Developmental changes in phosphatidylinositol transfer protein concentration and phospholipid transfer activities in rat type II cells.
The phospholipid transfer proteins (PLTPs) are cytosolic proteins that have been characterized by their ability to facilitate the transfer of phospholipids between membranes in vitro. The goals of this study were to determine whether PITP alpha concentration and phospholipid transfer activities are enriched in type II cells compared with whole lung and to determine the developmental changes in PITP alpha concentration and phospholipid transfer activities during late gestation and newborn period. The concentration of PITP alpha in type II cell cytosol measured by enzyme-linked immunosorbent assay (ELISA) increased during late fetal gestation to 2.2-fold adult levels and declined 41% during the first postnatal day. However, compared to whole adult lung cytosol, type II cell cytosol was not significantly enriched with PITP alpha. Phospholipid transfer activities were determined by a vesicle-rat lung membrane transfer assay. In adult lung, transfer activities for all the phospholipids were enriched in adult type II cell cytosol compared to whole lung cytosol (phosphatidylglycerol [PG], 12.5-fold; phosphatidylinositol [PI], 9.2-fold; phosphatidylcholine [PC], 6.5-fold; and phosphatidylethanolamine [PE], 6.6-fold; P < .05 in each case). The rate of phospholipid transfer in type II cell cytosol increased during late fetal gestation to levels 4.9 (PG), 3.7 (PI), and 2.8 (PC) times greater than adult levels. In cytosol from cells from different stages, the order of transfer rate was PG > PI > PC > PE. PITP alpha immunodepletion of adult type II cytosol did not significantly affect phospholipid transfer activities, suggesting that other PLTPs are responsible for the majority of the observed transfer activities in these cells. Developmental increases in PITP alpha concentration and other PLTPs parallel developmental changes in type II cell surfactant phospholipid metabolism, suggesting a possible role of these transfer proteins in the unique function of the type II cell.
Viscardi
R M
RM
Department of Pediatrics, University of Maryland School of Medicine, Baltimore 21201, USA. rviscard@umaryland.edu
Strauss
K A
KA
D000818:Animals; D000831:Animals, Newborn; D002352:Carrier Proteins / Q000378:metabolism*; D003600:Cytosol / Q000378:metabolism; D005260:Female; D005333:Fetus / Q000166:cytology / Q000378:metabolism; D008297:Male; D008565:Membrane Proteins; D010716:Phosphatidylinositols / Q000378:metabolism*; D049294:Phospholipid Transfer Proteins; D010743:Phospholipids / Q000378:metabolism*; D011247:Pregnancy; D011650:Pulmonary Alveoli / Q000166:cytology / Q000254:growth & development / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013347:Subcellular Fractions / Q000378:metabolism
D002352:Carrier Proteins; D008565:Membrane Proteins; D010716:Phosphatidylinositols; D049294:Phospholipid Transfer Proteins; D010743:Phospholipids