Galectin-1-induced apoptosis in mature T cells is preceded by an early activation of AP-1 and mediated by a Bcl-2-dependent pathway

RABINOVICH G.; ALONSO C.; SOTOMAYOR C.; DURAND S.; BOCCO J.L.; RIERA C.

NATURE PUBLISHING GROUP

Lugar: Londres; Año: 2000 vol. 8 p. 747 - 747

alectins are emerging as a new class of bioactive molecules with specific immunomodulatory properties. Galectin-1 (Gal-1), a member of this family, has been shown to induce apoptosis of mature T cells and immature thymocytes. To gain insight into the intracellular signals transduced by Gal-1 upon binding to mature T cells, we investigated whether this protein triggered activation of the dimeric AP-1 transcription factor. A marked increase in the binding of nuclear extracts to synthetic oligonucleotides containing the AP-1 consensus sequence, could be detected by an electrophoretic mobility shift assay, when T cells were cultured for 30 min in the presence of Gal-1. This DNA-binding activity was preceded by a rapid increase in the levels of c-Jun mRNA, as determined by Northern blot analysis. Requirement of AP-1 for Gal-1-induced apoptosis was confirmed by the dose-dependent reduction on the level of DNA fragmentation observed when cells were pre-treated with curcumin (an inhibitor of