Heat shock induces apoptosis in mouse thymocytes and protects them from glucocorticoid-induced cell death.
Thymocyte death is a complex phenomenon under the control of different signals and stimuli. We evaluated the effect of elevated temperature (heat shock, HS) on mouse thymocyte apoptosis. Incubation of thymocytes at 43 degrees C for 20 min induced DNA fragmentation and cell death, but it was also able to decrease the apoptosis induced by dexamethasone (DEX), TPA or Ca2+ ionophore. The anti-apoptotic effect was correlated with induction of heat shock proteins (HSPs) and abolished by protein synthesis inhibition. On the other hand, HS-induced unlike DEX-induced apoptosis was not inhibited by protein synthesis and mRNA transcription inhibitors, the PKC inhibitors H-7 and staurosporine, or interleukin-4 (IL-4), but only by Zn2+. These results suggest that HS interferes in thymocyte death by either inducing or inhibiting thymocyte apoptosis and that the induction process mechanisms are different from those of GCH.
Migliorati
G
G
Istituto di Farmacologia Medica, Perugia University Medical School, Italy.
Nicoletti
I
I
Crocicchio
F
F
Pagliacci
C
C
D'Adamio
F
F
Riccardi
C
C
D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D016923:Cell Death; D004249:DNA Damage; D003907:Dexamethasone / Q000494:pharmacology*; D006360:Heat-Shock Proteins / Q000096:biosynthesis; D006358:Hot Temperature; D051379:Mice; D008809:Mice, Inbred C3H; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D013950:Thymus Gland / Q000166:cytology*
D006360:Heat-Shock Proteins; D000001:Calcimycin; D003907:Dexamethasone; D013755:Tetradecanoylphorbol Acetate