ArticleExperimental neurobiology2011
Rapid Disruption of Cellular Integrity of Zinc-treated Astroglia Is Regulated by p38 MAPK and Ca-dependent Mechanisms.
Article in Experimental neurobiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 8 citations in OpenAlex.
- Cytotoxic Effects of Mesaconitine, the Aconitum carmichaelii Debx Bioactive Compound, on HBEC-5i Human Brain Microvascular Endothelial Cells: Role of CaNeurotoxicity research · 2021Article
- Halodule pinifolia (Seagrass) attenuated lipopolysaccharide-, carrageenan-, and crystal-induced secretion of pro-inflammatory cytokines: mechanism and chemistry.Inflammopharmacology · 2021Article
- Activation of Autophagy Pathway Suppresses the Expression of iNOS, IL6 and Cell Death of LPS-Stimulated Microglia Cells.Biomolecules & therapeutics · 2013Article
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Authors and funding
3 authors at 1 institution in 1 country.
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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 Ca(2+) 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 Ca(2+) signaling.
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