Document Detail


Endogenous regulation of human Schlemm's canal cell volume by nitric oxide signaling.
MedLine Citation:
PMID:  20484594     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE: There is a time-course correlation between nitric oxide (NO)-induced decreases in trabecular meshwork (TM) cell volume and NO-induced increases in outflow facility. The Schlemm's canal (SC) cells may also provide resistance to aqueous humor outflow; therefore, this study tests the involvement of the nitric oxide synthase (NOS) and NO signaling pathway and the BK(Ca)-channel in mediating SC cell volume decreases.
METHODS: Cell volume was measured in low-passage human SC cells using calcein AM fluorescent dye; images were captured with a confocal microscope, and data were quantified using NIH ImageJ software.
RESULTS: Inhibition of endogenous NOS resulted in a 7% increase in SC cell volume. Exposure of SC cells to DETA-NO resulted in a 12% to 16% decrease in cell volume that was abolished by the soluble guanylyl cyclase (sGC) inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) (5 μM), the protein kinase G (PKG) inhibitor (RP)-8-Br-PET-cGMP-S (50 μM), and the high-conductance calcium-activated potassium channel (BK(Ca) channel) inhibitor iberiotoxin (50 nM). Hypertonic media significantly decreased SC cell volume by 14%, whereas hypotonic media significantly increased cell volume by 11.2%.
CONCLUSIONS: These data suggest that endogenous NOS regulates steady state cell volume and the involvement of the NOS/NO/sGC/cGMP/PKG pathway and the BK(Ca)-channel in mediating NO-induced reductions in SC cell volume. These decreases in cell volume correlated with the time-course for NO-induced increases in outflow facility, suggesting that the NO-induced reduction in SC cell volume may also influence outflow facility.
Authors:
Dorette Z Ellis; Najam A Sharif; William M Dismuke
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-05-19
Journal Detail:
Title:  Investigative ophthalmology & visual science     Volume:  51     ISSN:  1552-5783     ISO Abbreviation:  Invest. Ophthalmol. Vis. Sci.     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-10-28     Completed Date:  2010-12-07     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7703701     Medline TA:  Invest Ophthalmol Vis Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  5817-24     Citation Subset:  IM    
Affiliation:
Department of Pharmacodynamics, University of Florida College of Pharmacy, Gainesville, Florida 32610, USA. ellis@cop.ufl.edu
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MeSH Terms
Descriptor/Qualifier:
Cell Size*
Cells, Cultured
Cyclic GMP / metabolism
Cyclic GMP-Dependent Protein Kinases / antagonists & inhibitors,  metabolism
Enzyme Inhibitors / pharmacology
Fluoresceins / metabolism
Fluorescent Dyes / metabolism
Guanylate Cyclase / antagonists & inhibitors,  metabolism
Humans
Large-Conductance Calcium-Activated Potassium Channels / metabolism
NG-Nitroarginine Methyl Ester / pharmacology
Nitric Oxide / metabolism*
Nitric Oxide Synthase / antagonists & inhibitors,  physiology*
Osmolar Concentration
Signal Transduction / physiology*
Tissue Donors
Trabecular Meshwork / cytology*
Triazenes / pharmacology
Chemical
Reg. No./Substance:
0/1-hydroxy-2-oxo-3,3-bis(2-aminoethyl)-1-triazene; 0/Enzyme Inhibitors; 0/Fluoresceins; 0/Fluorescent Dyes; 0/Large-Conductance Calcium-Activated Potassium Channels; 0/Triazenes; 10102-43-9/Nitric Oxide; 148504-34-1/calcein AM; 50903-99-6/NG-Nitroarginine Methyl Ester; 7665-99-8/Cyclic GMP; EC 1.14.13.39/Nitric Oxide Synthase; EC 2.7.11.12/Cyclic GMP-Dependent Protein Kinases; EC 4.6.1.2/Guanylate Cyclase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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