Decreased abundance of proteins involved in cerebrospinal fluid production in slc4a10 knockout mice

Abstract

Deletion of slc4a10 from mice has been shown to cause a shift in the membrane localization of the Na+/H+ exchanger from luminal to basolateral in the choroid plexus (CP). No other acid/base transporters showed changes in localization or abundance. In addition to pH regulation, slc4a10 is believed to be the bottleneck for Na+ import from the blood side to the CP cell and thereby for the cerebrospinal fluid (CSF) production as such; slc4a10 knockout mice have decreased brain ventricles indicating decreased CSF secretion. Here, we investigated whether deletion of slc4a10 causes changes in abundance of AQP1 and Na, K ATPase in the choroid plexus as examples of prominent proteins involved in CSF secretion. Protein abundances were semi-quantified from the immunofluorescenceintensities of confocal micrographs. Images were acquiredin the focal plane with the highest signal intensity using fixed instrument settings. The Na, K ATPase abundance was decreased by 36.4% (n=4, p=0.02) and AQP1 by 42.7% (n=4, p=0.02) in the choroid plexus of slc4a10 knockout mice compared to wildtype littermates. Thus, the cells of the CP seem to compensate by decreasing the abundance of the molecular machinery involved in CSF secretion in response to the removal of the main basolateral Na+ loader. This substantiates the previous study in this mouse indicating that CP cells favor cell survival over CSF secretion. Supported by the Lundbeck Foundation