Document Detail


Developmental regulation of the effects of surfactant protein A on phospholipid uptake by fetal rat type II pneumocytes.
MedLine Citation:
PMID:  9436177     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Surfactant protein A (SP-A) enhances the uptake of phospholipid by type II cells derived from adult and late gestation fetal rat lung. The present study was performed to examine more fully the developmental biology of the effects of SP-A on phosphatidylcholine (PC) uptake, to determine the effect of SP-A on the cellular location of bound and internalized phospholipid and on the metabolism of internalized phospholipid by morphologically undifferentiated (18-day) and morphologically differentiated (19-day) fetal type II cells. SP-A enhanced uptake almost two-fold in a dose-dependent manner in 19-day fetal cells, but it had no effect on uptake by 18-day fetal cells at any concentration. Stimulation of uptake by 19-day fetal cells was saturable at concentrations above 1 microgram/ml SP-A. Maximal uptake was 1.12 nmol of PC/mg of protein, and the effective concentration that yields 50% maximal response, K phi, was 58.9 ng/ml (84.1 pM). The effect of SP-A on uptake by 19-day fetal cells was detectable as early as 1 min of exposure. Uptake correlated significantly with time both in the absence (r = 0.98, p < 0.001) and presence of 5 micrograms/ml SP-A (r = 0.979, p < 0.001). The rate of uptake in the presence of SP-A (0.019 +/- 0.002 nmol of PC/mg of protein/min) was twice the rate of uptake in controls (0.009 +/- 0.001 nmol of PC/mg of protein/min). SP-A had no effect on binding to plasma membranes and uptake of phospholipid into lamellar bodies by 18-day fetal cells. On the other hand, SP-A significantly enhanced binding of dipalmitoyl phosphatidylcholine to plasma membranes (two- to threefold) and uptake into lamellar bodies (threefold) of 19-day fetal cells. SP-A caused a significant reduction in the degradation of internalized phospholipid by differentiated fetal type II cells. Based on the lack of effect of exogenous SP-A on 18-day fetal cells, we conclude that the response to SP-A is under developmental control. SP-A enhances the initial binding to the plasma membranes of fetal type II cells and subsequent internalization into the lamellar bodies. This effect is associated with a protection of internalized phospholipid from metabolic degradation. Both of these processes are developmentally regulated during the transition from the canalicular to the saccular phase of lung development.
Authors:
M J Kresch; C Christian
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Lung     Volume:  176     ISSN:  0341-2040     ISO Abbreviation:  Lung     Publication Date:  1998  
Date Detail:
Created Date:  1998-03-04     Completed Date:  1998-03-04     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  7701875     Medline TA:  Lung     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  45-61     Citation Subset:  IM    
Affiliation:
Department of Pediatrics, University of Connecticut Health Center, Farmington 06030-2203, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Binding Sites
Cell Division / drug effects
Cell Membrane Permeability / drug effects
Cells, Cultured
Dose-Response Relationship, Drug
Drug Carriers
Female
Fetus
Follow-Up Studies
Glycoproteins / pharmacology*
Liposomes
Lung / drug effects,  metabolism*
Phosphatidylcholines / administration & dosage,  pharmacokinetics*
Pregnancy
Proteolipids / pharmacology*
Pulmonary Surfactant-Associated Protein A
Pulmonary Surfactant-Associated Proteins
Pulmonary Surfactants / pharmacology*
Rats
Rats, Sprague-Dawley
Grant Support
ID/Acronym/Agency:
R29-HL49099/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Drug Carriers; 0/Glycoproteins; 0/Liposomes; 0/Phosphatidylcholines; 0/Proteolipids; 0/Pulmonary Surfactant-Associated Protein A; 0/Pulmonary Surfactant-Associated Proteins; 0/Pulmonary Surfactants

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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