Aim: 

The aim of this study was to determine whether there is a link between the knockout of the key Na⁺ loader slc4a10 and the water channel aquaporin 1 (AQP1) in two epithelia with high transport rate; the choroid plexus (CP) and the proximal tubule.

Methods: 

Protein abundances in the CP were semi-quantified from the immunofluorescence intensities of confocal micrographs. Images were acquired in the focal plane with the highest signal intensity for each antibody using fixed instrument settings.

Results: 

The Na, K ATPase abundance was decreased by 36.4% (n=4, p =0.02) and AQP1 was decrased by 42.7% (n=4, p =0.02) in the choroid plexus of slc4a10 knockout mice compared to wildtype littermates. Similarly, we investigated the abundance of slc4a10 and Na,K ATPase in the choroid plexus of the AQP1 knockout mouse; a mouse with a similar choroid plexus phenotype. In the AQP1 knockout mice we find no difference in relative immunofluorescence intensity for slc4a10 (AQP1 wildtype 100±10%, AQP1 knockout 73±11%, n=5, p =0.12) or Na, K ATPase (AQP1 wildtype 100±19%, AQP1 knockout 158±32%, n=5, p =0.15). In the proximal tubule of the AQP1 knockout mouse, the abundance of NBCe1 was reduced by 31% (n=5, p =0.02) and Na, K ATPase was reduced by 23% (n=5, p =0.03). The abundance of NHE3 was unchanged.

Conclusion: 

In contrast to current belief, lack of slc4a10 seems not be the only cause for decreased brain ventricle volume in slc4a10-knockout mice and similarly, lack of AQP1 may not be the only cause for decreased proximal tubule reabsorption in AQP1-knockout mice. More investigations are needed to determine whether AQP1 is more important in cell volume regulation than transport in choroid plexus and proximal tubules.