Altered cellular localization of aquaporin-1 in experimental hydrocephalus in mice and reduced ventriculomegaly in aquaporin-1 deficiency

摘要: Hydrocephalus is a pathological accumulation of cerebrospinal fluid (CSF) in the cerebral ventricles that constitutes significant cause neurological morbidity and mortality. Surgical treatment involving shunt placement associated with high failure rate complications due to infection, motivating development alternative, non-surgical therapies. Here, we investigated role hydrocephalus water channel aquaporin-1 (AQP1), which expressed at apical membrane choroid plexus epithelium believed facilitate CSF production. AQP1 expression subcellular localization were studied kaolin-induced model mice effect deficiency on severity was determined. While total choroidal protein not significantly altered hydrocephalus, ~50% redistributed from intracellular vesicles. We found ventricular size AQP1-deficient smaller than wild-type mice, both baseline following hydrocephalus. The reduced plasma involves endocytosis, may be compensatory mechanism reduce secretion. suggests inhibition or down-regulation as potential adjunctive for