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Inhibition of CLC-2 chloride channel expression interrupts expansion of fetal lung cysts.

Authors: Blaisdell, CJ  Morales, MM  Andrade, AC  Bamford, P  Wasicko, M  Welling, P 
Citation: Blaisdell CJ, etal., Am J Physiol Lung Cell Mol Physiol 2004 Feb;286(2):L420-6.
Pubmed: (View Article at PubMed) PMID:14711803
DOI: Full-text: DOI:10.1152/ajplung.00113.2003

Normal lung morphogenesis is dependent on chloride-driven fluid transport. The molecular identity of essential fetal lung chloride channel(s) has not been elucidated. CLC-2 is a chloride channel, which is expressed on the apical surface of the developing respiratory epithelium. CLC-2-like pH-dependent chloride secretion exists in fetal airway cells. We used a 14-day fetal rat lung submersion culture model to examine the role of CLC-2 in lung development. In this model, the excised fetal lung continues to grow, secrete fluid, and become progressively cystic in morphology (26). We inhibited CLC-2 expression in these explants, using antisense oligonucleotides, and found that lung cyst morphology was disrupted. In addition, transepithelial voltage (V(t)) of lung explants transfected with antisense CLC-2 was inhibited with V(t) = -1.5 +/- 0.2 mV (means + SE) compared with -3.7 +/- 0.3 mV (means + SE) for mock-transfected controls and -3.3 +/- 0.3 mV (means + SE) for nonsense oligodeoxynucleotide-transfected controls. This suggests that CLC-2 is important for fetal lung fluid production and that it may play a role in normal lung morphogenesis.


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CRRD Object Information
CRRD ID: 1358647
Created: 2005-06-22
Species: All species
Last Modified: 2005-06-22
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.