scholarly journals Igf2 Deficiency Results in Delayed Lung Development at the End of Gestation

Endocrinology ◽  
2006 ◽  
Vol 147 (12) ◽  
pp. 5584-5591 ◽  
Author(s):  
Delia Silva ◽  
Maria Venihaki ◽  
Wei-Hui Guo ◽  
Mary Frances Lopez
Keyword(s):  
Fetal Lung ◽  
Plasma Corticosterone ◽  
Mrna Levels ◽  
Wild Type ◽  
Lung Maturation ◽  
Morphological Alterations ◽  
Lung Histology ◽  
Igf I ◽  
Fetal Lung Maturation

IGF-II is a polypeptide hormone with structural homology to insulin and IGF-I. IGF-II plays an important role in fetal growth as mice with targeted disruption of the IGF-II gene (Igf2) exhibit severe growth retardation. The role of IGFs in the fetal lung has been suggested by several studies, including those that have identified IGF mRNA expression, and that of their receptors and binding proteins in the lungs at different stages of development. In this study, we used mice carrying a null mutation of Igf2 (Igf2−/− mice) to determine whether the absence of IGF-II had any effect in fetal lung maturation. Our results showed that the lungs of Igf2−/− fetuses had thicker alveolar septae and poorly organized alveoli when compared with those of Igf2+/+ on d 17.5 and 18.5 of gestation. These morphological alterations may be the result of exposure to lower levels of glucocorticoids because plasma corticosterone levels were significantly lower in Igf2−/− mothers compared with wild-type controls. In support of this, fetuses from homozygous knockout matings, where mothers were treated with 15 μg/ml corticosterone, and Igf2−/− fetuses obtained from heterozygous matings had similar lung histology to those of wild-type fetuses. Finally, we found that IGF-I and SP-B mRNA levels were up-regulated in the lungs of Igf2−/− fetuses at the end of gestation. This study suggests that Igf2 plays an important role in the development of the fetal lung and may affect fetal lung maturation by regulating maternal factors, such as corticosterone levels, during pregnancy.

Ovine surfactant protein cDNAs: use in studies on fetal lung growth and maturation after prolonged hypoxemia

2000 ◽  
Vol 278 (4) ◽  
pp. L754-L764 ◽  
Author(s):  
Geert A. Braems ◽  
Li-Juan Yao ◽  
Kevin Inchley ◽  
Anne Brickenden ◽  
Victor K. M. Han ◽  
...  
Keyword(s):  
Pulmonary Surfactant ◽  
Specific Binding ◽  
Fetal Lung ◽  
Surfactant Protein ◽  
Mrna Levels ◽  
Fetal Hypoxia ◽  
Lung Maturation ◽  
Igf I ◽  
Surfactant Apoprotein ◽  
Mild Hypoxia

cDNAs for ovine surfactant-associated protein (SP) A, SP-B, and SP-C have been cloned and shown to possess strong similarity to cDNAs for surfactant apoproteins in other species. These reagents were employed to examine the effect of fetal hypoxia on the induction of surfactant apoprotein expression in the fetal lamb. Postnatal lung function is dependent on adequate growth and maturation during fetal development. Insulin-like growth factor (IGF) I and IGF-II, which are present in all fetal tissues studied, possess potent mitogenic and proliferative actions, and their effects can be modulated by IGF-specific binding proteins (IGFBPs). Hypoxia can lead to increases in circulating cortisol and catecholamines that can influence lung maturation. Therefore, the effects of mild hypoxia in chronically catheterized fetal lambs at gestational days 126– 130 and 134– 136 (term 145 days) on the expression of pulmonary surfactant apoproteins and IGFBPs were examined. Mild hypoxia for 48 h resulted in an increase in plasma cortisol that was more pronounced at later gestation, and in these animals, there was a twofold increase in SP-A mRNA. SP-B mRNA levels also increased twofold, but this was not significant. SP-C mRNA was not altered. No significant changes in apoprotein mRNA were observed with the younger fetuses. However, these younger animals selectively exhibited reduced IGFBP-5 mRNA levels. IGF-I mRNA was also reduced at 126–130 days, although this conclusion is tentative due to low abundance. IGF-II levels were not affected at either gestational age. We conclude that these data suggest that mild prolonged fetal hypoxia produces alterations that could affect fetal cellular differentiation early in gestation and can induce changes consistent with lung maturation closer to term.

