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First published online 26 July 2005
doi: 10.1242/jcs.02507

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Hydrogen peroxide alters membrane and cytoskeleton properties and increases intercellular connections in astrocytes

¹ Department of Biological Engineering, University of Missouri-Columbia, Columbia, MO 65211, USA
² Department of Biochemistry, University of Missouri-Columbia, Columbia, MO 65211, USA
³ Department of Pharmacology and Physiology, University of Missouri-Columbia, Columbia, MO 65211, USA

^* Author for correspondence (e-mail: Leejam{at}missouri.edu)

Accepted 23 May 2005

Excess hydrogen peroxide (H₂O₂) is produced in the pathogenesis of brain injuries and neurodegenerative diseases. H₂O₂ may damage cells through direct oxidation of lipids, proteins and DNA or it can act as a signaling molecule to trigger intracellular pathways leading to cell death. In this study, H₂O₂ caused plasma membranes of primary astrocytes to become more gel-like, while artificial membranes of vesicles composed of rat brain lipid extract became more liquid crystalline-like. Besides the effects on membrane phase properties, H₂O₂ promoted actin polymerization, induced the formation of cell-to-cell tunneling nanotube (TNT)-like connections among astrocytes and increased the colocalization of myosin Va with F-actin. Myosin Va was also observed in the H₂O₂-induced F-actin-enriched TNT-like connections. Western blot analysis suggests that H₂O₂ triggered the phosphorylation of the p38 mitogen-activated protein kinase (MAPK), and that SB203580, a specific inhibitor of p38 MAPK, suppressed the changes in membrane phase properties and cytoskeleton resulting from H₂O₂ treatment. These results suggest that H₂O₂ alters astrocyte membranes and the cytoskeleton through activation of the p38 MAPK pathway.

Key words: actin, cytoneme, nanotube, oxidative stress, p38 MAPK

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