urine-derived SIX2-positive renal progenitor cell line.
Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Stem cell research and regenerative medicine: meeting report from the Royan International Stem Cell Congress 2025.Journal of biological engineering · 2026Article
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8 authors.
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Abstract
backgroundCKD affects approximately 850 million people worldwide and is a leading cause of mortality. Podocytes, cells in the kidney are terminally differentiated and incapable of division in vivo making the establishment of primary cultures particularly challenging. The ability of cells to proliferate and avoid senescence is closely linked to telomere length. However, cellular senescence ensues when telomere length becomes critically shortened.
methodsWe present the successful rejuvenation of a human SIX2-positive renal progenitor cell line derived from the urine of a 30-year-old West African male (UM30-OSN). To achieve partial reprogramming, plasmids expressing the Yamanaka factors OCT4, SOX2, NANOG, c-Myc, and KLF4 were employed.
resultsUM30-OSN expresses the pluripotency-associated marker SSEA4, renal stem cell markers such as SIX2, CD133 and CD24, determined by immunofluorescence, FACS and qPCR. Expression analysis revealed downregulation of senescence markers p21 and p53 and upregulation of proliferation-associated genes PCNA, KI67 and TERT, confirming rejuvenation. Upon podocyte differentiation, UM30-OSN cells expressed podocyte-specific markers NPHS1, NPHS2, SYNPO and CD2AP. Comparative transcriptome analyses revealed a correlation co-efficiency (R
conclusionGiven their robust proliferation capacity, UM30-OSN cells represent a valuable additional model for investigating kidney-associated diseases such the contribution of APOL1 high-risk variants to kidney injury and fibrosis.
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