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The Journal of Neuroscience, April 15, 2002, 22(8):3025-3032
Target Depletion of Distinct Tumor Necrosis Factor Receptor
Subtypes Reveals Hippocampal Neuron Death and Survival through
Different Signal Transduction Pathways
Libang
Yang1,
Kristina
Lindholm1,
Yoshihiro
Konishi1,
Rena
Li2, and
Yong
Shen1, 3
1 Haldeman Laboratory of Molecular and Cellular
Neurobiology and 2 L. J. Roberts Center for
Alzheimer's Disease Research, Sun Health Research Institute, Sun City,
Arizona 85351, and 3 Molecular and Cellular Biology
Program, Arizona State University, Tempe, Arizona 85287
Tumor necrosis factor receptor-I (TNFRI) and TNFRII are two TNFR
subtypes in the immune system, but their roles in the brain remain
unclear. Here we present a novel interaction between TNFR subtypes and
TNF- in the brain. Our studies on target-depleted TNFR in mice show
that TNF- has little effect on hippocampal neurons in which TNFRI,
containing an "intracellular death domain," is absent (TNFRI
 /), whereas neurons from TNFRII knock-out mice are vulnerable to
TNF- even at low doses. Moreover, little nuclear factor- B
(NF-B) translocation is induced by TNF- in neurons of
TNFRI /, whereas NF-B subunit p65 is still translocated from the
cytoplasm into the nucleus in neurons from wild-type and TNFRII /
mice. Furthermore, p38 mitogen-activated protein (MAP) kinase
activity is upregulated in neurons from both wild-type and TNFRI /,
but no alteration of p38 MAP kinase was found in neurons from TNFRII.
Results from overexpression of TNF receptors further support the above
findings. NT2 neuronal-like cells transiently transfected with TNFRI
are very sensitive to TNF-, whereas TNF- is not toxic and even
seems to be trophic to the cells with TNFRII overexpression. Last, our
radioligand-binding experiments demonstrate that TNF- binds TNFRI
with high affinity (Kd of 0.6 nM), whereas TNFRII shows lower binding affinity
(Kd of 1.14 nM) to TNF- in NT2 transfected cells. Together, these studies reveal novel neuronal responses of TNF- in mediating consequences of TNF receptor
activation differently. Subsequent neuronal death or survival may
ultimately depend on a particular subtype of TNF receptor that is
predominately expressed in neurons of the brain during neural
development or with neurological diseases.
Key words:
TNF-; TNF receptor; NF-B; p38 MAP kinase; neurodegeneration; neuronal survival
Copyright © 2002 Society for Neuroscience 0270-6474/02/2283025-08$05.00/0
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