ANALYSIS OF APOPTOSIS MORPHOLOGY IN EPSTEIN-BARR-VIRUS POSITIVE AND NEGATIVE BURKITTS-LYMPHOMA CELLS

Citation
H. Ishii et al., ANALYSIS OF APOPTOSIS MORPHOLOGY IN EPSTEIN-BARR-VIRUS POSITIVE AND NEGATIVE BURKITTS-LYMPHOMA CELLS, Archives of histology and cytology, 60(2), 1997, pp. 143-152
Citations number
35
Categorie Soggetti
Cell Biology
ISSN journal
09149465
Volume
60
Issue
2
Year of publication
1997
Pages
143 - 152
Database
ISI
SICI code
0914-9465(1997)60:2<143:AOAMIE>2.0.ZU;2-T
Abstract
In recent studies of cycloheximide (CHS)induced apoptosis in sublines of established Burkitt's lymphoma cell lines (BJA-B) both with and wit hout Epstein-Barr virus (EBV) infection, we noticed two distinct types of apoptosis morphology. In the present paper, we have classified the se, and further carried out a statistical analysis of their incidence in untreated and CHX-treated EBV-free (EBV(-)) and EBV-infected (EBV()) BJA-B cells. Classification: Both types of apoptosis morphology dem onstrated typical nuclear and cytoplasmic condensation. However, ''Typ e 1 apoptotic cells'' (AP1) maintained a spherical or ovoid shape, but ''Type 2 apoptotic cells'' (AP2) were typified by the lobulation of t heir nuclear and cytoplasmic structures to form ''clover leaf'' shapes , Statistical analysis of incidence: The numbers of AP1 and AP2 cells were analysed using a chi(2) test, with results as follows: EBV(-) cel ls underwent AP1 in preference to AP2 (90.5% versus 9.5%) (p < 0.001), whilst EBV(+) cells had comparably more AP2, making AP1 and AP2 appro ximately equal (49.3% versus 50.7%) (p > 0.1). In EBV(-) cells, treatm ent with CHX had little effect on the ratios of differing apoptotic mo rphology. In contrast, in the EBV(+) cells, cell death was altered fro m AP2 (50.7% --> 25.2%) towards AP1 (49.3% --> 74.8%) (p < 0.001). We propose that cellular proteins known to be associated with EBV infecti on not only protect the cells from apoptosis, but also affect the phen otype of apoptosis. This knowledge may be useful for defining possible mechanisms of apoptosis induction and/or inhibition in specific model s.