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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Lauf, Peter K. Misri, Sandeep Chimote, Ameet A. Adragna, Norma C. |
| Description | Country affiliation: United States Author Affiliation: Lauf PK ( Cell Biophysics Group, 054 Biological Sciences Bldg., Wright State Univ. Boonshoft School of Medicine, Dayton, OH 45435, USA. Peter.Lauf@wright.edu) |
| Abstract | This study explores the nature of K fluxes in human lens epithelial cells (LECs) in hyposmotic solutions. Total ion fluxes, Na-K pump, Cl-dependent Na-K-2Cl (NKCC), K-Cl (KCC) cotransport, and K channels were determined by 85Rb uptake and cell K (Kc) by atomic absorption spectrophotometry, and cell water gravimetrically after exposure to ouabain +/- bumetanide (Na-K pump and NKCC inhibitors), and ion channel inhibitors in varying osmolalities with Na, K, or methyl-d-glucamine and Cl, sulfamate, or nitrate. Reverse transcriptase polymerase chain reaction (RT-PCR), Western blot analyses, and immunochemistry were also performed. In isosmotic (300 mosM) media approximately 90% of the total Rb influx occurred through the Na-K pump and NKCC and approximately 10% through KCC and a residual leak. Hyposmotic media (150 mosM) decreased K(c) by a 16-fold higher K permeability and cell water, but failed to inactivate NKCC and activate KCC. Sucrose replacement or extracellular K to >57 mM, but not Rb or Cs, in hyposmotic media prevented Kc and water loss. Rb influx equaled Kc loss, both blocked by clotrimazole (IC50 approximately 25 microM) and partially by 1-[(2-chlorophenyl) diphenylmethyl]-1H-pyrazole (TRAM-34) inhibitors of the IK channel KCa3.1 but not by other K channel or connexin hemichannel blockers. Of several anion channel blockers (dihydro-indenyl)oxy]alkanoic acid (DIOA), 4-2(butyl-6,7-dichloro-2-cyclopentylindan-1-on-5-yl)oxybutyric acid (DCPIB), and phloretin totally or partially inhibited Kc loss and Rb influx, respectively. RT-PCR and immunochemistry confirmed the presence of KCa3.1 channels, aside of the KCC1, KCC2, KCC3 and KCC4 isoforms. Apparently, IK channels, possibly in parallel with volume-sensitive outwardly rectifying Cl channels, effect regulatory volume decrease in LECs. |
| File Format | HTM / HTML |
| ISSN | 03636143 |
| e-ISSN | 15221563 |
| Journal | American Journal of Physiology - Cell Physiology |
| Issue Number | 3 |
| Volume Number | 294 |
| Language | English |
| Publisher | American Physiological Society |
| Publisher Date | 2008-03-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Discipline Cell Biology Cell Size Epithelial Cells Metabolism Intermediate-conductance Calcium-activated Potassium Channels Ion Channel Gating Lens, Crystalline Potassium Acetates Pharmacology Blotting, Western Bumetanide Cell Line Cell Membrane Permeability Drug Effects Chloride Channels Clotrimazole Cyclopentanes Dose-response Relationship, Drug Immunohistochemistry Indans Indenes Antagonists & Inhibitors Genetics Kinetics Cytology Niflumic Acid Nitrobenzoates Osmosis Ouabain Phloretin Potassium Channel Blockers Pyrazoles Reverse Transcriptase Polymerase Chain Reaction Rubidium Sodium Potassium Chloride Symporter Inhibitors Sodium-potassium-chloride Symporters Sodium-potassium-exchanging Atpase Spectrophotometry, Atomic Symporters Voltage-dependent Anion Channels Research Support, Non-u.s. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Physiology |
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