Literature DB >> 1928369

Alveolar uptake of lipid and protein components of surfactant.

A B Fisher1, C Dodia, A Chander.   

Abstract

We investigated the clearance of radiolabeled natural surfactant from the alveolar space of the isolated perfused rat lung. 3H, 35S-natural surfactant was prepared from rat lungs that had been perfused with [methyl-3H]choline and [35S]methionine. The biosynthesized material contained greater than 95% of 3H in phosphatidylcholine (PC) and approximately 80% of 35S in surfactant protein A. Natural surfactant (1 mumol PC) was instilled into the trachea; lungs were analyzed 5 min later or after 2 h perfusion to determine surfactant uptake, defined as lung lavage-resistant 3H or 35S [% of instilled disintegrations per minute(dpm)]. Uptake at 5 min was 31.4 +/- 0.37% for 3H and 31.9 +/- 0.85% for 35S (mean +/- SE, n = 4). At 2 h, uptake was 46.6 +/- 0.96% for 3H and 45.8 +/- 1.1% for 35S (n = 7). In the presence of 0.1 mM 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP), uptake at 2 h for both 3H and 35S was stimulated to approximately 57% of instilled dpm (n = 4). Microsomes and plasma membranes isolated from lung homogenates had a ratio of 3H to 35S that was similar to the original surfactant, whereas 3H/35S in isolated lamellar bodies was increased 2.1-fold. Degradation of lipid was indicated by finding 13.4 +/- 0.65% of homogenate 3H in the aqueous fraction of lung extract after 2 h perfusion; only 2.3 +/- 0.47% of 35S dpm were soluble in trichloroacetic acid, suggesting significantly less protein breakdown. Lipid degradation was increased more than twofold by 8-BrcAMP, whereas protein degradation was not changed significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

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Year:  1991        PMID: 1928369     DOI: 10.1152/ajplung.1991.261.4.L334

Source DB:  PubMed          Journal:  Am J Physiol        ISSN: 0002-9513


  8 in total

1.  Role of the PI3-kinase signaling pathway in trafficking of the surfactant protein A receptor P63 (CKAP4) on type II pneumocytes.

Authors:  Altaf S Kazi; Jian-Qin Tao; Sheldon I Feinstein; Li Zhang; Aron B Fisher; Sandra R Bates
Journal:  Am J Physiol Lung Cell Mol Physiol       Date:  2010-09-24       Impact factor: 5.464

2.  Pathway to lamellar bodies for surfactant protein A.

Authors:  Aron B Fisher; Chandra Dodia; Peter Ruckert; Jian-Qin Tao; Sandra R Bates
Journal:  Am J Physiol Lung Cell Mol Physiol       Date:  2010-04-09       Impact factor: 5.464

3.  Protection against LPS-induced acute lung injury by a mechanism-based inhibitor of NADPH oxidase (type 2).

Authors:  Intae Lee; Chandra Dodia; Shampa Chatterjee; Sheldon I Feinstein; Aron B Fisher
Journal:  Am J Physiol Lung Cell Mol Physiol       Date:  2014-01-31       Impact factor: 5.464

4.  Binding of adenovirus capsid to dipalmitoyl phosphatidylcholine provides a novel pathway for virus entry.

Authors:  Larissa Balakireva; Guy Schoehn; Eric Thouvenin; Jadwiga Chroboczek
Journal:  J Virol       Date:  2003-04       Impact factor: 5.103

5.  Immunotargeting of antioxidant enzyme to the pulmonary endothelium.

Authors:  V R Muzykantov; E N Atochina; H Ischiropoulos; S M Danilov; A B Fisher
Journal:  Proc Natl Acad Sci U S A       Date:  1996-05-28       Impact factor: 11.205

Review 6.  Eosinophil-associated lung diseases. A cry for surfactant proteins A and D help?

Authors:  Julie G Ledford; Kenneth J Addison; Matthew W Foster; Loretta G Que
Journal:  Am J Respir Cell Mol Biol       Date:  2014-11       Impact factor: 6.914

Review 7.  The serpentine path to a novel mechanism-based inhibitor of acute inflammatory lung injury.

Authors:  Aron B Fisher
Journal:  J Appl Physiol (1985)       Date:  2014-04-17

8.  A competitive inhibitor of phospholipase A2 decreases surfactant phosphatidylcholine degradation by the rat lung.

Authors:  A B Fisher; C Dodia; A Chander; M Jain
Journal:  Biochem J       Date:  1992-12-01       Impact factor: 3.857

  8 in total

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