Sublethal hydrogen peroxide inhibits alveolar type II cell surfactant phospholipid biosynthetic enzymes

1995 ◽  
Vol 268 (1) ◽  
pp. L129-L135 ◽  
Author(s):  
C. Crim ◽  
W. J. Longmore
Keyword(s):  
Cell Injury ◽  
Phospholipid Metabolism ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Reactive Oxygen Metabolites ◽  
Type Ii ◽  
Intracellular Atp ◽  
Alveolar Type Ii Cell ◽  
Atp Levels ◽  
Type Ii Cell

Alveolar type II cell injury by phagocytic cell-derived reactive oxygen metabolites represents a potential mechanism for the altered surfactant metabolism found in patients with the adult respiratory distress syndrome (ARDS). Previous studies demonstrated altered surfactant phospholipid metabolism after sublethal oxidant exposure. In this study, we measured intracellular ATP levels and the activities of several enzymes involved in surfactant phospholipid biosynthesis after sublethal H2O2 exposure of cultured rat alveolar type II cells. Intracellular ATP levels were reduced by 46.6% after exposure to 75 microM H2O2. The activity of CTP:phosphorylcholine cytidyltransferase was unchanged after H2O2 exposure when measured in whole cell homogenates. However, when measured in the microsomal fraction, cytidyltransferase activity significantly fell after exposure of type II cells to 75 microM H2O2. Activity in the cytosolic fractions remained unchanged. Similarly, microsomal cholinephosphotransferase was reduced after H2O2 exposure. We conclude that H2O2 decreases surfactant phosphatidylcholine biosynthesis independently of its ability to deplete intracellular ATP content. These deleterious effects may partially explain the diminished alveolar surfactant observed in patients with ARDS.

scholarly journals Phospholipid-transfer activities in cytosols from lung, isolated alveolar type II cells and alveolar type II cell-derived adenomas

1983 ◽  
Vol 215 (3) ◽  
pp. 637-642 ◽  
Author(s):  
G L Pool ◽  
D G Bubacz ◽  
R H Lumb ◽  
R J Mason
Keyword(s):  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Transfer Protein ◽  
Alveolar Type Ii Cell ◽  
Phospholipid Transfer ◽  
Type Ii Cell ◽  
Specific Proteins ◽  
Isolated Rat

We have examined phospholipid-transfer activities in cytosols from rat and mouse whole lung, isolated rat alveolar type II cells and alveolar type II cell-derived mouse pulmonary adenomas. We report an enrichment in phosphatidylcholine and phosphatidylglycerol (but not phosphatidylinositol) protein-catalysed transfer in the type II cell and adenoma cytosols compared with the whole-lung cytosols. The activities from these cytosols were resolved using column chromatofocusing, which clearly demonstrated the presence of a phosphatidylcholine-specific transfer protein in each of the four tissues. In addition, two proteins (rat) or three proteins (mouse) catalysing both phosphatidylcholine and phosphatidylglycerol transfer were resolved from whole lung, whereas in both the rat isolated alveolar type II cells and the mouse type II cell-derived adenomas one of these less specific proteins is not present.

Derivation of tumorigenic and non-tumorigenic mouse alveolar type-II cell lines from fetal type-II cells after a combinedin vivo/in vitro carcinogen treatment

1992 ◽  
Vol 52 (2) ◽  
pp. 290-297 ◽  
Author(s):  
L. C. J. M. Oomen ◽  
J. Calafat ◽  
A. A. W. Ten Have-Opbroek ◽  
J. Egberts ◽  
P. Demant
Keyword(s):  
Cell Lines ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cell ◽  
Type Ii Cell

scholarly journals The cytoprotective role of DJ-1 and p45 NFE2 against human primary alveolar type II cell injury and emphysema

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Li Hui Tan ◽  
Karim Bahmed ◽  
Chih-Ru Lin ◽  
Nathaniel Marchetti ◽  
Sudhir Bolla ◽  
...  
Keyword(s):  
Cell Injury ◽  
Alveolar Type ◽  
Type Ii ◽  
Alveolar Type Ii Cell ◽  
Type Ii Cell

Generation and characterization of monoclonal antibodies to alveolar type II cell lamellar body membrane

1998 ◽  
Vol 275 (1) ◽  
pp. L172-L183 ◽  
Author(s):  
K. Zen ◽  
K. Notarfrancesco ◽  
V. Oorschot ◽  
J. W. Slot ◽  
A. B. Fisher ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
Membrane Protein ◽  
Lamellar Body ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Rat Lung ◽  
Lamellar Bodies ◽  
Alveolar Type Ii Cell ◽  
Type Ii Cell

