Targeting Germinal Matrix Hemorrhage–Induced Overexpression of Sodium‐Coupled Bicarbonate Exchanger Reduces Posthemorrhagic Hydrocephalus Formation in Neonatal Rats

摘要

BackgroundGerminal matrix hemorrhage (GMH) is a leading cause of mortality and lifelong morbidity in preterm infants. Posthemorrhagic hydrocephalus (PHH) is a common complication of GMH. A sodium‐coupled bicarbonate exchanger (NCBE) encoded by solute carrier family 4 member 10 gene is expressed on the choroid plexus basolateral membrane and may play a role in cerebrospinal fluid production and the development of PHH. Following GMH, iron degraded from hemoglobin has been linked to PHH. Choroid plexus epithelial cells also contain iron‐responsive element‐binding proteins (IRPs), IRP1, and IRP2 that bind to mRNA iron‐responsive elements. The present study aims to resolve the following issues: (1) whether the expression of NCBE is regulated by IRPs; (2) whether NCBE regulates the formation of GMH‐induced hydrocephalus; and (3) whether inhibition of NCBE reduces style="fixed-case">PHH development.