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Vol. 12, Issue 10, 3139-3151, October 2001
-induced Apoptosis in Human Burkitt Lymphoma B Cells BL41
and
*Institut National de la Santé et de la Recherche
Médicale U542 and Claude Bernard Research Center, Hopital Paul
Brousse, 94807 Villejuif, France; and On binding to its receptor, transforming growth factor Department of
Pediatrics, Women and Infant's Hospital, Brown University, Providence,
Rhode Island 02905
(TGF)
induces apoptosis in a variety of cells, including human B lymphocytes.
We have previously reported that TGF-mediated apoptosis is
caspase-dependent and associated with activation of caspase-3. We show
here that caspase-8 inhibitors strongly decrease TGF-mediated apoptosis in BL41 Burkitt's lymphoma cells. These inhibitors act upstream of the mitochondria because they inhibited the loss of mitochondrial membrane potential observed in TGF-treated cells. TGF induced caspase-8 activation in these cells as shown by the cleavage of specific substrates, including Bid, and the appearance of
cleaved fragments of caspase-8. Our data show that TGF induces an
apoptotic pathway involving sequential caspase-8 activation, loss of
mitochondrial membrane potential, and caspase-9 and -3 activation.
Caspase-8 activation was Fas-associated death domain protein
(FADD)-independent because cells expressing a dominant negative mutant
of FADD were still sensitive to TGF-induced caspase-8 activation and
apoptosis. This FADD-independent pathway of caspase-8 activation is
regulated by p38. Indeed, TGF-induced activation of p38 and two
different inhibitors specific for this mitogen-activated protein
kinase pathway (SB203580 and PD169316) prevented TGF-mediated caspase-8 activation as well as the loss of mitochondrial membrane potential and apoptosis. Overall, our data show that p38 activation by
TGF induced an apoptotic pathway via FADD-independent activation of
caspase-8.
Present address: Nicolas Schrantz,
Department of Immunology-IMM14/R221, The Scripps Research Institute,
10550 N. Torrey Pines Rd., La Jolla, CA 92037.
§
Corresponding author. E-mail address:
vazquez{at}infobiogen.fr.
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