Regulation of Ncbe in the Choroid Plexus of Mice after Hemorrhage-Induced Hydrocephalus

FASEB J. 2022 May;36 Suppl 1. doi: 10.1096/fasebj.2022.36.S1.R3405.ABSTRACTThe choroid plexus (CP) is a small tissue located inside brain ventricles. It is responsible for the production of most of the cerebrospinal fluid (CSF); approximately 500 mL of CSF per day in the adult human [1, 2]. CSF production occurs as a net result of transcellular movement of salt and water, carried out by various cellular transporters. Ncbe is a sodium-coupled bicarbonate transporter located in the basolateral membrane of the choroid plexus epithelial (CPE) cells. It transports Na+ and HCO3 - into the cell in exchange for Cl- . Ncbe is the main sodium loader of the cell and CSF production is probably dependent on this transporter [3]. Posthemorrhagic hydrocephalus (PHH) is a pathological state, caused by an accumulation of CSF in the ventricular system following intraventricular hemorrhage. CSF buildup is caused by a disproportion in CSF production and reabsorption. This leads to an expansion of the brain ventricles. Intraventricular hemorrhage (IVH) is known to cause inflammation in the CP, which is coupled to an over-production of CSF [4-6]. Initially we hypothesized that IVH would stimulate Ncbe in the CPE through increased protein abundance as well as transporter activity. This would lead to increased CSF formation, similar to the response found after treatment with e.g. the cyclic-AMP agonist forskolin [7]. Our preliminary data, however, suggest that Ncbe abundance is reduced by 24% (n=4, ...
Source: Pharmacological Reviews - Category: Drugs & Pharmacology Authors: Source Type: research