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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Hering-smith, Kathleen S. Hamm, L. Lee Tripathi, Piyush Yu, Miao Perez, Ronaldo Hou, Mingli Gong, Yongfeng Yang, Jing Hou, Jianghui Gonzales, Ernie |
| Description | Author Affiliation: Gong Y ( Department of Internal Medicine-Renal Division, Center for Investigation of Membrane Excitability Diseases, and Department of Physiology, Binzhou Medical College, Yantai 264003, China); Yu M ( Department of Medicine, Tulane University Health Science Center, New Orleans, LA 70112); Yang J ( Department of Internal Medicine-Renal Division, Center for Investigation of Membrane Excitability Diseases, and.); Gonzales E ( Department of Neurology, Washington University Medical School, St Louis, MO 63110); Perez R ( Department of Neurology, Washington University Medical School, St Louis, MO 63110); Hou M ( Department of Neurobiology, Harvard Medical School, Boston, MA 02115.); Tripathi P ( Department of Internal Medicine-Renal Division.); Hering-Smith KS ( Department of Medicine, Tulane University Health Science Center, New Orleans, LA 70112); Hamm LL ( Department of Medicine, Tulane University Health Science Center, New Orleans, LA 70112); Hou J ( Department of Internal Medicine-Renal Division, Center for Investigation of Membrane Excitability Diseases, and jhou@wustl.edu lhamm@tulane.edu.); |
| Abstract | The paracellular pathway through the tight junction provides an important route for transepithelial chloride reabsorption in the kidney, which regulates extracellular salt content and blood pressure. Defects in paracellular chloride reabsorption may in theory cause deregulation of blood pressure. However, there is no evidence to prove this theory or to demonstrate the in vivo role of the paracellular pathway in renal chloride handling. Here, using a tissue-specific KO approach, we have revealed a chloride transport pathway in the kidney that requires the tight junction molecule claudin-4. The collecting duct-specific claudin-4 KO animals developed hypotension, hypochloremia, and metabolic alkalosis due to profound renal wasting of chloride. The claudin-4-mediated chloride conductance can be regulated endogenously by a protease-channel-activating protease 1 (cap1). Mechanistically, cap1 regulates claudin-4 intercellular interaction and membrane stability. A putative cap1 cleavage site has been identified in the second extracellular loop of claudin-4, mutation of which abolished its regulation by cap1. The cap1 effects on paracellular chloride permeation can be extended to other proteases such as trypsin, suggesting a general mechanism may also exist for proteases to regulate the tight junction permeabilities. Together, we have discovered a theory that paracellular chloride permeability is physiologically regulated and essential to renal salt homeostasis and blood pressure control. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 36 |
| Volume Number | 111 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2014-09-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Blood Pressure Chlorides Metabolism Claudin-4 Kidney Renal Reabsorption Serine Endopeptidases Animals Drug Effects Cell Membrane Cell Membrane Permeability Electrolytes Blood Urine HEK293 Cells Kidney Tubules, Collecting Mice, Knockout Organ Specificity Protein Binding Protein Transport RNA Interference Recombinant Proteins Pharmacology Telemetry Trypsin Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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