Role of heat shock proteins in oxygen radical-induced gastric apoptosis

Anna M Leung1, Maria J Redlak1, Thomas A Miller1

  • 1Department of Surgery, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond, Virginia.

Abstract

Insights

Heat shock pretreatment protects gastric mucosal cells from oxidative damage by increasing heat shock proteins (Hsps). This study highlights the protective role of Hsps against reactive oxygen species (ROS)-induced apoptosis.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Gastroenterology

Background:

  • Gastric mucosal injury is often caused by reactive oxygen species (ROS).
  • Oxidative stress induces cell death via caspase-mediated apoptosis in the gastric mucosa.
  • Heat shock proteins (Hsps) are known to protect cells from various cytotoxic agents.

Purpose of the Study:

  • To investigate the protective effects of heat shock pretreatment against ROS-induced gastric mucosal damage.
  • To determine the role of heat shock proteins (Hsps) in mitigating oxidative stress in gastric cells.

Main Methods:

  • AGS cells were pretreated with heat shock, geldanamycin, or quercetin.
  • Cells were exposed to hydrogen peroxide (H2O2) to induce oxidative stress.
  • Apoptosis was measured by caspase-3 activation, PARP cleavage, and DNA-histone complex formation.
  • Heat shock protein (Hsp) levels (Hsp70 and Hsp90) were analyzed via Western blot.

Main Results:

  • Heat shock pretreatment increased Hsp70 expression and significantly reduced H2O2-induced apoptosis.
  • Geldanamycin increased Hsp70 but decreased Hsp90, leading to increased apoptosis.
  • Quercetin decreased Hsp70, also resulting in increased apoptosis.

Conclusions:

  • Heat shock pretreatment confers protection to gastric mucosal cells against H2O2-induced apoptosis.
  • Hsp70 and Hsp90 play critical roles in this protective mechanism.
  • Disruptions in Hsp metabolism may contribute to mucosal injury from oxygen free radicals.

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