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Dexamethasone‐induced killing of neoplastic cells of lymphoid derivation: Lack of early calcium involvement
Author(s) -
Bansal Neelam,
Houle Antoinette G.,
Melnykovych George
Publication year - 1990
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041430114
Subject(s) - fragmentation (computing) , calcium , egta , dexamethasone , dna fragmentation , apoptosis , glucocorticoid , calmodulin , incubation , cell culture , antagonist , medicine , biology , endocrinology , steroid , dna , microbiology and biotechnology , chemistry , programmed cell death , biochemistry , receptor , hormone , genetics , ecology
The role of calcium influx in dexamethasone‐induced fragmentation of DNA was studied in the glucocorticoid‐sensitive human lymphoid line of T cell derivation (CEM‐C7). Reduction of calcium content in the medium or the use of EGTA increased DNA fragmentation and appeared to slightly enhance the effect of dexamethasone. Incubation of isolated nuclei in the presence of high concentrations of calcium did not bring about significant DNA fragmentation. Calmida‐zolium, an antagonist of calmodulin dependent reactions did not reduce the sensitivity of CEM‐C7 cells to dexamethasone nor did it modify the response to dexamethasone of the resistant CEM‐C1 line. It appears that in contrast to rodent thymocytes, massive calcium influx is not per se responsible for the initiation of directed cell killing (apoptosis).