title: Altered cyclic expression of epithelial Na+ channel subunits and cystic fibrosis transmembrane conductance regulator in mouse endometrium by a low sodium diet.
abstract: Epithelial Na+ channel (ENaC) and cystic fibrosis transmembrane conductance (CFTR) have been shown to exhibit cyclic expression patterns in the uterus and demonstrated to play important roles in regulating uterine fluid absorption and secretion. The present study investigated the effect of a low Na+ diet on the cyclic expression of uterine ENaC subunits and CFTR in mice. Ten to 12 weeks old ICR mice with synchronized estrus cycle were fed with a low sodium diet for at least 2 weeks and the mRNA level of these ion channels was examined by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). Functional channel activities in primary cultures of endometrial epithelia were assessed by the short-circuit current (Isc) technique. The characteristic cyclic expression of ENaC subunits throughout the estrus cycle remained unchanged but their expression levels towards the diestrus stage were drastically elevated. The cyclic expression pattern of CFTR was disrupted with suppressed expression throughout the cycle. Isc measurements showed that treatment of cultured endometrial epithelial cells with aldosterone, the major hormone expected to be elevated during the low sodium diet, resulted in prominent increase in ENaC channel activity. The altered cyclic expression of uterine ENaC and CFTR by a low sodium diet suggests that these ion channels may be affected by elevated circulating aldosterone, which may disrupt reproductive events in the uterus.
authors.affiliation: Epithelial Cell Biology Research Center, Department of Physiology, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong.
authors.forename: Lai Ling
authors.initials: LL
authors.lastname: Tsang
authors.forename: Ling Nga
authors.initials: LN
authors.lastname: Chan
authors.forename: Hsiao Chang
authors.initials: HC
authors.lastname: Chan
mesh_terms: D000450:Aldosterone / Q000378:metabolism; D000818:Animals; D002478:Cells, Cultured; D019005:Cystic Fibrosis Transmembrane Conductance Regulator / Q000235:genetics / Q000378:metabolism*; D004594:Electrophysiology; D004717:Endometrium / Q000166:cytology / Q000378:metabolism*; D004847:Epithelial Cells / Q000166:cytology / Q000378:metabolism; D053503:Epithelial Sodium Channels; D005260:Female; D005786:Gene Expression Regulation; D051379:Mice; D021122:Protein Subunits / Q000235:genetics / Q000378:metabolism*; D015222:Sodium Channels / Q000235:genetics / Q000378:metabolism*; D012982:Sodium, Dietary
chemical_list: D053503:Epithelial Sodium Channels; D021122:Protein Subunits; D015222:Sodium Channels; D012982:Sodium, Dietary; D019005:Cystic Fibrosis Transmembrane Conductance Regulator; D000450:Aldosterone