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J. Biol. Chem., Vol. 277, Issue 10, 7955-7961, March 8, 2002

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Molecular Mechanisms Involved in CD43-mediated Apoptosis of TF-1 Cells
ROLES OF TRANSCRIPTION, Daxx EXPRESSION, AND ADHESION MOLECULES^*

Luká ermák^§, árka ímová^§, Alexandros Pintzas^¶, Václav Hoejí, and Ladislav Andra

From the  Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, Prague 4, CZ-14220, Czech Republic, and the ^¶ Institute of Biological Research and Biotechnology, National Hellenic Research Foundation, Athens 116 35, Greece

CD43 (leukosialin, sialophorin), an abundant leukocyte surface sialoglycoprotein, regulates leukocyte adhesion and transmits activating signals in T cells and dendritic cells. Immobilized anti-CD43 monoclonal antibody (mAb) MEM-59 has been previously shown to induce apoptosis of hematopoietic progenitors. In this study we show that it also triggers apoptosis of the myeloid progenitor-derived cell line TF-1. The kinetics of the MEM-59-induced apoptosis were unusually slow, with the first apoptotic cells appearing 36-48 h after their contact with the immobilized antibody; in 5 days, 90% of the cells were dead. CD43-mediated apoptosis was enhanced by coimmobilized anti-CD45 mAb and partly suppressed by coimmobilized anti-CD50 (ICAM-3) or anti-CD99 mAb. The MEM-59-triggered apoptosis of TF-1 cells was also inhibited by the overexpression of an apoptotic regulator, Daxx. CD43-mediated apoptosis was preceded by the repression of the DNA binding activity of the transcription factor AP-1. DNA array screening revealed that the expression of several genes encoding apoptosis-regulating proteins, including 14-3-3 proteins and the granulocyte macrophage colony-stimulating factor (GM-CSF) receptor -subunit, was repressed in TF-1 cells bound to immobilized MEM-59. The down-regulation of 14-3-3 proteins and GM-CSF receptor  was accompanied by translocation of the proapoptotic protein Bad to the mitochondria. These results suggest that engagement of CD43 may, presumably through the repressing transcription, initiate a Bad-dependent apoptotic pathway.

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