ArticleJournal of the American Society of Nephrology : JASN2015
Adam10 mediates the choice between principal cells and intercalated cells in the kidney.
Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 53 citations in OpenAlex.
- Clinical implications of plasma sADAM10: integrating renal function, histopathology and prognostic outcomes in chronic kidney disease and kidney transplantation.Frontiers in immunology · 2026Article
- Developmental Hypoxia Enhances Kidney Organoid Complexity and Maturity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Dmrt2 and Hmx2 direct intercalated cell diversity in the mammalian kidney through antagonistic and supporting regulatory processes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Developmental and Cell Fate Analyses Support a Postnatal Origin for the Cortical Collecting System in the Mouse Kidney.Journal of the American Society of Nephrology : JASN · 2025Article
- Absence of E-Cadherin and β-Catenin in the Basal Plasma Membrane of Collecting Duct Cells During NDI Development and Recovery.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2023Article
- The pathophysiology of distal renal tubular acidosis.Nature reviews. Nephrology · 2023Review
- Comparative whole-genome transcriptome analysis in renal cell populations reveals high tissue specificity of MAPK/ERK targets in embryonic kidney.BMC biology · 2022Article
- Article
- Renal cystic disease in tuberous sclerosis complex.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- ADAMs family in kidney physiology and pathology.EBioMedicine · 2021Review
- Key metalloproteinase-mediated pathways in the kidney.Nature reviews. Nephrology · 2021Review
- Contribution of ADAM17 and related ADAMs in cardiovascular diseases.Cellular and molecular life sciences : CMLS · 2021Review
- Review
- The Mechanisms of Cellular Plasticity in Collecting Duct Cells: Intermediate Cell Type and Notch-mediated Transdifferentiation.Function (Oxford, England) · 2021Article
- Loss of Adam10 Disrupts Ion Transport in Immortalized Kidney Collecting Duct Cells.Function (Oxford, England) · 2021Article
- Foxi1 inactivation rescues loss of principal cell fate selection in Hes1-deficient kidneys but does not ensure maintenance of principal cell gene expression.Developmental biology · 2020Article
- Adaptive response of the murine collecting duct to alkali loading.Pflugers Archiv : European journal of physiology · 2020Article
- The Renal Physiology of Pendrin-Positive Intercalated Cells.Physiological reviews · 2020Review
- Cellular and Molecular Mechanisms of Kidney Development: From the Embryo to the Kidney Organoid.Frontiers in cell and developmental biology · 2020Review
- Notch signaling is essential in collecting duct epithelial cell fate determination during development and maintenance of cell type homeostasis in adult.Annals of translational medicine · 2019Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
A disintegrin and metalloproteinase domain 10 (Adam10), a member of the ADAM family of cell membrane-anchored proteins, has been linked to the regulation of the Notch, EGF, E-cadherin, and other signaling pathways. However, it is unclear what role Adam10 has in the kidney in vivo. In this study, we showed that Adam10 deficiency in ureteric bud (UB) derivatives leads to a decrease in urinary concentrating ability, polyuria, and hydronephrosis in mice. Furthermore, Adam10 deficiency led to a reduction in the percentage of aquaporin 2 (Aqp2)(+) principal cells (PCs) in the collecting ducts that was accompanied by a proportional increase in the percentage of intercalated cells (ICs). This increase was more prominent in type A ICs than in type B ICs. Foxi1, a transcription factor important for the differentiation of ICs, was upregulated in the Adam10 mutants. The observed reduction of Notch activity in Adam10 mutant collecting duct epithelium and the similar reduction of PC/IC ratios in the collecting ducts in mice deficient for mindbomb E3 ubiquitin protein ligase 1, a key regulator of the Notch and Wnt/receptor-like tyrosine kinase signaling pathways, suggest that Adam10 regulates cell fate determination through the activation of Notch signaling, probably through the regulation of Foxi1 expression. However, phenotypic differences between the Adam10 mutants, the Mib1 mutants, and the Foxi1 mutants suggest that the functions of Adam10 in determining the fate of collecting duct cells are more complex than those of a simple upstream factor in a linear pathway involving Notch and Foxi1.
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