ArticleProceedings of the National Academy of Sciences of the United States of America2010
Deletion of hensin/DMBT1 blocks conversion of beta- to alpha-intercalated cells and induces distal renal tubular acidosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 50 papers.
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50 citing papers in PubMed, 95 citations in OpenAlex.
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- 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
- A Possible Link between Cell Plasticity and Renin Expression in the Collecting Duct: A Narrative Review.International journal of molecular sciences · 2024Review
- Apical cell expansion maintained by Dusky-like establishes a scaffold for corneal lens morphogenesis.Science advances · 2024Article
- GDF15, an Emerging Player in Renal Physiology and Pathophysiology.International journal of molecular sciences · 2024Review
- Potential Novel Role of Membrane-Associated Carbonic Anhydrases in the Kidney.International journal of molecular sciences · 2023Review
- The proximal tubule through an NBCe1-dependent mechanism regulates collecting duct phenotypic and remodeling responses to acidosis.American journal of physiology. Renal physiology · 2023Article
- Mapping the human kidney using single-cell genomics.Nature reviews. Nephrology · 2022Review
- Nrf2 deficiency causes hepatocyte dedifferentiation and reduced albumin production in an experimental extrahepatic cholestasis model.PloS one · 2022Article
- Connecting tubules develop from the tip of the ureteric bud in the human kidney.Histochemistry and cell biology · 2021Article
- No effect of deleted in malignant brain tumors 1 deficiency on chemotherapy induced murine intestinal mucositis.Scientific reports · 2021Article
- 3D Mapping Reveals a Complex and Transient Interstitial Matrix During Murine Kidney Development.Journal of the American Society of Nephrology : JASN · 2021Article
- Kidney intercalated cells are phagocytic and acidify internalized uropathogenic Escherichia coli.Nature communications · 2021Article
- FOXI1 expression in chromophobe renal cell carcinoma and renal oncocytoma: a study of The Cancer Genome Atlas transcriptome-based outlier mining and immunohistochemistry.Virchows Archiv : an international journal of pathology · 2021Article
- 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
- Screening and function discussion of a hereditary renal tubular acidosis family pathogenic gene.Cell death & disease · 2020Article
Corrections and comments
- Erratum issuedCheema, Faisal [corrected to Cheema, Faisal H]
Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
Acid-base transport in the renal collecting tubule is mediated by two canonical cell types: the β-intercalated cell secretes HCO(3) by an apical Cl:HCO(3) named pendrin and a basolateral vacuolar (V)-ATPase. Acid secretion is mediated by the α-intercalated cell, which has an apical V-ATPase and a basolateral Cl:HCO(3) exchanger (kAE1). We previously suggested that the β-cell converts to the α-cell in response to acid feeding, a process that depended on the secretion and deposition of an extracellular matrix protein termed hensin (DMBT1). Here, we show that deletion of hensin from intercalated cells results in the absence of typical α-intercalated cells and the consequent development of complete distal renal tubular acidosis (dRTA). Essentially all of the intercalated cells in the cortex of the mutant mice are canonical β-type cells, with apical pendrin and basolateral or diffuse/bipolar V-ATPase. In the medulla, however, a previously undescribed cell type has been uncovered, which resembles the cortical β-intercalated cell in ultrastructure, but does not express pendrin. Polymerization and deposition of hensin (in response to acidosis) requires the activation of β1 integrin, and deletion of this gene from the intercalated cell caused a phenotype that was identical to the deletion of hensin itself, supporting its critical role in hensin function. Because previous studies suggested that the conversion of β- to α-intercalated cells is a manifestation of terminal differentiation, the present results demonstrate that this differentiation proceeds from HCO(3) secreting to acid secreting phenotypes, a process that requires deposition of hensin in the ECM.
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