Effect of penetrating brain injury on aquaporin-4 expression using a rat model

Chris J. Neal, Eleanor Y. Lee, Andrea Gyorgy, James M. Ecklund, Denes V. Agoston*, Geoffrey S.F. Ling

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

30 Scopus citations


Cerebral edema (CE) is a frequent and potentially lethal consequence of various neurotraumas, including penetrating brain injury (PBI). Aquaporin-4 (AQP4) water channel is predominantly expressed by astrocytes and plays an important role in regulating water balance in the normal and injured brain. Using a rat model of PBI, we show that AQP4 immunoreactivity was substantially increased in the peri-injury area at both 24 and 72 h after PBI. The increase in AQP4 expression was paralleled by increased GFAP expression. The two proteins were co-expressed by peri-vascular astrocytes, whereas reactive astroglia identified by their stellar morphology did not express AQP4 at either time points after injury. Western analysis confirmed the increase in AQP4 immunoreactivity observed in the injured tissue. The apparent increase in AQP4 immunoreactivity was likely due to de novo AQP4 protein synthesis, as most of the increased AQP4 immunoreactivity was found in the soluble (cytosolic) fraction. Our results demonstrate dynamic spatial and temporal changes in AQP4 expression that contribute to the molecular pathophysiology of PBI.

Original languageEnglish
Pages (from-to)1609-1617
Number of pages9
JournalJournal of Neurotrauma
Issue number10
StatePublished - Oct 2007


  • Brain
  • Edema
  • Injury
  • Water channel


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