Heat shock proteins stress response

Exposure of cells to a variety of stresses induces a modification of cell metabolism called the heat shock or stress response [215], which is accompanied by the rapid synthesis of the so-called heat-shock proteins (HSPs). HSPs are considered to have essential protective function in cells. They are classified according to their function or apparent molecular weight into four families the HSP90 family, the HSP70 family, the HSP60 family and other low-molecular weight HSPs. 

Almoguera, C., M.A. Coca, and J. Jordano. 1993. Tissue-specific expression of sunflower heat shock proteins in response to water stress. Plant J. 4 947-958. 

Blake, M.J., Udelsman, R., Feulner, G.J., Norton, D.D., Holbrook, N.J. (1991). Stress induced heat shock protein 70 expression in adrenal cortex An ACTH-sensitive. age-dependent response. Proc. Natl. Acad. Sci. USA 88, 9873-9877,... 

Li, G. Laszio, A. (1985). Thermotolerance in mammalian cells A possible role for the heat shock proteins. In Changes in Eukaryotic Gene Expression in Response to Environmental Stress (Atkinson, B.G. Walden, D.B. eds.), pp. 349-371, Academic Press, Orlando. 

Heat shock proteins (HSPs) are synthesized by cells in response to an increase in temperature, as well to various other stressful stimuli. Their main function is to ensure intracellular protein homeostasis, thus preserving the cells viability in the presence of aggression. Current evidence points to a protective role for HSPs in several aspects of critical disease, such as ischemia-reperfusion, ARDS, and multiple organ failure. The increase of a few degrees Celsius above the normal environmental temperature of cells leads to the heat shock response 1) rapid expression of heat shock genes, 2) suppression of normal protein synthesis, and 3) the ability of cells to survive a second and otherwise lethal heat challenge (thermotolerance). 

Exposure of cells to elevated temperatures, or heat shock, induces the transcription and translation of a set of proteins known as the heat-shock proteins (HSPs) or the stress proteins. This event usually occurs with the concomitant inhibition of biosynthesis of other cellular components. The response is believed to be an attempt by the cells to protect themselves from injury, and there is some evidence to indicate that it may also be linked to oxidative stress. Evidence in favour of this idea comes from observations such as the following ... 

At the top of this list of false positives are the heat shock proteins. These could be termed real positives as they may reflect the fact that the bait protein does not fold appropriately and thus binds as in a normal cell stress response to the heat shock proteins. 

Heat-shock proteins (Hsps) are proteins expressed virtually in all organisms as a response of exposure to a stress, such as elevated temperature (fever), protein degradation, mechanical or chemical stress. As chaperone proteins they are concerned with the intracellular folding and refolding, assembly and translocation of damaged proteins. 

Proteomics in parasitic flatworms can be completed on intracellular fractions (e.g. microsomal or cytosol) or at the host-interface on excretory-secretory (ES) products. ES analysis can be completed during in vitro culture or in vivo by, for example, bile or gut content analysis. In all cases, a rapid and careful preparation is vital to prevent altered pro-teomic profiles due to stress responses (upreg-ulation of heat shock proteins) and action of proteases. Parasitic flatworms are best extracted from fresh host material, washed with a buffered saline solution at approximately the host s body temperature. In F. hepatica, for example, this will allow regurgitation of gut contents to remove digested material from, and removal of host material adherent to the outer surfaces of the parasite (Jefferies et al., 2001), both of which can subsequently complicate separation and identification. 

Cellular responses to metal ions include changes of patterns of gene expression. Many of these changes are non-specific shock effects for example, subsets of the heat shock proteins are synthesised in response to Cd (Czarnecka et al., 1984 Lin et al., 1984 Delhaize et al., 1989). However, some mRNAs are specifically induced by Cd (Delhaize et al., 1989). Thus, by examining metal-regulated gene expression, whether specific or non-specific, it may be possible to determine the relative roles of proteins and polypeptides specific to metal homeostasis and metal tolerance, as opposed to functions involved in general stress responses. 

---