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Homeostatic Imbalances in Body Temperature01:19

Homeostatic Imbalances in Body Temperature

Hyperthermia occurs when the body's temperature becomes unusually high, often due to heat exposure, intense physical activity, or certain illnesses. This condition can create a dangerous cycle where elevated body temperature increases the metabolic rate, generating more heat and potentially leading to organ failure and brain damage. A severe form of hyperthermia, called heat stroke, can raise body temperature to life-threatening levels. Fever, on the other hand, is a controlled form of...
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Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
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Measurements of Physiological Stress Responses in C. Elegans
10:36

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Published on: May 21, 2020

Hyperthermia induces the ER stress pathway.

Xu Xu1, Sounak Gupta, Wenli Hu

  • 1Department of Biology, Center for Cellular Dynamics, Pennsylvania State University, University Park, Pennsylvania, United States of America.

Plos One
|August 31, 2011
PubMed
Summary

Mild fever (40°C) activates the endoplasmic reticulum (ER) stress pathway and heat shock response, unlike intense heat shock. This suggests coordinated cellular adaptation to febrile hyperthermia.

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Area of Science:

  • Cellular Biology
  • Stress Response Pathways

Background:

  • The endoplasmic reticulum (ER) chaperone GRP78/BiP, a Hsp70 homolog, is typically induced by ER stress, not heat shock.
  • Previous studies overlooked febrile hyperthermia's physiological relevance in temperature elevation.
  • This study investigates GRP78/BiP and ER stress pathway responses to 40°C exposure.

Purpose of the Study:

  • To investigate the cellular response to mild hyperthermia (40°C).
  • To determine if the ER stress pathway is activated by physiologically relevant temperature increases.
  • To compare the effects of mild hyperthermia versus intense heat shock on cellular stress responses.

Main Methods:

  • AD293 cells were exposed to 43°C heat shock to confirm ER stress gene inhibition.
  • Five mammalian cell types, including AD293, were subjected to 40°C hyperthermia for varying durations.
  • Induction of the ER stress pathway was assessed by analyzing downstream targets and heat shock response.

Main Results:

  • Intense heat shock (43°C) inhibited the ER stress pathway, as expected.
  • Mild hyperthermia (40°C) induced partial or full ER stress pathway activation.
  • Cells deficient in Perk or Gcn2 showed heightened sensitivity to hyperthermia-induced ER stress.

Conclusions:

  • The ER stress pathway is activated by hyperthermia, paralleling Hsp70 induction.
  • Cells possess parallel ER and cytoplasmic pathways for adapting to febrile hyperthermia.
  • These pathways coordinate cellular adaptation during disease or infection-related fever.