Monoclonal antibodies against the limiting membrane of alveolar type II cell lamellar bodies were obtained after immunization of mice with a membrane fraction prepared from lamellar bodies isolated from rat lungs. The specificity of the antibodies was investigated with Western blot analysis, indirect immunofluorescence, and electron-microscopic immunogold studies of freshly isolated or cultured alveolar type II cells, alveolar macrophages, and rat lung tissue. One of the monoclonal antibodies identified, MAb 3C9, recognized a 180-kDa lamellar body membrane (lbm180) protein. Immunogold labeling of rat lung tissue with MAb 3C9 demonstrated that lbm180 protein is primarily localized at the lamellar body limiting membrane and is not found in the lamellar body contents. Most multivesicular bodies of type II cells were also labeled, as were some small cytoplasmic vesicles. Golgi complex labeling and plasma membrane labeling were weak. The appearance of lbm180 protein by immunofluorescence in fetal rat lung cryosections correlated with the biogenesis of lamellar bodies. The lbm180 protein decreased with time in type II cells cultured on plastic. The lbm180 protein is an integral membrane protein of lamellar bodies and was also found in the pancreas and the pancreatic βHC9 cell line but not in the rat brain, liver, kidney, stomach, or intestine. The present study provides evidence that the lbm180 protein is a lung lamellar body and/or multivesicular body membrane protein and that its antibody, MAb 3C9, will be a valuable reagent in further investigations of the biogenesis and trafficking of type II cell organelles.

Uptake of antioxidants in surfactant liposomes by cultured alveolar type II cells is enhanced by SP-A

1993 ◽  
Vol 265 (4) ◽  
pp. L330-L339 ◽  
Author(s):  
F. J. Walther ◽  
R. David-Cu ◽  
M. C. Supnet ◽  
M. L. Longo ◽  
B. R. Fan ◽  
...  
Keyword(s):  
Antioxidant Activity ◽  
Surface Activity ◽  
Alveolar Epithelium ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Adult Rats ◽  
Alveolar Type Ii Cell ◽  
Type Ii Cell

Antioxidant delivery may be targeted toward the alveolar epithelium by encapsulating superoxide dismutase (SOD) and catalase in liposomes made from pulmonary surfactant. We studied whether antioxidant-surfactant liposomes increase cellular antioxidant activity in alveolar type II cells and whether this effect is influenced by the presence of surfactant protein A (SP-A). Cu,Zn SOD and catalase were encapsulated in liposomes made from synthetic phospholipids with or without 5% SP-A or from natural cow surfactant. Alveolar type II cells from adult rats were preincubated for 20 h, and liposome mixtures were added for 24 h, followed by measurement of cellular SOD and catalase activities (U/mg DNA). Antioxidant-surfactant liposomes increased alveolar type II cell antioxidant activity sharply. Uptake of SOD/catalase from liposomes with synthetic phospholipids and SP-A was twice that from liposomes without SP-A and did not further improve in the presence of SP-B and -C. Encapsulation of antioxidants diminished the surface activity of the surfactant liposomes, but this feature was absent in the presence of SP-A. These data suggest that: 1) antioxidant-surfactant liposomes augment alveolar type II cell antioxidant activity, 2) liposomal uptake is facilitated by the presence of SP-A, and 3) inhibition of surface activity of surfactant by encapsulated antioxidants can be reversed by SP-A.

Stimulation of net active ion transport across alveolar type II cell monolayers

1986 ◽  
Vol 250 (2) ◽  
pp. C222-C227 ◽  
Author(s):  
G. R. Cott ◽  
K. Sugahara ◽  
R. J. Mason
Keyword(s):  
Ion Transport ◽  
Alveolar Epithelium ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Cell Monolayers ◽  
Alveolar Type Ii Cell ◽  
Active Ion Transport ◽  
Type Ii Cell

The active transcellular transport of electrolytes across the alveolar epithelium probably plays an important role in alveolar fluid homeostasis by helping to maintain the alveolus relatively free of fluid. To better understand the factors regulating active ion transport across alveolar epithelial cells, we examined the effect of a number of pharmacologically active agents on the bioelectric properties of alveolar type II cells in primary culture. Alveolar type II cells were isolated from adult male rats and cultured on collagen-coated Millipore filters for 6-14 days. The bioelectric properties of these monolayers were determined in Ussing-type chambers. The addition of 10(-3) M 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP) increased the short-circuit current (Isc) from 2.9 +/- 0.75 to 6.9 +/- 0.73 microA/cm2 (means +/- SE; n = 8) and decreased the transepithelial resistance. Cholera toxin, 3-isobutyl-1-methylxanthine, and terbutaline sulfate produced similar increases in Isc and decreases in resistance. The Isc stimulated by 8-BrcAMP was Na but not Cl dependent and could be blocked by amiloride but not by furosemide. Thus 8-BrcAMP and agents that increase intracellular cAMP can stimulate a Na-dependent net active ion transport across alveolar type II cell monolayers. Similar regulatory mechanisms may be involved in controlling solute and fluid movement across the alveolar epithelium in vivo.

