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Increased Cerebral Capillary Density in Aquaporin‐4 Knockout Mouse
Author(s) -
Xu Kui,
Almotah Khalil,
Zhang Yifan,
Radford Thomas S,
Yu Xin,
Boron Walter F,
LaManna Joseph C
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.721.9
Subject(s) - aquaporin 4 , cerebral blood flow , central nervous system , chemistry , blood–brain barrier , medicine , endocrinology , knockout mouse , cerebral edema , arterial blood , pathology , receptor
In the brain, Aquaporin 4 (AQP4) is highly expressed in the blood–brain barrier and brain–CSF interfaces. AQP4 functions as an efficient water‐selective transporting protein and plays an important role in cerebral water balance. It has been shown that knocking out of AQP4 in mice reduces brain edema after acute water intoxication and ischemic stroke. The specific localization of AQP4 to these anatomical and cellular regions of the central nervous system may also suggest a role for AQP4 as a gas channel to facilitate oxygen transport. In this study we investigated the role of AQP4 on cerebral capillary density and cerebral blood flow using AQP4 knockout (AQP4‐KO) mice in comparison with the wild‐type (WT) mice. Cerebral blood flow was measured using arterial spin labeling ( ASL) MRI in WT mice (n = 7) and AQP4‐KO mice (n = 4). Mice were then perfusion fixed and cerebral capillary density was identified by GLUT‐1 immunohistochemistry staining and was quantified from the number of the positive counts per unit area (number/mm 2 ). Results showed that the cerebral blood flows were similar in the WT and the AQP4‐KO groups (Mean ± SD, 182 ± 30 vs. 178 ± 52, ml/min/100g tissue). The AQP4‐KO mice exhibited a 24% increase in capillary density as compared to the WT mice (Mean ± SD, 504 ± 49 vs. 406 ± 32, N/mm 2 ). Our results showed that the deletion of AQP4 increased the capillary density without altered blood flow in mouse brain, suggesting a compensation for decreased gas transport in the KO mice. Support or Funding Information NIH R01 NS 38632