Document Detail


Chloride influx provokes lamellipodium formation in microglial cells.
MedLine Citation:
PMID:  18209472     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Lamellipodium extension and retraction is the driving force for cell migration. Although several studies document that activation of chloride channels are essential in cell migration, little is known about their contribution in lamellipodium formation. To address this question, we characterized chloride channels and transporters by whole cell recording and RT-PCR, respectively, as well as quantified lamellipodium formation in murine primary microglial cells as well as the microglial cell-line, BV-2, using time-lapse microscopy. The repertoire of chloride conducting pathways in BV-2 cells included, swelling-activated chloride channels as well as the KCl cotransporters, KCC1, KCC2, KCC3, and KCC4. Swelling-activated chloride channels were either activated by a hypoosmotic solution or by a high KCl saline, which promotes K(+) and Cl(-) influx instead of efflux by KCCs. Conductance through swelling-activated chloride channels was completely blocked by flufenamic acid (200 microM), SITS (1 mM) and DIOA (10 microM). By exposing primary microglial cells or BV-2 cells to a high KCl saline, we observed a local swelling, which developed into a prominent lamellipodium. Blockade of chloride influx by flufenamic acid (200 microM) or DIOA (10 microM) as well as incubation of cells in a chloride-free high K(+) saline suppressed formation of a lamellipodium. We assume that local swellings, established by an increase in chloride influx, are a general principle in formation of lamellipodia in eukaryotic cells.
Authors:
Susanna Zierler; Eva Frei; Stephan Grissmer; Hubert H Kerschbaum
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-01-16
Journal Detail:
Title:  Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology     Volume:  21     ISSN:  1015-8987     ISO Abbreviation:  Cell. Physiol. Biochem.     Publication Date:  2008  
Date Detail:
Created Date:  2008-01-22     Completed Date:  2008-03-26     Revised Date:  2010-02-17    
Medline Journal Info:
Nlm Unique ID:  9113221     Medline TA:  Cell Physiol Biochem     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  55-62     Citation Subset:  IM    
Affiliation:
Department of Cell Biology, Paris-Lodron- University of Salzburg, Salzburg, Austria.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Line
Cell Size / drug effects
Chloride Channels / metabolism*
Extracellular Fluid / drug effects,  metabolism
Extracellular Space / drug effects,  metabolism
Ion Channel Gating / drug effects
Membrane Transport Modulators / pharmacology
Mice
Microglia / cytology*,  drug effects,  metabolism*
Models, Biological
Osmolar Concentration
Potassium / pharmacology
Pseudopodia / drug effects,  metabolism*
Sodium Chloride / pharmacology
Chemical
Reg. No./Substance:
0/Chloride Channels; 0/Membrane Transport Modulators; 7440-09-7/Potassium; 7647-14-5/Sodium Chloride
Comments/Corrections
Erratum In:
Cell Physiol Biochem. 2009;24(5-6):635

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


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