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Calcium‐dependent DNA fragmentation in human synovial cells exposed to cold shock
Author(s) -
Perotti Mariarosa,
Toddei Filippo,
Mirabelli Francesca,
Vairetti Mariapia,
Bellomo Giorgo,
McConkey David J.,
Orrenius Sten
Publication year - 1990
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(90)80040-p
Subject(s) - dna fragmentation , fragmentation (computing) , endonuclease , microbiology and biotechnology , apoptosis , programmed cell death , cytosol , protein kinase c , dna damage , chemistry , apoptotic dna fragmentation , dna , biology , biochemistry , kinase , enzyme , ecology
Exposure of confluent human synovial McCoy's cells to near‐freezing temperatures followed by rewarming at 37°C resulted in endonuclease activation and cell death characteristic of a suicide process known as apoptosis. Both DNA fragmentation and cell killing were dependent on a sustained increase in the cytosolic Ca 2+ concentration. Sensitivity to cold shock‐induced endonuclease activation was critically dependent on the cell cycle (proliferative) status and limited to confluent cells, whereas cells in the logarithmic growth phase were completely resistant. However, DNA fragmentation was promoted in the proliferating McCoy's cells pretreated with H‐7 or sphingosine, inhibitors of protein kinase C. In addition, phorbol ester, known to activate PKC, inhibited DNA fragmentation in the confluent cells. Our findings indicate that cold shock‐induced DNA fragmentation in McCoy's cells is dependent on a sustained Ca 2+ increase, and sensitivity to the process appears to be regulated by the status of protein kinase C.