Alveolar type II cell cNOS activity and ATP levels are increased by lung surfactant or DPPC vesicles

1997 ◽  
Vol 273 (2) ◽  
pp. L339-L346 ◽  
Author(s):  
P. R. Miles ◽  
L. Bowman ◽  
A. Rengasamy ◽  
L. Huffman
Keyword(s):  
Nitric Oxide ◽  
Lung Surfactant ◽  
Specific Inhibitor ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
O2 Consumption ◽  
No Formation ◽  
Atp Levels ◽  
Type Ii Cell

In a previous study, we reported that nitric oxide (.NO) affects surfactant synthesis and ATP levels in alveolar type II cells and suggested that there is constitutive nitric oxide synthase (cNOS) activity in the cells. In the present study, we performed experiments to confirm further the presence of cNOS and to determine the effects of lung surfactant on type II cell .NO and ATP levels. The supernatant from freshly isolated cells contains .NO (0.26 +/- 0.08 nmol/10(6) cells). During incubation, the cells produce additional .NO at a rate of approximately 0.3 nmol.10(5) cells-1.h-1. .NO formation is inhibited by 28-46% by three inhibitors of cNOS and inducible NOS (iNOS), NG-monomethyl-L-arginine (L-NMMA), L-N5-(1-iminoethyl)ornithine hydrochloride, and NG-nitro-L-arginine methyl ester, but a specific inhibitor of iNOS, aminoguanidine, has no effect. The production of .NO is reduced in Ca(2+)-free medium, is stimulated by the Ca2+ ionophore A-23187, and is independent of extracellular L-arginine. One known type of cNOS, endothelial NOS (eNOS), can be detected in the cells by using Western blot analysis. Incubation of the cells with lung surfactant leads to a relatively rapid (approximately 15 min), concentration-dependent increase in .NO formation that reaches levels as high as 238 +/- 14% of control. The surfactant effects appear to be caused by its major component, dipalmitoyl phosphatidylcholine (DPPC). Exposure of type II cells to DPPC results in maximal increases in .NO formation, ATP content, and O2 consumption, which are 268 +/- 32, 234 +/- 24, and 131 +/- 6% of control, respectively. The DPPC-induced increases in .NO, ATP, and O2 consumption are inhibited by L-NMMA. These results confirm the presence of type II cell cNOS and suggest that it may have a role in the cellular processing of lung surfactant.

Surfactant treatment effects on alveolar type II cell morphology in rabbit lungs

1993 ◽  
Vol 74 (3) ◽  
pp. 1240-1247 ◽  
Author(s):  
K. E. Pinkerton ◽  
J. Lewis ◽  
A. M. Mulder ◽  
M. Ikegami ◽  
A. H. Jobe
Keyword(s):  
Volume Fraction ◽  
Lamellar Body ◽  
Exogenous Surfactant ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Lamellar Bodies ◽  
Alveolar Type Ii Cells ◽  
Alveolar Type Ii Cell ◽  
Type Ii Cell

The effects of exogenous surfactant administration on alveolar type II cells and the lung parenchyma were examined in adult rabbits. Natural surfactant was instilled into the left lobe of New Zealand White rabbits while the right lobe served as the control. Four hours post-instillation, the lungs were fixed by vascular perfusion. Surfactant instillation did not change alveolar type II cell size but was associated with a significant reduction in the volume fraction of lamellar bodies in type II cells (20.4% in control lobes compared with 11.9% in surfactant-treated lobes). The size distribution of lamellar body profiles was different in surfactant-treated lobes compared with control lobes, with a significant decrease in lamellar bodies > 0.8 microns in diameter and a twofold increase in lamellar bodies 0.2–0.4 microns in diameter. Composite body profile number was also increased by 87% (P < 0.05) after instillation of surfactant compared with control. Saline instillation decreased lamellar body volume fraction in type II cells but three times less than surfactant instillation. These observations are consistent with a strong stimulus for secretion of endogenous surfactant 4 h after surfactant instillation in normal adult rabbit lungs, whereas the increase in composite bodies is consistent with new lamellar body formation, probably from both de novo synthesized and exogenous natural rabbit surfactant. These observations confirm that the secretory and synthetic processes of alveolar type II cells are significantly affected by exogenous surfactant instillation.

Isolation and culture of alveolar type II cells

1990 ◽  
Vol 258 (4) ◽  
pp. L134-L147 ◽  
Author(s):  
L. G. Dobbs
Keyword(s):  
Cell Biology ◽  
Full Range ◽  
Cell Phenotype ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Mixed Cell ◽  
Cell Functions ◽  
Alveolar Type Ii Cell ◽  
Type Ii Cell

The alveolar type II cell performs many important functions within the lung, including regulation of surfactant metabolism, ion transport, and alveolar repair. Because type II cells comprise only 15% of all lung cells, it is difficult to attribute specific functions to type II cells from studies of whole lungs or mixed cell cultures. At the present time, there is no passaged line that exhibits the full range of known type II cell functions. For these reasons, investigators have used isolated type II cells to study alveolar cell biology, biochemistry, and molecular biology. This review addresses many of the issues involved in isolating and culturing type II cells, including the choice of a method of isolating cells, the importance of using specific markers of the differentiated type II cell phenotype, and the problems of maintaining these differentiated phenotypic characteristics in tissue culture.

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