Trigeminal ganglion neurons are protected by the heat shock proteins hsp70 and hsp90 from thermal stress but not from programmed cell death following nerve growth factor withdrawal.
A prior mild thermal stress (heat shock) can protect neuronal cells against a subsequent exposure to either severe thermal stress or the induction of programmed cell death (apoptosis). By micro-injecting trigeminal ganglion neurons with expression constructs we show that over-expression of the individual heat shock proteins hsp70 and hsp90 can protect these cells against severe thermal stress but not against apoptosis. However, the protective effect of prior heat shock against subsequent apoptosis is dependent upon its ability to induce heat shock protein (hsp) synthesis rather than, for example, the inhibition of other protein synthesis associated with heat shock. The significance of these effects is discussed in terms of the role of different hsps in protecting neuronal cells from distinct stresses.
Wyatt
S
S
Department of Molecular Pathology, University, College London Medical School, UK.
Mailhos
C
C
Latchman
D S
DS
D000818:Animals; D016923:Cell Death / Q000187:drug effects*; D002478:Cells, Cultured; D018840:HSP70 Heat-Shock Proteins / Q000494:pharmacology*; D018841:HSP90 Heat-Shock Proteins / Q000494:pharmacology*; D051379:Mice; D008815:Mice, Inbred Strains; D009414:Nerve Growth Factors / Q000494:pharmacology*; D014276:Trigeminal Nerve / Q000187:drug effects*
D018840:HSP70 Heat-Shock Proteins; D018841:HSP90 Heat-Shock Proteins; D009414:Nerve Growth Factors