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Related Experiment Video

Updated: Jun 25, 2026

Use of a Hanging-weight System for Liver Ischemia in Mice
05:53

Use of a Hanging-weight System for Liver Ischemia in Mice

Published on: August 7, 2012

Age-related decrease in proteasome expression contributes to defective nuclear factor-kappaB activation during

Nadine Huber1, Nozomu Sakai, Thorsten Eismann

  • 1Laboratory of Trauma, Sepsis and Inflammation Research, Department of Surgery, University of Cincinnati, Cincinnati, OH 45267-0558, USA.

Hepatology (Baltimore, Md.)
|February 12, 2009
PubMed
Summary
This summary is machine-generated.

Aging impairs liver repair after ischemia/reperfusion (I/R) by reducing proteasome function. This age-related defect in PSMD4 expression hinders NF-kappaB activation, leading to increased liver injury.

Related Experiment Videos

Last Updated: Jun 25, 2026

Use of a Hanging-weight System for Liver Ischemia in Mice
05:53

Use of a Hanging-weight System for Liver Ischemia in Mice

Published on: August 7, 2012

Area of Science:

  • Hepatology
  • Immunology
  • Aging Research

Background:

  • Hepatic ischemia/reperfusion (I/R) causes liver injury via inflammation regulated by nuclear factor kappaB (NF-kappaB).
  • Previous studies show age-dependent differences in hepatic I/R injury, with young mice exhibiting greater NF-kappaB activation but less injury than old mice.

Purpose of the Study:

  • To investigate the mechanism by which aging alters NF-kappaB activation in the liver during I/R.
  • To identify age-related molecular differences in the hepatic response to I/R.

Main Methods:

  • Partial hepatic I/R was performed on young and old mice.
  • Livers were analyzed using RNA microarray and protein expression assays.
  • Gene expression related to protein ubiquitinylation and the proteasome was assessed.

Main Results:

  • Old mice showed down-regulation of ubiquitin-proteasome pathway genes during I/R.
  • Expression of the proteasome subunit PSMD4 was reduced in old mice.
  • Increased phosphorylation and ubiquitinylation of IkappaB alpha were observed in old mice, with reduced proteasomal degradation.

Conclusions:

  • Age-related defects in hepatic NF-kappaB signaling during I/R are linked to decreased PSMD4 expression.
  • Reduced PSMD4 impairs the recruitment of phosphorylated, ubiquitinylated IkappaB alpha to the proteasome.
  • This mechanism results in defective NF-kappaB activation and increased liver injury in aged mice.