Rapid Disruption of Cellular Integrity of Zinc-treated Astroglia Is Regulated by p38 MAPK and Ca(2+)-dependent Mechanisms.
- Author:
Joo Young IM
1
;
Hyo Jin JOO
;
Pyung Lim HAN
Author Information
- Publication Type:Original Article
- Keywords: astroglia; zinc; morphology protection; p38 inhibitors; actin filament
- MeSH: Actin Cytoskeleton; Astrocytes; Calcimycin; Cell Death; p38 Mitogen-Activated Protein Kinases; Phosphotransferases; Zinc
- From:Experimental Neurobiology 2011;20(1):45-53
- CountryRepublic of Korea
- Language:English
- 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.
