Abstract
In previous work we showed that programed cell death (PCD) in thymocytes is mediated by a sustained increase in cytosolic Ca2+ concentration, resulting in the activation of an endogenous endonuclease, DNA fragmentation, and cell death. In this study we investigated the roles of Ca2+ and DNA fragmentation in target cell killing by natural killer (NK) cells. The effector cells induced a rapid, sustained increase in cytosolic Ca2+ concentration in Jurkat target cells. Buffering the target cell cytosolic Ca2+ with the Ca2+-selective dye, quin-2, prevented target cell killing. Extensive DNA fragmentation was associated with killing in every target tested, and this response was also blocked by quin-2. The endonuclease inhibitor, aurintricarboxylic acid, inhibited both DNA fragmentation and killing without influencing the Ca2+ increase in target cells. Thus, it is concluded that NK cell killing depends on a Ca2+ increase and appears to involve endogenous endonuclease activation in target cells.
Original language | English (US) |
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Pages (from-to) | 2661-2664 |
Number of pages | 4 |
Journal | FASEB Journal |
Volume | 4 |
Issue number | 9 |
DOIs | |
State | Published - 1990 |
Externally published | Yes |
Keywords
- aurintricarboxylic acid
- calcium buffering
- endonuclease activation
- programed cell death
ASJC Scopus subject areas
- Biotechnology
- Biochemistry
- Molecular Biology
- Genetics