6533b853fe1ef96bd12ac2e3

RESEARCH PRODUCT

CD38 expression enhances sensitivity of lymphoma T and B cell lines to biochemical and receptor-mediated apoptosis

Armando GregoriniDaniela ColombaStella ColombaCristina CintiMarco Tomasetti

subject

Lymphoma B-CellCD30Ultraviolet RaysTocopherolsApoptosisCD38BiologyLymphoma T-CellJurkat cellsTNF-Related Apoptosis-Inducing LigandJurkat Cellsimmune system diseasesAnnexinCell Line Tumorhemic and lymphatic diseasesmedicineHumansVitamin EAnnexin A5B cellhemic and immune systemsHydrogen PeroxideCell BiologyGeneral MedicineOligonucleotides AntisenseFlow CytometryADP-ribosyl Cyclase 1Antigens DifferentiationMolecular biologyBCL10medicine.anatomical_structureApoptosisAnnexin A5K562 CellsFluorescein-5-isothiocyanate

description

CD38 has been widely characterised both as an ectoenzyme and as a receptor. In the present paper, we investigated the role of CD38 as possible modulator of apoptosis. CD38-positive (CD38(+)) and negative (CD38(-)) fractions, obtained by sorting CD38(+) cells from lymphoma T (Jurkat) and lymphoma B (Raji) and by transfecting lymphoma LG14 and myeloid leukemia K562 cell lines, were used. Cellular subpopulations were exposed to different triggers (H(2)O(2), UV-B, alpha-TOS and hrTRAIL) and the extent of apoptosis was determined by Annexin V-FITC/PI assay. Our data showed that, in lymphoma cells, propensity to apoptosis was significantly linked to CD38 expression and that, remarkably, such response was independent of the nature of the trigger used. Inhibition of CD38 expression by antisense oligonucleotides treatment resulted in CD38-silenced fractions which were as prone to apoptosis as CD38(-) ones. Notably, susceptibility of K562 to apoptosis-inducing challenges was not affected by CD38 expression.

yearjournalcountryeditionlanguage
2006-09-01Cell Biology International
https://doi.org/10.1016/j.cellbi.2006.05.004