Exp Neurobiol.  2011 Mar;20(1):45-53. 10.5607/en.2011.20.1.45.

Rapid Disruption of Cellular Integrity of Zinc-treated Astroglia Is Regulated by p38 MAPK and Ca(2+)-dependent Mechanisms

Affiliations
  • 1Departments of Brain & Cognitive Sciences, and Chemistry & Nano Science, Ewha Womans University, Seoul 120-750, Korea. plhan@ewha.ac.kr

Abstract

Cultured cortical primary astroglia treated with zinc died while rapidly detached from culture plates, a distinct part of zinc-treated astroglia. In the present study, we investigated the mechanism underlying the rapid change in the morphologic integrity of zinc-treated astroglia. Among the early cellular events occurring in zinc-treated astroglia, strong activation of p38 MAPK and JNK was evident. Although inhibitors of p38 (SB203580 and SB202190) or JNK (SP600125) did not protect zinc-insulted astroglia from cell death, the p38 inhibitors, but not the JNK inhibitor, suppressed actin filament and cell morphology disruption. The Ca2+ ionophore, A23187, also suppressed actin filament and cell morphology disruption, but not cell death, of zinc-insulted astroglia. However, A23187 did not inhibit p38 MAPK activation in zinc-treated astroglia. Together these results suggest that zinc influx in astroglia results in rapid loss of the morphologic integrity via mechanisms regulated by p38 kinase and/or Ca2+ signaling.

Keyword

astroglia; zinc; morphology protection; p38 inhibitors; actin filament

MeSH Terms

Actin Cytoskeleton
Astrocytes
Calcimycin
Cell Death
p38 Mitogen-Activated Protein Kinases
Phosphotransferases
Zinc
Calcimycin
Phosphotransferases
Zinc
p38 Mitogen-Activated Protein Kinases
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