Up-regulation of type 2 iodothyronine deiodinase mRNA in reactive astrocytes following traumatic brain injury in the rat

Lanling Zou, Lynn A. Burmeister, Scot D. Styren, Patrick M. Kochanek, Steven T. DeKosky

Research output: Contribution to journalArticlepeer-review

26 Scopus citations

Abstract

Type 2 5'-deiodinase (5'-D2), which converts thyroxine to the more active thyroid hormone 3,5,3'-triiodothyronine (T3), is believed to be an important source of intracellular T3 in the brain. The activity of this enzyme is increased in hypothyroidism and decreased in hyperthyroidism, and as such, it serves an important role to protect the brain from wide fluctuations in T3 during changes in thyroidal state. Although it has been hypothesized that T3 may facilitate neuronal regeneration after CNS injury, the 5'-D2 response to brain injury is unknown. To assess the 5'-D2 mRNA response to injury, we performed in situ hybridization following traumatic brain injury. In unlesioned animals, 5'-D2 mRNA was undetectable. At 3 days posttrauma, 5'-D2 mRNA was detected in ipsilateral cortex near the contusion. A significant further increase of 5'-D2 mRNA was noted 7 days posttrauma in both hippocampus and cortex. Similar response was also observed on the contralateral side. Colocalization of 5'-D2 mRNA with glial fibrillary acidic protein indicates that reactive astrocytes were the major cellular source for the trauma-induced 5'-D2 expression. These data demonstrate for the first time, a trauma-induced, astrocytic up-regulation of 5'-D2 mRNA, suggesting a potential role for T3 action in adult brain's response to injury and recovery.

Original languageEnglish (US)
Pages (from-to)887-890
Number of pages4
JournalJournal of Neurochemistry
Volume71
Issue number2
DOIs
StatePublished - Aug 1998

Keywords

  • 3,5,3'- Triiodothyronine
  • Astrocytes
  • In situ hybridization
  • Thyroid hormone
  • Traumatic brain injury
  • Type 2 5'-deiodinase
  • mRNA

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