Fetal lung surfactant lipid synthesis from glycogen during organ culture

Farrell, Philip M.; Bourbon, Jacques R.

doi:10.1016/0005-2760(86)90142-6

Cited by 33 publications

(13 citation statements)

References 20 publications

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“…In our experiments, inositol not only increased surfactant phospholipid concentrations but also diminished glycogen concentration, i.e. it increased its utilization presumably for surfactant biosynthesis (26). Supplementation studies suggest that the lung of the malnourished rat poorly uses exogenous precursors for surfactant lipid biosynthesis, probably because of an overall reduced anabolic activity.…”

Section: Discussionmentioning

confidence: 41%

“…Our results also show that malnutrition slows down the mobilization of lung glycogen stores after birth, which is consistent with the previous findings by Curle and Adamson (3). This delay in glycogen breakdown with possible reduction of glycogen utilization for providing precursors of surfactant lipids (26,27) appears to reflect a delay in perinatal lung biochemical maturation. Changes in water content suggest that malnutrition also decreased lung fluid reabsorption at birth.…”

Section: Discussionmentioning

confidence: 99%

“…The lung samples were homogenized in ice-cold 10 mM Tris-HC1 buffer, pH 7.4, containing 1 mM EDTA and 154 mM NaCI. All sucrose solutions were prepared in this buffer, and ultracentrifugations were as described previously (26). The presumed surfactant fraction was obtained as the Frosolono's 1B band at the interface between 0.25 and 0.68 M sucrose layers (14).…”

Section: Surfactant Fraction Isolation Surfactant and Nonsurfactantmentioning

confidence: 99%

“…Nonsurfactant fraction gathered pellets and supernatants above and below the surfactant band of each centrifugation. It was composed of nuclei, mitochondria, microsomes, lysosomes, and cytosol (26).…”

Section: Surfactant Fraction Isolation Surfactant and Nonsurfactantmentioning

confidence: 99%

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Effects of Maternal Protein-Calorie Malnutrition on the Phospholipid Composition of Surfactant Isolated from Fetal and Neonatal Rat Lungs. Compensation by Inositol and Lipid Supplementation

Guarner¹,

Tordet²,

Bourbon³

1992

Pediatr Res

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ABSTRACT. The effects of a maternal protein-calorie malnutrition during gestation and lactation were analyzed on fetal and postnatal lung growth and maturation, including a surfactant fraction isolated from lung tissue. There was a considerable reduction in body weight and in wet and dry lung weights of malnourished pups. Lung protein and DNA concentrations were similar in both groups except in late gestation (lung hyperplasia) and 2 and 1 5 d after delivery (hypocellularity). Lung glycogen breakdown was slowed down in malnourished newborns. Surfactant material was decreased the most perinatally and the reduction was more marked than for the nonsurfactant fraction of the lung. Disaturated phosphatidylcholine, the major surface active surfactant component, was decreased the most a t birth (1.70 f 0.31 nmol/mg wet wt versus 3.

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Section: Discussionmentioning

confidence: 41%

Section: Discussionmentioning

confidence: 99%

Section: Surfactant Fraction Isolation Surfactant and Nonsurfactantmentioning

confidence: 99%

Section: Surfactant Fraction Isolation Surfactant and Nonsurfactantmentioning

confidence: 99%

See 2 more Smart Citations

Effects of Maternal Protein-Calorie Malnutrition on the Phospholipid Composition of Surfactant Isolated from Fetal and Neonatal Rat Lungs. Compensation by Inositol and Lipid Supplementation

Guarner¹,

Tordet²,

Bourbon³

1992

Pediatr Res

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“…Although total PC was found to be reduced in the whole lung of HIF-2 Ϫ/Ϫ mice (8), the surfactant compartment was not explored specifically in this model, and it is not clear whether this was related directly to the observed reduction of VEGF production, or whether the prevention of neonatal respiratory distress observed following intra-amniotic administration of VEGF was linked to an increase in surfactant phospholipids. Reduced glycogen stores after VEGF treatment were interpreted by the authors as an improved maturation of the lung and as the result of a probable utilization for surfactant phospholipid synthesis (8), because glycogen has been demonstrated to be a precursor of the latter (10). However, improved morphological maturation of the lung (i.e., thinning of septa) after VEGF treatment evidenced by histological examination However, it appears from both the present and previous (8) findings that VEGF is able to exert a direct stimulating effect on the expression level of the SP-B transcript in isolated type II cells.…”

Section: Discussionmentioning

confidence: 99%

Effects of vascular endothelial growth factor on isolated fetal alveolar type II cells

Raoul¹,

Chailley‐Heu²,

Barlier-Mur³

et al. 2004

American Journal of Physiology-Lung Cellular and Molecular Phys

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Previous investigations gained from in vivo or lung explant studies suggested that VEGF is an autocrine proliferation and maturation factor for developing alveolar type II cells. The objective of this work was to determine whether VEGF exerted its growth and maturation effects directly on isolated type II cells. These were isolated from 19-day fetal rat lung and cultured in defined medium. The presence of VEGF receptor-2 was assessed in cultured cells at the pre- and posttranslational levels. Recombinant VEGF165, formerly found to be active on lung explants, failed to enhance type II cell proliferation estimated by thymidine and 5-bromo-2′-deoxy-uridine incorporation. It increased choline incorporation in saturated phosphatidylcholine by 27% but did not increase phospholipid surfactant pool size. VEGF (100 ng/ml) left unchanged the transcript level of surfactant proteins (SP)-A, SP-C, and SP-D but increased SP-B transcripts to four times the control steady-state level. VEGF slightly retarded, but did not prevent, the in vitro transdifferentiation of type II into type I cells, as assessed by immunolabeling of the type I cell marker T1α. We conclude that, with the exception of SP-B expression, which appears to be controlled directly, the previously observed effects of this VEGF isoform on type II cells are likely to be exerted indirectly through reciprocal paracrine interactions involving other lung cell types.

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Ultrastructural features of type II alveolar epithelial cells in early embryonic mouse lung

1988

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Immunofluorescence studies of type II alveolar epithelial cells indicate that they first appear in the pseudoglandular period of mouse lung development (around day 14.2). They are the only cell type to line the prospective pulmonary acinus at this time. The ultrastructural characteristics of this cell are defined by investigating embryos aged 13-16 days with transmission and scanning electron microscopy. Early embryonic type II cells appear as low-columnar or cuboid cells having large, approximately round nuclei and distinct ultrastructural features, including a well-developed Golgi apparatus with many associated vesicles, multivesicular bodies, dense bodies, and large apical and basal glycogen fields. These fields represent a distinctive property of the cell. Frequently, they show compartmentalization due to the presence of membrane systems, and association with dense bodies of various sizes.

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Fetal lung surfactant lipid synthesis from glycogen during organ culture

Cited by 33 publications

References 20 publications

Effects of Maternal Protein-Calorie Malnutrition on the Phospholipid Composition of Surfactant Isolated from Fetal and Neonatal Rat Lungs. Compensation by Inositol and Lipid Supplementation

Effects of Maternal Protein-Calorie Malnutrition on the Phospholipid Composition of Surfactant Isolated from Fetal and Neonatal Rat Lungs. Compensation by Inositol and Lipid Supplementation

Effects of vascular endothelial growth factor on isolated fetal alveolar type II cells

Ultrastructural features of type II alveolar epithelial cells in early embryonic mouse lung

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