The Function Of Hsp90 In Heat-induced Apoptosis In Jurkat Cells

When the human cells are in the "heat" environment, they are affected by heat shock or heat stress. As an environmental physic inducer, "heat" can transfer signals into the nuclear mediated by receptors on cell surface or other ways and regulate the expression of specific genes. Heat shock can cause heat-sensitive proteins in the cell unfold, form soluble global intermediates and re-accumulate, which lead the activation of HSF and synthesis of heat shock proteins. Heat shock has intimate relation with cell cycle and apoptosis. Local heat therapy has been applied as supplementary way in the clinic treatment of some cancers. However, the essence and mechanism of cellular heat stress still remain to be disclosed.Hsp90 is one of the most abundant proteins in cytosol of eukaryotic cells. Hsp90 may have a general role in refolding of the misfolded proteins that accumulate in response to various stress treatments and perhaps upon mutational alteration of proteins. Moreover, hsp90 has many other significant functions in cells, such as regulating activity of steroid receptors, transcription factors and some kinases in signal pathways. However, the functions of hsp90 in the apoptosis induces by heat shock is poorly understood.First of all, we research on heat shock temperature and its duration which can define Jurkat cell apoptosis. Heat shock at both 42℃ for 2h and 45℃ for 15min cause obvious cleavage of PARP, increased sub-diploid cells and appearance of DNA ladder during recovery at 37℃. This proves that the above heat shock condition can induce apoptosis, whereas heat shock at 45℃ for 15min induces more severe apoptosis than that of 42℃ for 2h. Continuous heat shock at 42°C increases the expression of hsp90 slightly, while has no obvious influence on the expression of Bcl-2, Bad, Bcl-x, CAS, Fas ligand and TIAR proteins. The decreased expression of procaspase-2 and procaspase-3, the notable cleavage of PARP, which is a substrate of caspase-3, indicates that the two caspases are activated under this heat shock condition.During the recovery from heat shock at 42℃ for 2h, procaspase-3 increases slightly and then decrease, procaspase-2 decreases gradually. The above two procaspases decrease...