Upregulation of Heat Shock Proteins Rescues Motoneurones from Axotomy-Induced Cell Death in Neonatal Rats

@article{Kalmar2002UpregulationOH,
  title={Upregulation of Heat Shock Proteins Rescues Motoneurones from Axotomy-Induced Cell Death in Neonatal Rats},
  author={Bernadett Kalmar and Geoffrey Burnstock and Gerta Vrb{\'o}va and Rudolf Urbanics and P{\'e}ter Csermely and Linda Greensmith},
  journal={Experimental Neurology},
  year={2002},
  volume={176},
  pages={87-97}
}
Heat shock proteins (hsps) are induced in a variety of cells following periods of stress, where they promote cell survival. In this study, we examined the effect of upregulating hsp expression by treatment with BRX-220, a co-inducer of hsps, on the survival of injured motoneurones. Following sciatic nerve crush at birth, rat pups were treated daily with BRX-220. The expression of hsp70 and hsp90, motoneurone survival, and muscle function was examined at various intervals later and the number of… 

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References

SHOWING 1-10 OF 57 REFERENCES
The effect of neonatal nerve injury on the expression of heat shock proteins in developing rat motoneurones.
TLDR
It is possible that the upregulation of hsp27 observed in injured mot oneurones may play a role in protecting motoneurones from apoptotic cell death following nerve injury, as assessed by TUNEL and caspase-3 immunoreactivity.
Exogenous heat shock cognate protein Hsc 70 prevents axotomy-induced death of spinal sensory neurons.
TLDR
Application of exogenous Hsc70 prevented axotomy-induced death of virtually all sensory neurons, but did not significantly alter motoneuron death, suggesting that HSc70 may prove to be useful in the repair of peripheral sensory nerve damage.
A Role for HSP27 in Sensory Neuron Survival
TLDR
In vitro, overexpression of human HSP27 in neonatal rat sensory and sympathetic neurons significantly increases survival after NGF withdrawal, with nearly twice as many neurons surviving at 48 hr as well as in P0 DRG cultures, suggesting that HSP 27 in sensory neurons plays a role in promoting survival after axotomy or neurotrophin withdrawal.
Astrocyte survival and HSP70 heat shock protein induction following heat shock and acidosis
TLDR
This study determined whether induction of heat shock proteins protects cultured astrocytes against acidosis and induced hsp70 mRNA and HSP70 protein.
Alterations of nerve-muscle interaction during postnatal development influence motoneurone survival in rats.
Synthesis of Heat Shock/Stress Proteins during Cellular Injury
  • T. Nowak
  • Biology
    Annals of the New York Academy of Sciences
  • 1993
TLDR
Comprehensive evaluations of hsp72 mRNA and protein expression provide practical means of identifying cell populations responding to diverse injuries and may reveal the contributions of specific gene products to the tolerant state.
Heat shock proteins increase resistance to apoptosis.
TLDR
Results demonstrate that an increase in cellular levels of hsp 27 or 70, either by a mild heat shock treatment or by stable transfection, increases the resistance of U937 and Wehi-s cells to apoptotic cell death.
HSP70 protects murine astrocytes from glucose deprivation injury
...
...