Alterations of Cullin-5 mRNA levels in the rat central nervous system following hemorrhagic shock

Thomas E. Ceremuga*, Xiang Lan Yao, Hasan B. Alam, Joseph T. McCabe

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


Hemorrhagic shock is a clinical syndrome that manifests as hypoperfusion, hypoxia, and ischemia initiating various cellular stress responses involved in the synthesis and release of an assortment of pro-inflammatory molecules, cytokines, chemokines, and reactive oxidant species (ROS). The ROS have been shown to oxidize and damage proteins making them targets for ubiquitination and proteasomal degradation. Cullin-5 (cul-5), an E3 ligase that binds ubiquitin to proteins targeted for degradation via the proteasome, was investigated for its gene expression during hemorrhagic shock. Male Long-Evans rats were subjected to volume controlled (27 ml kg-1) hemorrhage over 10 min and kept in shock for 60 min. Quantitative realtime polymerase chain reaction showed cul-5 mRNA levels were significantly increased in the brainstem and cerebellum, and decreased in the hypothalamus of rats as a result of hemorrhagic shock (n = 6) compared to sham-treated rats (n = 6). Cul-5 mRNA levels in the cerebral cortex, small intestine, kidney, liver, lung, or pituitary gland did not significantly change after hemorrhagic shock. This is the first report of cul-5 mRNA regulation by hemorrhagic shock. Evidence indicates this protein may have a regulatory role in ubiquitin-proteasomal protein degradation in response to hemorrhagic shock.

Original languageEnglish (US)
Pages (from-to)211-216
Number of pages6
JournalNeurological research
Issue number2
StatePublished - Mar 2003
Externally publishedYes


  • Cullin-5
  • Gene expression
  • Ischemia
  • Proteasome
  • Protein degradation
  • Ubiquitination

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology


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