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Lack of heat shock response triggers programmed cell death in a rat histiocytic cell line
Author(s) -
Sreedhar A.S,
Pardhasaradhi B.V.V,
Begum Zareena,
Khar Ashok,
Srinivas Usha K
Publication year - 1999
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/s0014-5793(99)00970-9
Subject(s) - heat shock , programmed cell death , apoptosis , microbiology and biotechnology , dna fragmentation , hsp70 , fragmentation (computing) , cell culture , heat shock protein , biology , cell , chemistry , biochemistry , genetics , ecology , gene
Stress response is a universal phenomenon. However, a rat histiocytic cell line, BC‐8, showed no heat shock response and failed to synthesize heat shock protein 70 (hsp70) upon heat shock at 42°C for 30 min. BC‐8 is a clone of AK‐5, a rat macrophage tumor line that is adapted to grow in culture and has the same chromosome number and tumorigenic potential as AK‐5. An increase in either the incubation temperature or time or both to BC‐8 cells leads to loss of cell viability. In addition, heat shock conditions activated apoptotic cell death in these cells as observed by cell fragmentation, formation of nuclear comets, apoptotic bodies, DNA fragmentation and activation of ICE‐like cysteine proteases. Results presented here demonstrate that BC‐8 cells cannot mount a typical heat shock response unlike all other eukaryotic cells and that in the absence of induction of hsps upon stress, these cells undergo apoptosis at 42°C.