Final published version
Research output: Contribution to Journal/Magazine › Journal article › peer-review
Research output: Contribution to Journal/Magazine › Journal article › peer-review
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TY - JOUR
T1 - Altered aquaporins in the brains of mice submitted to intermittent hypoxia model of sleep apnea
AU - Baronio, Diego
AU - Martinez, Denis
AU - Fiori, Cintia Zappe
AU - Bambini-Junior, Victorio
AU - Forgiarini, Luiz Felipe
AU - Pase da Rosa, Darlan
AU - Kim, Lenise Jihe
AU - Cerski, Marcelle Reesink
N1 - Copyright © 2012 Elsevier B.V. All rights reserved.
PY - 2013/1/15
Y1 - 2013/1/15
N2 - 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.
AB - 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.
KW - Animals
KW - Aquaporins/metabolism
KW - Brain/metabolism
KW - Disease Models, Animal
KW - Glial Fibrillary Acidic Protein/metabolism
KW - Hypoxia/complications
KW - Male
KW - Mice
KW - Mice, Inbred C57BL
KW - Nerve Growth Factors/metabolism
KW - Organ Size
KW - S100 Calcium Binding Protein beta Subunit
KW - S100 Proteins/metabolism
KW - Sleep Apnea Syndromes/etiology
KW - Statistics, Nonparametric
KW - Water/metabolism
U2 - 10.1016/j.resp.2012.10.012
DO - 10.1016/j.resp.2012.10.012
M3 - Journal article
C2 - 23123204
VL - 185
SP - 217
EP - 221
JO - Respiratory physiology & neurobiology
JF - Respiratory physiology & neurobiology
SN - 1569-9048
IS - 2
ER -