Document Detail


Elevated hydrostatic pressure activates sodium/hydrogen exchanger-1 in rat optic nerve head astrocytes.
MedLine Citation:
PMID:  19419999     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Optic nerve head astrocytes become abnormal in eyes that have elevated intraocular pressure, and cultured astrocytes display altered protein expression after being subjected for > or = 1 days to elevated hydrostatic pressure. Here we show that 2-h elevated hydrostatic pressure (15 or 30 mmHg) causes phosphorylation of ERK1/2, ribosomal S6 protein kinase (p90(RSK)), and Na/H exchanger (NHE)1 in cultured rat optic nerve head astrocytes as judged by Western blot analysis. The MEK/ERK inhibitor U0126 abolished phosphorylation of NHE1 and p90(RSK) as well as ERK1/2. To examine NHE1 activity, cytoplasmic pH (pH(i)) was measured with BCECF and, in some experiments, cells were acidified by 5-min exposure to 20 mM ammonium chloride. Although baseline pH(i) was unaltered, the rate of pH(i) recovery from acidification was fourfold higher in pressure-treated astrocytes. In the presence of either U0126 or dimethylamiloride (DMA), an NHE inhibitor, hydrostatic pressure did not change the rate of pH(i) recovery. The findings are consistent with NHE1 activation due to phosphorylation of ERK1/2, p90(RSK), and NHE1 that occurs in response to hydrostatic pressure. These responses may precede long-term changes of protein expression known to occur in pressure-stressed astrocytes.
Authors:
Amritlal Mandal; Mohammad Shahidullah; Nicholas A Delamere; Marcos A Terán
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2009-05-06
Journal Detail:
Title:  American journal of physiology. Cell physiology     Volume:  297     ISSN:  1522-1563     ISO Abbreviation:  Am. J. Physiol., Cell Physiol.     Publication Date:  2009 Jul 
Date Detail:
Created Date:  2009-07-02     Completed Date:  2009-08-17     Revised Date:  2013-06-02    
Medline Journal Info:
Nlm Unique ID:  100901225     Medline TA:  Am J Physiol Cell Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  C111-20     Citation Subset:  IM    
Affiliation:
Dept. of Physiology, Univ. of Arizona, Tucson, AZ 85724, USA.
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MeSH Terms
Descriptor/Qualifier:
Amiloride / analogs & derivatives,  pharmacology
Animals
Animals, Newborn
Astrocytes / drug effects,  enzymology,  metabolism*
Butadienes / pharmacology
Cells, Cultured
Hydrogen-Ion Concentration
Hydrostatic Pressure
Kidney / metabolism
Mitogen-Activated Protein Kinase 1 / metabolism
Mitogen-Activated Protein Kinase 3 / metabolism
Nitriles / pharmacology
Opossums
Optic Disk / cytology,  drug effects,  enzymology,  metabolism*
Phosphorylation
Protein Kinase Inhibitors / pharmacology
Rats
Ribosomal Protein S6 Kinases, 90-kDa / metabolism
Signal Transduction
Sodium-Hydrogen Antiporter / antagonists & inhibitors,  metabolism*
Time Factors
Grant Support
ID/Acronym/Agency:
EY-014069/EY/NEI NIH HHS
Chemical
Reg. No./Substance:
0/Butadienes; 0/Nitriles; 0/Protein Kinase Inhibitors; 0/Slc9a1 protein, rat; 0/Sodium-Hydrogen Antiporter; 0/U 0126; 1214-79-5/5-dimethylamiloride; 2609-46-3/Amiloride; EC 2.7.11.1/Ribosomal Protein S6 Kinases, 90-kDa; EC 2.7.11.24/Mitogen-Activated Protein Kinase 1; EC 2.7.11.24/Mitogen-Activated Protein Kinase 3
Comments/Corrections

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