Loss of the NHE2 Na+/H+ Exchanger in Mice Results in Dilation of Folliculo-Stellate Cell Canaliculi

• Published in: BioMed research international Vol. 2011; no. 2011; pp. 1 - 14
• Main Authors: Miller, Marian L., Andringa, Anastasia, Schultheis, Patrick J., Shull, Gary E.
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Puplishing Corporation 01.01.2011; Hindawi Publishing Corporation; Hindawi Limited
• Subjects: Animals; Basement Membrane - pathology; Blotting, Northern; Colon - metabolism; Cystic fibrosis; Female; Growth hormones; Histocytochemistry; In Situ Hybridization; Intercellular Junctions; Laboratory animals; Lipid Metabolism; Lipids; Male; Mice; Mice, Transgenic; Microscopy, Electron; Microvilli; Pituitary Gland, Anterior - metabolism; Pituitary Gland, Anterior - pathology; Pituitary Gland, Posterior - metabolism; Pituitary Gland, Posterior - pathology; RNA, Messenger; Sodium-Hydrogen Exchangers - genetics; Sodium-Hydrogen Exchangers - metabolism; Studies
• ISSN: 1110-7243; 2314-6133; 1110-7251; 2314-6141
• DOI: 10.1155/2011/510827

Genetic ablation of the NHE2 Na+/H+ exchanger causes gastric achlorhydria, absorptive defects in kidney and colon, and low fertility. Here we show that NHE2 is expressed in the pituitary, with the highest mRNA expression in pars distalis and lower expression in pars intermedia. In pars distalis of NHE2-null mice, prominent cyst-like dilatations of folliculo-stellate (FS) cell canaliculi developed with age, and there were increased FS cell area, accumulation of lipid in FS cell cytoplasm, redundancies in FS cell basement membrane, and other changes. The expansion of the canaliculi indicates that NHE2 is a major absorptive Na+/H+ exchanger in the luminal membranes lining the extensive network of channels formed by FS cells, which may provide a means of intrapituitary communication. The results suggest that NHE2 contributes to homeostatic regulation of the volume and composition of the canalicular fluid and may counter the secretory activity of the CFTR Cl− channel, which is known to be expressed in pituitary.