ArticleHistochemistry and cell biology2005
Impaired formation of desmosomal junctions in ADPKD epithelia.
Article in Histochemistry and cell biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 34 citations in OpenAlex.
- Intestinal barrier function declines during polycystic kidney disease progression.American journal of physiology. Renal physiology · 2025Article
- Adult human kidney organoids originate from CD24Nature genetics · 2022Article
- Polycystins as components of large multiprotein complexes of polycystin interactors.Cellular signalling · 2020Review
- Autosomal dominant polycystic kidney disease: Disrupted pathways and potential therapeutic interventions.Journal of cellular physiology · 2019Review
- Newly synthesized polycystin-1 takes different trafficking pathways to the apical and ciliary membranes.Traffic (Copenhagen, Denmark) · 2018Article
- Polycystin and calcium signaling in cell death and survival.Cell calcium · 2018Review
- Polycystins and mechanotransduction: From physiology to disease.World journal of experimental medicine · 2015Article
- Polycystin-1 and Gα12 regulate the cleavage of E-cadherin in kidney epithelial cells.Physiological genomics · 2015Article
- Polycystins and partners: proposed role in mechanosensitivity.The Journal of physiology · 2014Review
- Cell polarity and cystic kidney disease.Pediatric nephrology (Berlin, Germany) · 2013Review
- Polycystin-1 surface localization is stimulated by polycystin-2 and cleavage at the G protein-coupled receptor proteolytic site.Molecular biology of the cell · 2010Article
- Homophilic and heterophilic polycystin 1 interactions regulate E-cadherin recruitment and junction assembly in MDCK cells.Journal of cell science · 2009Article
- Tight junction composition is altered in the epithelium of polycystic kidneys.The Journal of pathology · 2008Article
- Treatment of autosomal dominant polycystic kidney disease (ADPKD): the new horizon for children with ADPKD.Pediatric nephrology (Berlin, Germany) · 2008Review
- Polycystic kidney diseases: from molecular discoveries to targeted therapeutic strategies.Cellular and molecular life sciences : CMLS · 2008Review
- The histochemistry and cell biology vade mecum: a review of 2005-2006.Histochemistry and cell biology · 2006Review
- Recent progress in histochemistry and cell biology: the state of the art 2005.Histochemistry and cell biology · 2005Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in polycystin-1 (PC-1) are responsible for autosomal dominant polycystic kidney disease (ADPKD), characterized by formation of fluid-filled tubular cysts. The PC-1 is a multifunctional protein essential for tubular differentiation and maturation found in desmosomal junctions of epithelial cells where its primary function is to mediate cell-cell adhesion. To address the impact of mutated PC-1 on intercellular adhesion, we have analyzed the structure/function of desmosomal junctions in primary cells derived from ADPKD cysts. Primary epithelial cells from normal kidney showed co-localization of PC-1 and desmosomal proteins at cell-cell contacts. A striking difference was seen in ADPKD cells, where PC-1 and desmosomal proteins were lost from the intercellular junction membrane, despite unchanged protein expression levels. Instead, punctate intracellular expression for PC-1 and desmosomal proteins was detected. The N-cadherin, but not E-cadherin was expressed in adherens junctions of ADPKD cells. These data together with co-sedimentation analysis demonstrate that, in the absence of functional PC-1, desmosomal junctions cannot be properly assembled and remain sequestered in cytoplasmic compartments. Taken together, our results demonstrate that PC-1 is crucial for formation of intercellular contacts. We propose that abnormal expression of PC-1 causes disregulation of cellular adhesion complexes leading to increased proliferation, loss of polarity and, ultimately, cystogenesis.
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