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The Journal of Neuroscience, March 1, 1999, 19(5):1754-1770
Fas/Apo [Apoptosis]-1 and Associated Proteins in the
Differentiating Cerebral Cortex: Induction of Caspase-Dependent Cell
Death and Activation of NF- B
Zulfiqar F.
Cheema1,
Stephen B.
Wade1,
Masataka
Sata2,
Kenneth
Walsh2,
Farida
Sohrabji1, and
Rajesh C.
Miranda1
1 Department of Human Anatomy and Medical Neurobiology,
Texas A & M University Health Science Center, College Station, Texas
77843, and 2 Division of Cardiovascular Research, St.
Elizabeth's Medical Center, Tufts University School of Medicine,
Boston, Massachusetts 02135
The developing cerebral cortex undergoes a period of substantial
cell death. The present studies examine the role of the suicide receptor Fas/Apo[apoptosis]-1 in cerebral cortical development. Fas
mRNA and protein are transiently expressed in subsets of cells within
the developing rat cerebral cortex during the peak period of apoptosis.
Fas-immunoreactive cells were localized in close proximity to Fas
ligand (FasL)-expressing cells. The Fas-associated signaling protein
receptor interacting protein (RIP) was expressed by some Fas-expressing
cells, whereas Fas-associated death domain (FADD) was undetectable in
the early postnatal cerebral cortex. FLICE-inhibitory protein (FLIP),
an inhibitor of Fas activation, was also expressed in the postnatal
cerebral cortex. Fas expression was more ubiquitous in embryonic
cortical neuroblasts in dissociated culture compared to in
situ within the developing brain, suggesting that the
environmental milieu partly suppresses Fas expression at this
developmental stage. Furthermore, FADD, RIP, and FLIP were also
expressed by subsets of dissociated cortical neuroblasts in culture.
Fas activation by ligand (FasL) or anti-Fas antibody induced
caspase-dependent cell death in primary embryonic cortical neuroblast
cultures. The activation of Fas was also accompanied by a rapid
downregulation of Fas receptor expression, non-cell cycle-related
incorporation of nucleic acids and nuclear translocation of the
RelA/p65 subunit of the transcription factor NF- B. Together, these
data suggest that adult cortical cell number may be established, in
part, by an active process of receptor-mediated cell suicide, initiated
in situ by killer (FasL-expressing) cells and that Fas may have functions in addition to suicide in the developing brain.
Key words:
CNS; rat; interleukin-1 -converting enzyme; ICE
protease inhibitors; FasL; FADD; FLIP; RIP; PCNA; BrdU
Copyright © 1999 Society for Neuroscience 0270-6474/99/1951754-17$05.00/0
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