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J Appl Physiol (June 6, 2003). doi:10.1152/japplphysiol.00208.2003
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Submitted on February 28, 2003
Accepted on June 4, 2003

Compositional changes in lipid microdomains of air-blood barrier plasma membranes in pulmonary interstitial edema

Paola Palestini1, Chiara Calvi1, Elena Conforti1, Rossella Daffara1, Laura Botto1, and Giuseppe Miserocchi1*

1 Department of Experimental, Environmental Medicine and Biotechnology, University of Milano-Bicocca, Monza, Italy

* To whom correspondence should be addressed. E-mail: giuseppe.miserocchi{at}unimib.it.

We evaluated in anaesthetized rabbits the compositional changes of plasmalemma lipid microdomains from lung tissue samples after inducing pulmonary interstitial edema (0.5 ml/kg for 3 h, leading to ~ 5% increase in extravascular water). Lipid microdomains (lipid rafts and caveolae) were present in the detergent resistant fraction (DRF ) obtained after discontinuous sucrose density gradient. DRF was enriched in caveolin-1, flotillin, AQP-1, GM1, cholesterol, sphingomyelin and phosphatidylserine and their contents significantly increased in interstitial edema The higher DRF content in caveolin, flotillin and AQP-1 and of the ganglioside GM1 suggest an increase in both caveolar domains and in lipid rafts, respectively. Compositional changes could be ascribed to endothelial and epithelial cells that provide most of plasma membrane surface area in the air-blood barrier. Alterations in lipid components in the plasmamembrane may reflect rearrangement of floating lipid platforms within the membrane and/or lipid translocation from intracellular stores. Lipid traffic could be stimulated by the marked increase in hydraulic interstitial pressure following initial water accumulation, from ~ -10 to ~ 5 cm H2O, due to the low compliance of the pulmonary tissue, in particular in the basement membranes and in the interfibrillar substance. Compositional changes in lipid microdomains represent a sign of cellular activation and suggest the potential role of mechanotransduction in response to developing interstitial edema.




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