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B
Department of Biochemistry and Molecular Biology, Colorado State University, Fort Collins, Colorado 80523-1870, USA
1Correspondence: Department of Biochemistry and Molecular Biology, Colorado State University, Fort Collins, CO 80523-1870, USA. E-mail:
S100ßß is a calcium binding, neurotrophic protein produced by
nonneuronal cells in the nervous system. The pathway by which it
enhances neuronal survival is unknown. Here we show that S100ßß
enhances survival of embryonic chick forebrain neurons in a
dose-dependent manner. In the presence of suboptimal amounts of
S100ßß, neuronal survival is enhanced by the immunosuppressants
FK506 and cyclosporin A at concentrations that inhibit calcineurin,
which is present in these cells. Rapamycin, an immunosuppressant that
does not inhibit calcineurin, did not enhance cell survival.
Cypermethrin, a direct and highly specific calcineurin inhibitor,
mimicked the immunophilin ligands in its neurotrophic effect. None of
the drugs stimulated neuronal survival in the absence of S100ßß. In
the presence of suboptimal amounts of S100ßß, FK506, cyclosporin A,
and cypermethrin (but not rapamycin) also increased NF-
B activity,
as measured by immunofluorescence of cells stained with antibody to the
active subunit (p65) and by immunoblotting of nuclear extracts.
Antioxidant and glucocorticoid inhibitors of NF-B decreased both the
amount of active NF-B and the survival of neurons caused by
S100ßß alone or in the presence of augmenting drugs. We conclude
that S100ßß enhances the survival of chick embryo forebrain neurons
through the activation of NF-B.—Alexanian, A. R., Bamburg,
J. R. Neuronal survival activity of S100ßß is enhanced by
calcineurin inhibitors and requires activation of NF-B.
Key Words: immunosuppressants • immunophilins • cyclosporin A • FK506 • rapamycin • cypermethrin
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