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The choroid plexus epithelium displays conventional cell polarization

The choroid plexus epithelium (CPE) has been studied extensively as a model cell in e.g. high rate fluid secretion because of the direct access to the luminal surface. The high‐rate secretion is orchestrated by an unusual plasma membrane distribution of key transport proteins in the CPE cells. Par example, the ubiquitously expressed Na, K‐ATPase accumulates in the luminal membrane domain of CPE cells. The same has been observed for other normally basolateral proteins such as NKCC1 and NHE1, but not for all basolateral proteins (e.g. AE2). The observation led to the hypotheses that the CPE cells exhibit an inverse cell polarity, despite a conventional localization of structural polarity elements in epithelial cells: basal membrane facing the interstitium, tight junctions close to the luminal surface and luminal specializations such as microvilli and cilia. In this study, we investigated the expression and subcellular distribution of basic cell polarity markers in the CPE cells. Immunohistochemical analysis revealed a basolateral domain accumulation of the membrane lipid PtdIns(3,4,5)P3, Scrib, E‐cadherin, and partitioning‐defective protein (Par) 1. Luminal membrane domain accumulation was observed for the atypical protein kinase aPKC, the plasma membrane target snare syntaxin‐3, whereas Par3 was localized at the tight junction area. These markers represent the molecular complexes known to determine luminal and basolateral identity and were, thus, all located as expected for mature and normally polarized epithelial cells. We conclude that these central polarity proteins are distributed normally in the choroid plexus cells, and that cell polarity as such does not seem to be involved in the unusual localizations of key transport proteins in these cells.