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Altered aquaporins in the brains of mice submitted to intermittent hypoxia model of sleep apnea

Research output: Contribution to Journal/MagazineJournal articlepeer-review

  • Diego Baronio
  • Denis Martinez
  • Cintia Zappe Fiori
  • Victorio Bambini-Junior
  • Luiz Felipe Forgiarini
  • Darlan Pase da Rosa
  • Lenise Jihe Kim
  • Marcelle Reesink Cerski
<mark>Journal publication date</mark>15/01/2013
<mark>Journal</mark>Respiratory physiology & neurobiology
Issue number2
Number of pages5
Pages (from-to)217-221
Publication StatusPublished
Early online date30/10/12
<mark>Original language</mark>English


Rostral fluid displacement has been proposed as a pathophysiologic mechanism of both central and obstructive sleep apnea. Aquaporins are membrane proteins that regulate water transport across the cell membrane and are involved in brain edema formation and resolution. The present study investigated the effect of intermittent hypoxia (IH), a model of sleep apnea, on brain aquaporins. Mice were exposed to intermittent hypoxia to a nadir of 7% oxygen fraction. Brain water content, Aquaporin-1 and Aquaporin-3 were measured in the cerebellum and hippocampus. Hematoxylin-eosin and immunohistochemistry stainings were performed to evaluate cell damage. Compared to the sham group, the hypoxia group presented higher brain water content, lower levels of Aquaporin-1 and similar levels of Aquaporin-3. Immunoreactivity to GFAP and S100B was stronger in the hypoxia group in areas of extensive gliosis, compatible with cytotoxic edema. These findings, although preliminary, indicate an effect of IH on aquaporins levels. Further investigation about the relevance of these data on the pathophysiology of OSA is warranted.

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