J. Lipid Res.
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A more recent version of this article appeared on September 1, 2004

Papers In Press, published online ahead of print June 21, 2004
J. Lipid Res., doi:10.1194/jlr.M400179-JLR200
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Submitted on May 10, 2004
Revised on May 27, 2004
Accepted on June 8, 2004

Upregulation of surfactant synthesis triggers ABCA1-mediated basolateral phospholipid efflux

Jiming Zhou, Yong You, Alan J. Ryan, and Rama K. Mallampalli

Internal Medicine, University of Iowa, Iowa City, IA 52242

Corresponding Author: rama-mallampalli{at}uiowa.edu

Alveolar type II lung epithelia produce surfactant, an essential surface-active material highly enriched with disaturated phosphatidylcholine (DSPC), which requires a key regulatory enzyme, CTP:phosphocholine cytidylyltransferase (CCTalpha ) for its synthesis prior to its export apically into the alveolus. In this study, we examined whether surfactant phosphatidylcholine (PC) synthesis and export are physiologically linked. Stable over-expression of CCTalpha in lung epithelial cell lines increased rates of PC synthesis and elevated cellular DSPC mass without altering total cellular PC content. Overexpression of CCTalpha was associated with: i) increased basolateral, rather than apical PC export catalyzed by the ATP binding cassette transporter 1 (ABCA1), ii) basolateral export of significant levels of unsaturated (nonsurfactant) PC, and iii) transcriptional activation of the ABCA1 gene via a liver X receptor/retinoic acid receptor-independent pathway. Cells exposed to PC vesicles exhibited a dose-dependent increase in ABCA1 transcriptional activity. These data provide the first evidence that surfactant PC synthesis is linked to its export via a basolateral lipid efflux pathway. This pathway is mediated, in part, by a phospholipid sensor, ABCA1, that appears to partake in autoregulation of both cellular content and composition of PC thereby providing a potentially novel exit route for a newly synthesized pool of PC distinct from surfactant.


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