Open AccessElevations in cytosolic free Ca 2+ are not required to trigger apoptosis in human leukaemia cells
Author(s) -
LEN S. V.,
ILFEATHER S. A. K.,
HALLETT M. B.,
CAMPBELL A. K.,
COTTER T. G.
Publication year - 1992
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1992.tb03021.x
Subject(s) - apoptosis , immunology , cytosol , biology , microbiology and biotechnology , medicine , biochemistry , enzyme
SUMMARY Previous studies have indicated that Ca 2+ is a trigger Tor apoptosis (programmed cell death) in thymocytes and related cell lines. Recently we have shown that levels of apoptosis in leukacmic cells are diminished in Ca 2+ ‐deficient conditions, indicating that Ca 2+ may be important in the mechanism of apoptosis in these cells. In the present study we investigated the possibility that Ca 2+ serves as a trigger for apoptosis in the human leukaemic cell line, HL‐60. Using fura‐2 to measure cytosolic free Ca 2+ concentrations, [Ca 2+ ] i , in cell suspensions, and by using ratio imaging of fura‐2 in single cells, we did not observe an early significant increase in [Ca 2+ ] f , in HL‐60 cells undergoing apoptosis. The latter stages of apoptosis were, however, accompanied by increasing [Ca 2+ ] f , these increases were apparently a result of, rather than a cause of, apoptosis. Furthermore, apoptosis could be induced in HL‐60 cells under conditions of vastly reduced [Ca 2+ ] i achieved by loading these cells with fura‐2 in the presence of EGTA. These results indicate that elevation of [Ca 2+ ] i is not a prerequisite for apoptosis in HL‐60 cells and that apoptosis can occur in these cells in the presence of low[Ca 2+ ] i .