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Tissue-level cytoprotection.

L E Hightower1, Brown, J L Renfro

  • 1Department of Molecular and Cell Biology, University of Connecticut, Storrs, CT 06269, USA.

Cell Stress & Chaperones
|February 24, 2001
PubMed
Summary
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Tissue models reveal heat shock proteins induce cytoprotection, altering functions like transport and leukocyte adhesion. This cytoprotected state acts as an anti-inflammatory brake, limiting tissue damage during inflammation.

Area of Science:

  • Cellular biology
  • Physiology
  • Immunology

Background:

  • In vitro and ex vivo tissue models offer biological complexity between cell cultures and whole animals.
  • Differentiated cellular functions are altered in cytoprotected tissues, impacting physiological processes.

Purpose of the Study:

  • To investigate how cytoprotection affects differentiated functions in tissue models.
  • To explore the role of heat shock proteins in inflammation and wound healing.

Main Methods:

  • Utilized primary tissue cultures of winter flounder renal secretory epithelium.
  • Employed ex vivo preparations of rat intestinal tissues to study microcirculation.
  • Examined transepithelial transport and leukocyte-endothelium interactions.

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Main Results:

  • Cytoprotected tissues showed altered transepithelial transport and leukocyte attachment/transmigration.
  • Heat shock proteins are induced in wound responses and can act as proinflammatory cytokines.
  • Intracellular heat shock proteins confer cytoprotection against hostile wound environments.

Conclusions:

  • The cytoprotected state, mediated by heat shock proteins, is proposed to be anti-inflammatory.
  • Cytoprotection acts as a regulatory mechanism, limiting excessive inflammatory responses.
  • Heat shock response plays a critical role in vertebrate inflammation and wound healing.