Journal
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
Volume 284, Issue 6, Pages L981-L989Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00392.2002
Keywords
liposomes; lamellar bodies; alveolar type II cells; perfused rat lung; 1-palmitoyl-2-[12-(7-nitro-2-1,3-benzoxadiazol-4-yl) amino] dodecanoyl-phosphatidylcholine
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Funding
- NHLBI NIH HHS [HL-19737] Funding Source: Medline
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We evaluated the contribution of endocytotic pathways to pulmonary uptake of surfactant lipids from the alveolar space. Resting and stimulated 8-bromoadenosine 3', 5'-cyclic monophosphate (8-Br-cAMP) uptake of unilamellar liposomes labeled with either [H-3] dipalmitoylphosphatidylcholine ([H-3] DPPC) or 1-palmitoyl-2-[ 12-(7-nitro-2-1,3-benzoxadiazol-4-yl) amino] dodecanoylphosphatidylcholine (NBD-PC) was studied in isolated perfused rat lungs and isolated type II cells. Amantadine and phenylarsine oxide, inhibitors of clathrin-mediated endocytosis, each decreased [H-3] DPPC uptake under resting conditions by similar to40%; their combination had no additional effect. Cytochalasin D, an inhibitor of actin-dependent processes, reduced liposome uptake by 55% and potentiated the effect of either clathrin inhibitor alone. Relative inhibition for all agents was higher in the presence of 8-Br-cAMP. The effect of inhibitors was similar for liposomes labeled with [H-3] DPPC or NBD-PC. By fluorescence microscopy, NBD-PC taken up by lungs was localized primarily to alveolar type II cells and was localized to lamellar bodies in both lungs and isolated cells. These studies indicate that both clathrin-mediated and actin-mediated pathways are responsible for endocytosis of DPPC-labeled liposomes by alveolar type II cells in the intact lung.
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