Comparison of effects of epidermal and insulin-like growth factors, gastrin releasing peptide and retinoic acid on fetal lung cell growth and maturation in vitro

Fraslon, Caroline; Bourbon, Jacques R.

doi:10.1016/0005-2760(92)90172-r

Cited by 56 publications

(33 citation statements)

References 33 publications

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“…In our previous work, we demonstrated that BLP is important for type II cell differentiation and surfactant synthesis as well as generalized cell proliferation in both murine and human fetal lung in organ culture and in murine lung in utero (40)(41)(42)(43). Subsequent work in other laboratories confirmed and extended this result to isolated rat primary type II cell cultures (44,45), in which BLP stimulated surfactant secretion as well as synthesis (44). The highest endogenous BLP levels occur at mid-gestation in primate lung, but often peak effects of BLP occur at subnanomolar concentrations (44,45).…”

Section: Discussionmentioning

confidence: 71%

Bombesin-like peptide mediates lung injury in a baboon model of bronchopulmonary dysplasia.

et al. 1998

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Section: Discussionmentioning

confidence: 71%

Bombesin-like peptide mediates lung injury in a baboon model of bronchopulmonary dysplasia.

et al. 1998

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“…Immunolabeling for cytokeratin and vimentin has shown epithelial cells obtained through this procedure to be over 95% pure (17). Purified type II cells were seeded directly on plastic for proliferation studies (15) and for transdifferentiation into type I cells (9), or after coating with Engelbreth-Holm-Swarm (EHS) basement membrane matrix to maintain type II cell phenotype (7,9) in surfactant studies. Cells were allowed to adhere overnight to the substratum under air-CO2 (95%:5% vol/vol) at 37°C in MEM containing 10% FBS.…”

Section: Methodsmentioning

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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“…2). Similarly, EGF did not increase the content or the synthcsis of DSPC, which normally has a time course of maturation very similar to the chronology of AOE systcnl maturation both it1 ritro and it1 rive (1)(2)(3). However.…”

Section: Discussionmentioning

confidence: 77%

Epidermal Growth Factor Increases Antioxidant Enzyme and Surfactant System Development during Hyperoxia and Protects Fetal Rat Lungs In Vitro from Hyperoxic Toxicity

1993

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IIBSTRIICr. Epidermal growth factor (EGF) has been shown to accelerate fetal lung maturation in rabbits, lambs, and rhesus monkeys in riro and increase surfactant synthesis in vitro. Its effect on the maturation of the lung antioxidant enzyme system, however, is unknown. We studied the effect of EGF (10 nhl) on 19-d fetal rat lung esplant cultures in serum-free medium in air/S% C 0 2 or >90% 0 2 / 5 % C 0 2 compared with similarly grown control cultures in air or hyperosia a t 72 h. Fetal lung activities of superoxide dismutase and catalase were unchanged by EGF in air, whereas glutathione peroxidase activity was significantly decreased ( p < 0.05 rersus air control). lIowever, in hyperosia, EGF-treated fetal lung cultures had significantly elevated superoside dismutase and catalase activities ( p < 0.01) versus 02-exposed controls, and glutathione perosidase activity similar to that of controls. 'l'he mRNA levels for all the antioxidant enzymes showed patterns similar to the enzyme activities escept in the case of Cu,Znsuperoside dismutase mKNA, which increased in EGF-air cultures. E G F decreased the rate of '11-choline incorporation into disaturated phosphatidylcholine in air (p < 0.01 versus air control), but increased disaturated phosphatidylcholine synthesis in response to hyperosia ( p < 0.01 rersus O 2 control). The histologic appearance of EGF-treated cultures in O2 was superior to that of 02-exposed controls, which showed thickened septa1 walls, decreased surfactant in the air spaces, and epithelial cell mitochondria1 swelling. EGF therefore accelerates antiosidant enzyme and disaturated phosphatidylcholine maturation under hyperosic conditions and protects fetal rat lung cultures from hyperosic injury. This accelerated 02-dependent maturation by EGF occurs at the pretranslational level. TNA, total nucleic acidIn all mammalian species studied to date, there is a late gestational increase in surfactant and a par;1IIeI increase in the AOE system ofthe lungs ( I , 2). These late gestational biochemical changes prepare the fctal lungs for the transition from a fluidfilled state in a relatively 0.-poor intrauterine environment to air breathing in a relatively 0.-rich environment at birth (3). The prematurely born infant with a poorly developed surfactant system is prone to develop severe RDS and requires early mechanical ventilation combined with 0. therapy. Prolonged 0. therapy is associated with the development of chronic lung disease or bronchopulmonary dysplasia believed to be due in part to a poorly developed AOE defense system to counteract toxic O2 radical species generated by hyperoxia (3. 4).Lung maturation is known to be regulated or modulated by a number of hormones, among them the polypeptide EGF (5). 111 viro, EGF has been shown to enhance maturation of alveolar type 11 cells and increase surfactant production in fetal rabbits (6, 7) and rhcsus monkeys (8). Similarly. E G F increased morphologic maturation of the fetal lung and decreased RDS in fetal lambs (9). EGF also caused similar effects ...

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Comparison of effects of epidermal and insulin-like growth factors, gastrin releasing peptide and retinoic acid on fetal lung cell growth and maturation in vitro

Cited by 56 publications

References 33 publications

Bombesin-like peptide mediates lung injury in a baboon model of bronchopulmonary dysplasia.

Bombesin-like peptide mediates lung injury in a baboon model of bronchopulmonary dysplasia.

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

Epidermal Growth Factor Increases Antioxidant Enzyme and Surfactant System Development during Hyperoxia and Protects Fetal Rat Lungs In Vitro from Hyperoxic Toxicity

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