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Ethanol increases p190RhoGAP activity, leading to actin cytoskeleton rearrangements
Author(s) -
Selva Javier,
Egea Gustavo
Publication year - 2011
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2011.07522.x
Subject(s) - rhoa , microbiology and biotechnology , cytoskeleton , gene silencing , actin , actin cytoskeleton , gtp' , biology , chemistry , biochemistry , signal transduction , cell , gene , enzyme
J. Neurochem. (2011) 10.1111/j.1471‐4159.2011.07522.x Abstract We previously reported that cells chronically exposed to ethanol show alterations in actin cytoskeleton organization and dynamics in primary cultures of newborn rat astrocytes, a well‐established in vitro model for foetal alcohol spectrum disorders. These alterations were attributed to a decrease in the cellular levels of active RhoA (RhoA‐GTP), which in turn was produced by an increase in the total RhoGAP activity. We here provide evidence that p190RhoGAPs are the main factors responsible for such increase. Thus, in astrocytes chronically exposed to ethanol we observe: (i) an increase in p190A‐ and p190B‐associated RhoGAP activity; (ii) a higher binding of p190A and p190B to RhoA‐GTP; (iii) a higher p120RasGAP‐p190A RhoGAP complex formation; and (iv) the recruitment of both p190RhoGAPs to the plasma membrane. The simultaneous silencing of both p190 isoforms prevents the actin rearrangements and the total RhoGAP activity increase triggered both by ethanol. Therefore, our data directly points p190RhoGAPs as ethanol‐exposure molecular targets on glial cells of the CNS.