ArticleProceedings of the National Academy of Sciences of the United States of America1996
Immunolocalization of ion transport proteins in human autosomal dominant polycystic kidney epithelial cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
37 citing papers in PubMed, 104 citations in OpenAlex.
- Physiologic mechanisms underlying polycystic kidney disease.Physiological reviews · 2025Review
- Pathogenic Pathways and Therapeutic Strategies in Autosomal Dominant Polycystic Kidney Disease (ADPKD).Journal of cellular signaling · 2025Article
- The Cyst Epithelium in Polycystic Kidney Disease Patients Displays Normal Apical-Basolateral Cell Polarity.International journal of molecular sciences · 2024Article
- Ouabain enhances renal cyst growth in a slowly progressive mouse model of autosomal dominant polycystic kidney disease.American journal of physiology. Renal physiology · 2023Article
- Pathogenic Relationships in Cystic Fibrosis and Renal Diseases: CFTR, SLC26A9 and Anoctamins.International journal of molecular sciences · 2023Review
- Review
- AMPK and Polycystic Kidney Disease Drug Development: An Interesting Off-Target Target.Frontiers in medicine · 2022Review
- The chloride channel CFTR is not required for cyst growth in an ADPKD mouse model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- In vitro 3D phenotypic drug screen identifies celastrol as an effective in vivo inhibitor of polycystic kidney disease.Journal of molecular cell biology · 2020Article
- Targeting and therapeutic peptide-based strategies for polycystic kidney disease.Advanced drug delivery reviews · 2020Review
- Autosomal dominant polycystic kidney disease: Disrupted pathways and potential therapeutic interventions.Journal of cellular physiology · 2019Review
- CFTR pharmacology.Cellular and molecular life sciences : CMLS · 2017Review
- Dendrimer-based selective autophagy-induction rescues ΔF508-CFTR and inhibits Pseudomonas aeruginosa infection in cystic fibrosis.PloS one · 2017Article
- Rationale for early treatment of polycystic kidney disease.Pediatric nephrology (Berlin, Germany) · 2015Review
- Molecular pathways and therapies in autosomal-dominant polycystic kidney disease.Physiology (Bethesda, Md.) · 2015Review
- Hypoxia-inducible factor-1α causes renal cyst expansion through calcium-activated chloride secretion.Journal of the American Society of Nephrology : JASN · 2014Article
- Novel role of ouabain as a cystogenic factor in autosomal dominant polycystic kidney disease.American journal of physiology. Renal physiology · 2013Review
- CFTR inhibitors.Current pharmaceutical design · 2013Review
- Calmodulin-sensitive adenylyl cyclases mediate AVP-dependent cAMP production and Cl- secretion by human autosomal dominant polycystic kidney cells.American journal of physiology. Renal physiology · 2012Article
- Prostaglandin E(2) mediates proliferation and chloride secretion in ADPKD cystic renal epithelia.American journal of physiology. Renal physiology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The kidneys of patients with autosomal dominant polycystic kidney disease become massively enlarged due to the progressive expansion of myriad fluid-filled cysts. The epithelial cells that line the cyst walls are responsible for secreting the cyst fluid, but the mechanism through which this secretion occurs is not well established. Recent studies suggest that renal cyst epithelial cells actively secrete Cl across their apical membranes, which in turn drives the transepithelial movement of Na and water. The characteristics of this secretory flux suggest that it is dependent upon the participation of an apical cystic fibrosis transmembrane conductance regulator (CFTR)-like Cl channel and basolateral Na,K-ATPase. To test this hypothesis, we have immunolocalized the CFTR and Na,K-ATPase proteins in intact cysts and in cyst epithelial cells cultured in vitro on permeable filter supports. In both settings, cyst epithelial cells were found to possess Na,K-ATPase exclusively at their basolateral surfaces; apical labeling was not detected. The CFTR protein was present at the apical surfaces of cyst epithelial cells that had been stimulated to secrete through incubation in forskolin. CFTR was detected in intracellular structures in cultured cyst epithelial cells that had not received the forskolin treatment. These results demonstrate that the renal epithelial cells that line cysts in autosomal dominant polycystic kidney disease express transport systems with the appropriate polarity to mediate active Cl and fluid secretion.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.