Fluid-percussion brain injury induces changes in aquaporin channel expression

A. A. Oliva, Y. Kang, J. S. Truettner, J. Sanchez-Molano, C. Furones, A. J. Yool, Coleen M Atkins

Research output: Contribution to journalArticle

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Abstract

Edema, the accumulation of excess fluid, is a major pathological change in the brain that contributes significantly to pathology and mortality after moderate to severe brain injury. Edema is regulated by aquaporin (AQP) channels which transport water across cellular membranes. Six AQPs are found in the brain (1, 3, 4, 5, 8, and 9), and previous studies have found that AQP4 is regulated after traumatic brain injury (TBI). To further understand how AQPs contribute to brain edema, we investigated whether expression of AQP1, 3, and 9 are also regulated after TBI. Adult male Sprague Dawley rats received moderate parasagittal fluid-percussion brain injury (FPI) or sham surgery. After induction of FPI, the injured, ipsilateral parietal cortex and hippocampus were dissected and analyzed by Western blotting. We observed a small decrease in AQP3 and 4 levels at 7 days after FPI in the ipsilateral, parietal cortex. Both AQP1 and 9 significantly increased within 30 min post-injury and remained elevated for up to 6 h in the ipsilateral, parietal cortex. Aqp1 and 9 mRNA levels were also significantly increased at 30 min post-FPI. Administration of an AQP1 and 4 antagonist, AqB013, non-significantly increased brain water content in sham, non-injured animals, and did not prevent edema formation 24 h after trauma in either the parietal cortex or hippocampus. These results indicate that Aqp1 and 9 mRNA and protein levels increase after moderate parasagittal FPI and that an inhibitor of AQP1 and 4 does not decrease edema after moderate parasagittal FPI.

Original languageEnglish
Pages (from-to)272-279
Number of pages8
JournalNeuroscience
Volume180
DOIs
StatePublished - Apr 28 2011

Fingerprint

Percussion
Aquaporins
Brain Injuries
Parietal Lobe
Edema
Hippocampus
Brain
Messenger RNA
Water
Brain Edema
Wounds and Injuries
Sprague Dawley Rats
Western Blotting
Pathology
Membranes
Mortality

Keywords

  • Aquaporin
  • Edema
  • Fluid-percussion
  • Traumatic brain injury
  • Water channel

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Oliva, A. A., Kang, Y., Truettner, J. S., Sanchez-Molano, J., Furones, C., Yool, A. J., & Atkins, C. M. (2011). Fluid-percussion brain injury induces changes in aquaporin channel expression. Neuroscience, 180, 272-279. https://doi.org/10.1016/j.neuroscience.2011.02.020

Fluid-percussion brain injury induces changes in aquaporin channel expression. / Oliva, A. A.; Kang, Y.; Truettner, J. S.; Sanchez-Molano, J.; Furones, C.; Yool, A. J.; Atkins, Coleen M.

In: Neuroscience, Vol. 180, 28.04.2011, p. 272-279.

Research output: Contribution to journalArticle

Oliva, AA, Kang, Y, Truettner, JS, Sanchez-Molano, J, Furones, C, Yool, AJ & Atkins, CM 2011, 'Fluid-percussion brain injury induces changes in aquaporin channel expression', Neuroscience, vol. 180, pp. 272-279. https://doi.org/10.1016/j.neuroscience.2011.02.020
Oliva AA, Kang Y, Truettner JS, Sanchez-Molano J, Furones C, Yool AJ et al. Fluid-percussion brain injury induces changes in aquaporin channel expression. Neuroscience. 2011 Apr 28;180:272-279. https://doi.org/10.1016/j.neuroscience.2011.02.020
Oliva, A. A. ; Kang, Y. ; Truettner, J. S. ; Sanchez-Molano, J. ; Furones, C. ; Yool, A. J. ; Atkins, Coleen M. / Fluid-percussion brain injury induces changes in aquaporin channel expression. In: Neuroscience. 2011 ; Vol. 180. pp. 272-279.
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