Estres del reticulo endoplasmático

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Heat/Stress Responses
Davis T. W. Ng
Pennsylvania State University, University Park, Pennsylvania, USA

All cells from simple bacteria to highly differentiated animal cells maintainspecialized mechanisms to monitor and respond to changes in their local environments. Unfavorable circumstances that threaten cellular homeostasis will elicit one or more stress response programs in an effortto preserve viability of the organism. The many forms of cellular stress include temperature variation, exposure to toxic compounds, oxidative and reductive stress, ionizing radiation, hypoxia,aging, mechanical injury, and the invasion of pathogens. Mounting the correct response can insure cell survival or initiate an apoptotic program depending on the severity of the stress. Stress responsesare also activated in numerous disease states and deficient responses are etiological for afflictions including Parkinson’s and Alzheimer’s diseases. More recently, stressregulated genes were intimatelylinked to aging and shown to be required for the extension of life in model organisms. As a general rule, stress responses remodel relevant cellular pathways to counteract specific effects of theinsult.

dinitrophenol, or sodium salicylate. Termed the heat shock response (HSR), it was later shown that the puffs signified activation of genes encoding heat shock proteins (Hsps). For virtually allorganisms, exposure to 5 – 108C above the optimal growth temperature leads to a robust HSR. Within the cell, an increase of this magnitude can have many deleterious effects including increased membranefluidity and the partial unfolding of proteins.

INPUTS
The HSR can be activated by a wide variety of conditions beyond temperature change. A few examples include exposure to ethanol, heavy metals,amino acid analogues, mechanical damage, and conditions of hypoxia, ischemia, and osmotic stress. As with temperature increases, these conditions are believed to increase the concentration of...