Generalized accumulation of stress proteins during the organism's adaptation to stress

Induction of adaptation to stress in rats by repeated transcranial electrostimulation

“…In general, the currently available evidence suggests that the protection afforded by adaptation to stressors and in particular to repeated ESs may result from the operation of two basic mechanisms: activation of the body systems that limit the stress reaction, thereby preventing its various damaging effects [7,12]; and accumulation in the target or-gans of stress proteins that possess dispersive properties and can thus prevent protein denaturation and the associated damage to cellular structures responsible for the so-called "adaptive stabilization of structures" [12,14]. This latter phenomenon, in turn, underlies numerous protective effects of stress adaptation [5,13].…”

Heat-shock proteins and cardioprotection

“…Adaptation of animals to periodic moderate stress was shown to increase heart resistance to ischemia and reperfusion and toxic concentrations of catecholamines and calcium. Various cellular structures of the heart (mitochondria, elements of the sarcoplasmic reticulum, and nuclei) differ in extremely high resistance to autolysis [1][2][3][4][5]22]. The contents of mRNA and HSP70 in the heart in adapted animals are increased [5].…”

Constitutive overexpression of the major inducible 70 kDa heat shock protein mediates large plaque formation by measles virus.

“…The identification of a host factor that reproducibly promotes the emergence of large plaque variants is the first step in defining the corresponding viral determinant of infection phenotype and the possible role of virus-HSP interaction as a determinant of virus virulence. In this capacity, hsp72 is an attractive candidate for a cellular protein modulating virulence since increases in hsp72 frequently accompany physiologic states associated with high morbidity, including psychological stress (Fukudo et al, 1997 ;Meerson et al, 1993).…”