Deleterious Effect of Tracheal Obstruction on Type II Pneumocytes in Fetal Sheep

Piedboeuf, Bruno; Laberge, Jean-Martin; Ghitulescu, Gabriela; Gamache, Marie; Petrov, Peter G.; Bélanger, Sylvie; Chen, Moy-Fong; Hashim, Ezat; Possmayer, Fred

doi:10.1203/00006450-199704000-00004

Cited by 103 publications

(78 citation statements)

References 22 publications

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“…The current studies show that decreased distension not only retards lung growth but also inhibits differentiation of type I cells. Previous studies have shown that increased lung distension in fetal sheep accelerates lung growth and decreases numbers of type II cells and surfactant (2,11,18,28,32,37). The cellular mechanisms involved in the responses to changes in distension of the fetal lung have not been defined.…”

Section: Discussionmentioning

confidence: 99%

“…However, they reported neither quantitative data for cell counts nor measurements of indicators of surfactant, which is produced by type II cells. Subsequently, other investigators have studied tracheal ligation in fetal sheep and have confirmed that an increase in lung distension results in a lower number of type II cells (6,11,37) and a higher percentage of type I cells (18). Tracheal ligation also results in lower concentrations in the lung of surfactant protein (SP)-A and saturated phosphatidylcholine (SatPC), the major surface-active lipid in pulmonary surfactant (28), as well as mRNA for SP-A, -B, and -C (32).…”

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confidence: 99%

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Effects of oligohydramnios on lung growth and maturation in the fetal rat

Kitterman

Chapin

Vanderbilt

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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Oligohydramnios (OH) retards fetal lung growth by producing less lung distension than normal. To examine effects of decreased distension on fetal lung development, we produced OH in rats by puncture of uterus and fetal membranes at 16 days of gestation; fetuses were delivered at 21 or 22 days of gestation. Controls were position-matched littermates in the opposite uterine horn. OH lungs had lower weights and less DNA, protein, and water, but no differences in saturated phosphatidylcholine, surfactant proteins (SP)-A and -B, and mRNA for SP-A, -B, -C, and -D. To evaluate effects on epithelial differentiation, we used RTI 40 and RTII70, proteins specific in lung to luminal surfaces of alveolar type I and II cells, respectively. At 22 days of gestation, OH lungs had less RTI40 mRNA (P Ͻ 0.05) and protein (P Ͻ 0.001), but RTII70 did not differ from controls. With OH, type I cells (in proportion to type II cells) covered less distal air space perimeter (P Ͻ 0.01). We conclude that OH, which retards lung growth, has little effect on surfactant and impedes formation of type I cells relative to type II cells. fetal lung development; lung distension; pulmonary epithelial differentiation; pulmonary hypoplasia; pulmonary surfactant IN LATE GESTATION, the fetal lung undergoes marked changes in preparation for the transition to extrauterine life. These changes include growth, enlargement of distal potential air spaces, thinning of the septa, maturation of the surfactant system, and differentiation of distal pulmonary epithelium into mature alveolar type I and type II cells. Several studies have shown that fetal lung growth is controlled primarily by mechanical factors, especially distension of the lung (for reviews, see Refs. 26 and 29) and that maturation of the surfactant system is controlled primarily by endocrine factors (for reviews, see Refs. 3 and 48). In contrast, relatively little is known about factors that regulate differentiation of the alveolar epithelium.In 1977, Alcorn and associates (2) reported that tracheal ligation in fetal sheep, which increased lung distension, caused accelerated lung growth and a qualitative reduction in the number of alveolar type II cells; conversely, chronic drainage of tracheal fluid, which inhibited lung distension, retarded lung growth and increased the number of type II cells. However, they reported neither quantitative data for cell counts nor measurements of indicators of surfactant, which is produced by type II cells. Subsequently, other investigators have studied tracheal ligation in fetal sheep and have confirmed that an increase in lung distension results in a lower number of type II cells (6,11,37) and a higher percentage of type I cells (18). Tracheal ligation also results in lower concentrations in the lung of surfactant protein (SP)-A and saturated phosphatidylcholine (SatPC), the major surface-active lipid in pulmonary surfactant (28), as well as mRNA for SP-A, -B, and -C (32). Conversely, transection of the cervical spinal cord (which abolishes fetal breathing movemen...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Effects of oligohydramnios on lung growth and maturation in the fetal rat

Kitterman

Chapin

Vanderbilt

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Tracheal obstruction in animal models has been shown to accelerate fetal lung growth (Alcorn and Mendelson, 1993;Piedboeuf et al, 1997). Conditions that are associated with lung liquid drainage are characterized by pulmonary hypoplasia and an excess of type II cells (Flecknoe et al, 2003;Laudy and Wladimiroff, 2000).…”

Section: Discussionmentioning

confidence: 99%

Differentiation of xenografted human fetal lung parenchyma

Pavlović

Floros

Phelps

et al. 2008

Early Human Development

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The goal of this study was to characterize xenografted human fetal lung tissue with respect to developmental stage-specific cytodifferentiation. Human fetal lung tissue (pseudoglandular stage) was grafted either beneath the renal capsule or the skin of athymic mice (NCr-nu). Tissues were analyzed from 3 to 42 days post-engraftment for morphological alterations by light and electron microscopy (EM), and for surfactant protein mRNA and protein by reverse transcription-polymerase chain reaction (RT-PCR) and immunocytochemistry (ICC), respectively. The changes observed resemble those seen in human lung development in utero in many respects, including the differentiation of epithelium to the saccular stage. Each stage occurred over approximately one week in the graft in contrast to the eight weeks of normal in utero development. At all time points examined, all four surfactant proteins (SP-A, SP-B, SP-C, and SP-D) were detected in the epithelium by ICC. Lamellar bodies were first identified by EM in 14 day xenografts. By day 21, a significant increase in lamellar body expression was observed. Cellular proliferation, as marked by PCNA ICC and elastic fiber deposition resembled those of canalicular and saccular in utero development. This model in which xenografted lung tissue in different stages of development is available may facilitate the study of human fetal lung development and the impact of various pharmacological agents on this process.

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“…But this drive for accelerated growth was found to have negative effects on type II cells, 33 which has prompted some investigators to study whether antenatal steroids could reverse these adverse effects of tracheal occlusion on lung maturation. 34,35 The preoperative care now reflects the fact that the pulmonary hypoplasia and pulmonary hypertension caused by CDH represent a physiologic emergency, not a surgical one.…”

Section: Development Of Modern Surgical Approachmentioning

confidence: 99%

The History of Congenital Diaphragmatic Hernia from 1850s to the Present

Golombek

2002

J Perinatol

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Deleterious Effect of Tracheal Obstruction on Type II Pneumocytes in Fetal Sheep

Cited by 103 publications

References 22 publications

Effects of oligohydramnios on lung growth and maturation in the fetal rat

Effects of oligohydramnios on lung growth and maturation in the fetal rat

Differentiation of xenografted human fetal lung parenchyma

The History of Congenital Diaphragmatic Hernia from 1850s to the Present

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