Lysophosphatidic acid rescues RhoA activation and phosphoinositides levels in astrocytes exposed to ethanol

Susana E. Martínez, Francisco Lázaro-Diéguez, Javier Selva, Fernando Calvo, Jaime Renau Piqueras, Piero Crespo, Enrique Claro, Gustavo Egea

Research output: Contribution to journalArticle

19 Scopus citations

Abstract

Long-term ethanol treatment substantially impairs glycosylation and membrane trafficking in primary cultures of rat astrocytes. Our previous studies indicated that these effects were attributable to a primary alteration in the dynamics and organization of the actin cytoskeleton, although the molecular mechanism(s) remains to be elucidated. As small Rho GTPases and phosphoinositides are involved in the actin cytoskeleton organization, we now explore the effects of chronic ethanol treatment on these pathways. We show that chronic ethanol treatment of rat astrocytes specifically reduced endogenous levels of active RhoA as a result of the increase of in the RhoGAP activity. Furthermore, ethanol-treated astrocytes showed reduced phosphoinositides levels. When lysophosphatidic acid was added to ethanol-treated astrocytes, it rapidly reverted actin cytoskeleton reorganization and raised active RhoA levels and phosphoinositides content to those observed in untreated astrocytes. Overall, our results indicate that the harmful effects of chronic exposure to ethanol on a variety of actin dynamics-associated cellular events are primarily because of alterations of activated RhoA and phosphoinositides pools.

Original languageEnglish (US)
Pages (from-to)1044-1052
Number of pages9
JournalJournal of Neurochemistry
Volume102
Issue number4
DOIs
StatePublished - Aug 2007
Externally publishedYes

Keywords

  • 5-bisphosphate
  • Actin cytoskeleton
  • Astrocytes
  • Ethanol
  • Fetal alcohol syndrome
  • Lysophosphatidic acid
  • Phosphatidylinositol 4
  • RhoA

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

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