ArticleThe Journal of physiology2009
Claudin-16 affects transcellular Cl- secretion in MDCK cells.
Article in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 51 citations in OpenAlex.
- Role of Stress on Driving the Intestinal Paracellular Permeability.Current issues in molecular biology · 2023Review
- The importance of kidney calcium handling in the homeostasis of extracellular fluid calcium.Pflugers Archiv : European journal of physiology · 2022Review
- Article
- Claudins in Renal Physiology and Pathology.Genes · 2020Review
- Blood-Brain Barrier Protein Claudin-5 Expressed in PairedFrontiers in physiology · 2020Article
- Phosphorylated claudin-16 interacts with Trpv5 and regulates transcellular calcium transport in the kidney.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Magnesium Handling in the Kidney.Advances in chronic kidney disease · 2018Review
- Mosaic expression of claudins in thick ascending limbs of Henle results in spatial separation of paracellular Na+ and Mg2+ transport.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Increased urothelial paracellular transport promotes cystitis.American journal of physiology. Renal physiology · 2015Article
- Familial hypomagnesaemia with hypercalciuria and nephrocalcinosis: clinical and molecular characteristics.Clinical kidney journal · 2015Article
- Biochemical and biophysical analyses of tight junction permeability made of claudin-16 and claudin-19 dimerization.Molecular biology of the cell · 2015Article
- Claudins and the modulation of tight junction permeability.Physiological reviews · 2013Review
- In vivo imaging of human breast cancer mouse model with high level expression of calcium sensing receptor at 3T.European radiology · 2012Article
- Altered expression of tight junction proteins in mammary epithelium after discontinued suckling in mice.Pflugers Archiv : European journal of physiology · 2012Article
- CNNM2, encoding a basolateral protein required for renal Mg2+ handling, is mutated in dominant hypomagnesemia.American journal of human genetics · 2011Article
- Tight junction pore and leak pathways: a dynamic duo.Annual review of physiology · 2011Review
- Tricellulin forms homomeric and heteromeric tight junctional complexes.Cellular and molecular life sciences : CMLS · 2010Article
- Two-path impedance spectroscopy for measuring paracellular and transcellular epithelial resistance.Biophysical journal · 2009Article
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Authors and funding
7 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Claudin-16 (paracellin-1) is a tight junction protein localized mainly in the thick ascending limb of Henle's loop and also in the distal nephron. Its defect causes familial hypomagnesaemia with hypercalciuria and nephrocalcinosis. This had been taken as an indication that claudin-16 conveys paracellular Mg(2+) and Ca(2+) transport; however, evidence is still conflicting. We studied paracellular ion permeabilities as well as effects of claudin-16 on the driving forces for passive ion movement. MDCK-C7 cells were stably transfected with wild-type (wt) and mutant (R146T, T233R) claudin-16. Results indicated that paracellular permeability to Mg(2+) but not to Ca(2+) is increased in cells transfected with wt compared to mutant claudin-16 and control cells. Increased basolateral Mg(2+) concentration activated a transcellular Cl(-) current which was greatly enhanced in cells transfected with wt and T233R claudin-16, as compared to R146T claudin-16-transfected or control cells. This current was triggered by the basolateral calcium-sensing receptor causing Ca(2+) release from internal stores, thus activating apical Ca(2+)-sensitive Cl(-) channels and basolateral Ca(2+)-sensitive K(+) channels. Immunohistochemical data suggest that the Cl(-) channel involved is bestrophin. We conclude that claudin-16 itself possesses only moderate paracellular Mg(2+) permeability but governs transcellular Cl(-) currents by interaction with apical Ca(2+)-activated Cl(-) channels, presumably bestrophin. As the transepithelial voltage generated by such a current alters the driving force for all ions, this may be the major mechanism to regulate Mg(2+) and Ca(2+) absorption in the kidney.
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