• KSBNS 2024


Original Article

Exp Neurobiol 2011; 20(1): 45-53

Published online March 31, 2011

© The Korean Society for Brain and Neural Sciences

Rapid Disruption of Cellular Integrity of Zinc-treated Astroglia Is Regulated by p38 MAPK and Ca2+-dependent Mechanisms

Joo-Young Im#, Hyo-Jin Joo# and Pyung-Lim Han*

Departments of Brain & Cognitive Sciences, and Chemistry & Nano Science, Ewha Womans University, Seoul 120-750, Korea

Correspondence to: #These authors equally contributed to this work.
*To whom correspondence should be addressed.
TEL: 82-2-3277-4130, FAX: 82-2-3277-3419


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.

Keywords: astroglia, zinc, morphology protection, p38 inhibitors, actin filament