Synthesis of heat shock/stress proteins during cellular injury.

Abstract

Several conclusions can be drawn from available data on the expression of stress proteins in brain with respect to their utility as markers of cellular injury. First, it is evident that all cell types in brain are capable of expressing stress proteins, although there is striking specificity in the population responding to a given insult. The apparent hierarchy of responsiveness indicated by hsp72 expression correlates well with the relative vulnerability of specific cell populations in a given model. With increasing severity of injury there can be an attenuation of the translational component of the stress response, in that hsp72 immunoreactivity fails to accumulate even though its mRNA is abundantly expressed. For this reason, hsp72 immunoreactivity provides an index of cell populations that have responded to an insult with a functional stress response. Such a response is not sufficient to guarantee survival, since many CA1 neurons that show significant hsp72 staining are eventually lost after global ischemia in the rat. However, brief insults that result in expression of hsp72 and other proteins encoded by induced mRNAs do result in tolerance to subsequent insults. Future studies may be expected to reveal the contributions of specific gene products to the tolerant state. Meanwhile, complementary evaluations of hsp72 mRNA and protein expression provide practical means of identifying cell populations responding to diverse injuries.