The Role of Prolactin in Fetal Lung Maturation

1992 ◽  
Vol 10 (03) ◽  
pp. 287-293
Author(s):  
Jeanne Snyder ◽  
Steven Dekowski
Keyword(s):  
Fetal Lung ◽  
Lung Maturation ◽  
Fetal Lung Maturation

Role of α-glucosidase in fetal lung maturation

1987 ◽  
Vol 917 (1) ◽  
pp. 203-210 ◽  
Author(s):  
Jacques R. Bourbon ◽  
Edith Doucet ◽  
Michel Rieutort
Keyword(s):  
Fetal Lung ◽  
Lung Maturation ◽  
Fetal Lung Maturation

scholarly journals Molecular regulation of lung maturation in near-term fetal sheep by maternal daily vitamin C treatment in late gestation

2021 ◽  
Author(s):  
Erin V. McGillick ◽  
Sandra Orgeig ◽  
Beth J. Allison ◽  
Kirsty L. Brain ◽  
Youguo Niu ◽  
...  
Keyword(s):  
Vitamin C ◽  
Lung Development ◽  
Fetal Lung ◽  
Late Gestation ◽  
Lung Maturation ◽  
Maternal Vitamin ◽  
Healthy Pregnancy ◽  
Daily Vitamin ◽  
Expression Of Genes ◽  
Fetal Lung Maturation

Abstract Background In the fetus, the appropriate balance of prooxidants and antioxidants is essential to negate the detrimental effects of oxidative stress on lung maturation. Antioxidants improve respiratory function in postnatal life and adulthood. However, the outcomes and biological mechanisms of antioxidant action in the fetal lung are unknown. Methods We investigated the effect of maternal daily vitamin C treatment (200 mg/kg, intravenously) for a month in late gestation (105–138 days gestation, term ~145 days) on molecular regulation of fetal lung maturation in sheep. Expression of genes and proteins regulating lung development was quantified in fetal lung tissue. The number of surfactant-producing cells was determined by immunohistochemistry. Results Maternal vitamin C treatment increased fetal lung gene expression of the antioxidant enzyme SOD-1, hypoxia signaling genes (HIF-2α, HIF-3α, ADM, and EGLN-3), genes regulating sodium movement (SCNN1-A, SCNN1-B, ATP1-A1, and ATP1-B1), surfactant maturation (SFTP-B and ABCA3), and airway remodeling (ELN). There was no effect of maternal vitamin C treatment on the expression of protein markers evaluated or on the number of surfactant protein-producing cells in fetal lung tissue. Conclusions Maternal vitamin C treatment in the last third of pregnancy in sheep acts at the molecular level to increase the expression of genes that are important for fetal lung maturation in a healthy pregnancy. Impact Maternal daily vitamin C treatment for a month in late gestation in sheep increases the expression of gene-regulating pathways that are essential for normal fetal lung development. Following late gestation vitamin C exposure in a healthy pregnancy, an increase in lung gene but not protein expression may act as a mechanism to aid in the preparation for exposure to the air-breathing environment after birth. In the future, the availability/development of compounds with greater antioxidant properties than vitamin C or more specific targets at the site of oxidative stress in vivo may translate clinically to improve respiratory outcomes in complicated pregnancies at birth.

Modeling Glucocorticoid-Mediated Fetal Lung Maturation: I. Temporal Patterns of Corticosteroids in Rat Pregnancy

2005 ◽  
Vol 317 (1) ◽  
pp. 117-126 ◽  
Author(s):  
Mahesh N. Samtani ◽  
Nancy A. Pyszczynski ◽  
Debra C. DuBois ◽  
Richard R. Almon ◽  
William J. Jusko
Keyword(s):  
Temporal Patterns ◽  
Fetal Lung ◽  
Lung Maturation ◽  
Fetal Lung Maturation
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