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J. Biol. Chem., Vol. 276, Issue 47, 43871-43878, November 23, 2001
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From the Laboratoire de Physiopathologie Cellulaire et
Moléculaire de la Rétine, INSERM-Université Louis
Pasteur EMI 9918, Clinique Médicale A, Centre Hospitalier
Régional Universitaire, BP. 426, 1 Place de
l'Hôpital, 67091 Strasbourg Cedex, France
Basic fibroblast growth factor (FGF2) stimulates
photoreceptor survival in vivo and in vitro,
but the molecular signaling mechanism(s) involved are unknown.
Immunohistochemical and immunoblotting analyses of pure photoreceptors,
inner retinal neurons, and Müller glial cells (MGC) in
vitro revealed differential expression of the high affinity FGF
receptors (FGFR1-4), as well as many cytoplasmic signaling
intermediates known to mediate the extracellular signal-regulated kinase (ERK1/2) pathway. FGF2-induced tyrosine phosphorylation in
vitro exhibited distinct profiles for each culture type, and FGF2-induced ERK1/2 activation was observed for all three preparations. Whereas U0126, a specific inhibitor of ERK kinase (MEK), completely abolished FGF2-induced ERK1/2 tyrosine phosphorylation and survival in
cultured photoreceptors, persistent ERK1/2 phosphorylation was observed
in cultured inner retinal cells and MGC. Furthermore U0126 treatment
entirely blocked nerve growth factor-induced ERK1/2 activation in MGC,
as well as FGF2-induced ERK1/2 activation in cerebral glial cells.
Taken together, these data indicate that FGF2-induced ERK1/2 activation
is entirely mediated by MEK within photoreceptors, which is responsible
for FGF2-stimulated photoreceptor survival. In contrast, inner
retina/glia possess alternative, cell type, and growth factor-specific
MEK-independent ERK1/2 activation pathways. Hence signaling and
biological effects elicited by FGF2 within retina are mediated by cell
type-specific pathways.
Alternate FGF2-ERK1/2 Signaling Pathways in Retinal Photoreceptor
and Glial Cells in Vitro*
,
*
This work was supported by the INSERM and the British
Retinitis Pigmentosa Society.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Supported by a grant from Pro Retina Germany.
§
To whom correspondence should be addressed. Tel.: 33-3-90-24-34-23;
Fax: 33-3-90-24-34-17; E-mail:
hicks@neurochem.u-strasbg.fr.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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