Increased expression of heat shock protein, transferrin, and β2-microglobulin in astrocytes during scrapie

Abstract Scrapie is a slow infection and neurodegenerative disease of animals characterized pathologically by formation of amyloid, astrocytosis, vacuolation and unjury and death of neurons. Our previous studies of scrapie point to: (i) a critical role for the astrocyte in responding to, and perhaps inadvertently contributing to, the neuropathological manifestations of infection; and (ii), the hypothesis that the astrocyte a executes a programed response to neurological injury analogous to the stress response. The expression of genes encoding tranferrin and β 2 -microglobulin has been shown to increase during scrapie and we sought in the studies reported here to determine whether this modulated expression would map to astrocytes. We also looked for changes in a heat shock protein that is induced in the stress response. We show that transferrin, β 2 -microglobulin and heat shock 72 kD protein all increase in astrocytes in the course of infection. We speculate in the discussion on the possible functions of the other proteins in neurodegenerative processes and why these functions so frequently reside in the astrocyte.