INVESTIGADORES
PASQUINI juana Maria
artículos
Título:
Fyn kinase is involved in oligodendroglial cell differentiation induced by apotransferrin
Autor/es:
PEREZ MJ, ORTIZ EH, ROFFE M, SOTO EF AND PASQUINI JM
Revista:
JOURNAL OF NEUROSCIENCE RESEARCH
Editorial:
WILEY-LISS, DIV JOHN WILEY & SONS INC
Referencias:
Año: 2009 vol. 87 p. 3378 - 3389
ISSN:
0360-4012
Resumen:
Mechanisms that regulate oligodendroglial cell (OLGc)differentiation are the focus of intensive research in the
field of cellular and molecular neurobiology. We have previously shown that the addition of apotransferrin
(aTf) to primary OLGc cultures accelerates their differentiation and induces an increase in the expression of
different components of the myelin cytoskeleton (CSK) such as actin, tubulin, and some of the microtubuleassociated
proteins, particularly the stable tubulin only peptide (STOP). Fyn protein-tyrosine kinase (Fyn kinase),
a member of the Src family, participates in signalling pathways that regulate OLGs/myelin cytoskeletal
reorganization. It is essential for myelin development in the central nervous system (CNS), and its absence
results in hypomyelination. In the present study, we used both primary cell and N19 cell line cultures to
investigate further the mechanisms of action involved in the accelerated differentiation of OLGcs induced by
aTf. In particular, we were interested in studying the participation of Fyn kinase in the different pathways
involved in the reorganization of the OLGc/myelin cytoskeleton. In agreement with results already published,
we found that in OLGcs, Fyn kinase is associated with Tau and tubulin. Using a dominant-negative of Tau in
which the Fyn-Tau-microtubules (MTs) interaction is blocked, we found that aTf was unable to induce OLGc
morphological differentiation. It was also observed that aTf decreases the activated RhoA content in coincidence
with a redistribution of actin immunoreactivity. These results give support to our hypothesis that Fyn
kinase plays a key role in the differentiation process of OLGcs promoted by aTf.