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Expression of the epithelial Na+ channel in the developing rat lung
H O'Brodovich1, C Canessa, J Ueda
1Department of Pediatrics, Hospital for Sick Children, Toronto, Ontario, Canada.
The American Journal of Physiology
|August 1, 1993
Summary
The immature fetal lung shows impaired sodium transport due to low alpha epithelial sodium channel (alpha rENaC) expression. This expression increases with lung development and can be induced by hormones.
Area of Science:
- Pulmonary physiology
- Molecular biology
- Developmental biology
Background:
- The mature fetal lung actively transports Na+ from the alveolar space, but the immature lung cannot.
- The apical membrane Na+ channel is the rate-limiting step for epithelial Na+ transport.
- The molecular basis for impaired Na+ transport in immature lungs is unknown.
Purpose of the Study:
- To determine the presence and developmental regulation of alpha epithelial sodium channel (alpha rENaC) transcripts in fetal and adult rat lungs.
- To investigate the role of alpha rENaC in fetal lung maturation and Na+ transport.
Main Methods:
- RNA isolation from fetal and adult rat lungs, alveolar epithelium, and kidneys.
- Northern blot analysis to detect alpha rENaC transcripts.
- Hormonal induction studies using thyroid-releasing hormone and dexamethasone in pregnant rats.
Main Results:
- Alpha rENaC transcripts were detected in fetal and adult lungs, similar to those in the colon.
- Low mRNA levels were observed in early fetal lungs (17-18 days gestational age), increasing significantly during the saccular stage (20 days gestational age).
- Hormonal treatment induced alpha rENaC expression in fetal lungs.
Conclusions:
- Alpha rENaC is expressed in mature fetal and adult alveolar epithelium.
- The expression of alpha rENaC is developmentally regulated and influenced by hormones crucial for lung maturation.
- Alpha rENaC likely plays a significant role in active Na+ transport in the developing and mature lung.