Fetal origins of neonatal lung disease: understanding the pathogenesis of bronchopulmonary dysplasia

Mestan, Karen K.; Steinhorn, Robin H.

doi:10.1152/ajplung.00314.2011

Cited by 22 publications

(29 citation statements)

References 27 publications

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“…Our further analysis revealed that Wnt/β-catenin is required for the maintenance of vascular smooth muscle cells through Klf2. Together, these findings not only provide important information about the normal mechanism by which RESEARCH REPORT Development 140 (17) epithelial Wnts control vasculature development, but provide important insights into birth defects, including alveolar capillary dysplasia, that present with abnormal alveologenesis and dysmorphic vasculature (Bishop et al, 2011;Mestan and Steinhorn, 2011). …”

Section: Wnt/β-catenin Regulates the Proliferation Of Vascular Smoothmentioning

confidence: 91%

“…In future studies it will be interesting to determine whether the reduced levels of Foxf1 also contribute to the abnormal lung morphogenesis in the Gpr177 ∆/∆ mutants. Notably, heterozygous loss-of-function FOXF1 mutations have been associated with the pathobiology of alveolar capillary dysplasia (ACD), which is characterized by the dramatically reduced numbers of capillary vessels and poor alveolar development (Bishop et al, 2011;Mestan and Steinhorn, 2011).…”

Section: Research Reportmentioning

confidence: 99%

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Gpr177 regulates pulmonary vasculature development

Jiang

et al. 2013

Development

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Establishment of the functional pulmonary vasculature requires intimate interaction between the epithelium and mesenchyme. Previous genetic studies have led to inconsistent conclusions about the contribution of epithelial Wnts to pulmonary vasculature development. This discrepancy is possibly due to the functional redundancy among different Wnts. Here, we use Shh-Cre to conditionally delete Gpr177 (the mouse ortholog of Drosophila Wntless, Wls), a chaperon protein important for the sorting and secretion of Wnt proteins. Deletion of epithelial Gpr177 reduces Wnt signaling activity in both the epithelium and mesenchyme, resulting in severe hemorrhage and abnormal vasculature, accompanied by branching defects and abnormal epithelial differentiation. We then used multiple mouse models to demonstrate that Wnt/β-catenin signaling is not only required for the proliferation and differentiation of mesenchyme, but also is important for the maintenance of smooth muscle cells through the regulation of the transcription factor Kruppel-like factor 2 (Klf2). Together, our studies define a novel mechanism by which epithelial Wnts regulate the normal development and maintenance of pulmonary vasculature. These findings provide insight into the pathobiology of congenital lung diseases, such as alveolar capillary dysplasia (ACD), that have abnormal alveolar development and dysmorphic pulmonary vasculature.

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Section: Wnt/β-catenin Regulates the Proliferation Of Vascular Smoothmentioning

confidence: 91%

Section: Research Reportmentioning

confidence: 99%

Gpr177 regulates pulmonary vasculature development

Jiang

et al. 2013

Development

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“…There are other nutritional components that have been shown to impact fetal lung development (24,36), but the focus of this manuscript will be on the maternal HFD. The fetal lung is particularly susceptible to in utero insults (27). For example, chorioamnionitis (inflammation of the fetal placental membranes) is associated with reduced microvascular and alveolar development in the lungs of fetal sheep (22,23).…”

mentioning

confidence: 99%

“…FGR is a pathological reduction in fetal growth potential (16). It is a major complication of pregnancy and increases the risk of fetal, perinatal, and lifelong morbidity and mortality (27).…”

mentioning

confidence: 99%

Maternal high-fat diet is associated with impaired fetal lung development

Mayor

Finch

Zehr

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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Maternal nutrition has a profound long-term impact on infant health. Poor maternal nutrition influences placental development and fetal growth, resulting in low birth weight, which is strongly associated with the risk of developing chronic diseases, including heart disease, hypertension, asthma, and type 2 diabetes, later in life. Few studies have delineated the mechanisms by which maternal nutrition affects fetal lung development. Here, we report that maternal exposure to a diet high in fat (HFD) causes placental inflammation, resulting in placental insufficiency, fetal growth restriction (FGR), and inhibition of fetal lung development. Notably, pre- and postnatal exposure to maternal HFD also results in persistent alveolar simplification in the postnatal period. Our novel findings provide a strong association between maternal diet and fetal lung development.

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“…In addition, IUGR syndrome adversely affects postnatal ontogenesis [4,5] and morphological and functional formation of digestive [5], respiratory [6], and reproductive organs [7]. Predisposition to metabolic and endocrine diseases [5,8], reduced fertility and productivity [7,9] are observed in the animals and their offspring.…”

mentioning

confidence: 99%

Metabolic Status of the Cows Under Intrauterine Growth Retardation of Embryo and Fetus

Нежданов¹,

Mikhalev²,

Chusova³

et al. 2016

S-h. biol.

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A b s t r a c tIntrauterine growth retardation of embryo and fetus (IUGR) in cows is a polyfactorial syndrome which is defined as an inconsistency between the sizes of forming embryos and fetuses and gestation periods. It is thought that the processes of embryo and fetus growth and development in cows are determined by morphofunctional integrity of gametes entering into the process of insemination and are mainly regulated by the character of maternal nutrition, state of metabolic homeostasis and maternal genitals. This work was devoted to the study of cows' metabolic status under intrauterine growth retardation of embryo and fetus. In 2013 at a large dairy complex (Agrotekh-Garant Ltd. Nashchekino, Anninskii Region, Voronezh Province) a total of 53 Red-motley Holstein cows with average annual productivity of 6.0-6.5 thousand kg were studied for protein metabolism indices (content of total proteins, protein fractions, serum urea), carbohydrates (blood concentration of glucose, lactic and pyruvic acids), vitamins (A, E, C), hormonal homeostasis (blood serum content of progesterone, dehydroepiandrosterone sulfate, testosterone, estradiol, cortisol, triiodothyronine), endogenous intoxication (concentration of middle molecular peptides, urea, creatinine, transaminase blood serum activity) and nitric oxide system on the days 38-40, 60-65, 110-115 and 230-240 of gestation. The impact of these indices on the development of embryo and fetus was also studied. Blood was collected from the jugular vein in the morning before feeding. The evaluation of genitals and metrics of embryo and fetus were done by the method of transrectal palpation and sonography with the use of bovine ultrasound scanner Easi-Scan-3 with 4.5-8.5 MHz linear transducer (BCF Technology Ltd, United Kingdom). The diameter of the fertilized horn, placenta size, body diameter and coccyx-parietal size of the fetus were determined. Coccyx-parietal size of 12-16 mm and body diameter of 7-9 mm were the criteria of development at the age of 38-40 days, 25-45 mm and 12-16 mm -at the age of 60-65 days, respectively. The diameter of the fertilized horn of 9-15 cm and placenta of 10-17 mm were the criteria of development at the age of 110-115 days. The animals with IUGR, diagnosed during 38-40 days of gestation, were included into the experiment on the days 230-240. It is stated that during early stages of fetus formation (38-40 days) the retardation of its growth and development is connected with hypoprogesteronemia determined by hypoplasia of the yellow body. The cows with IUGR also demonstrated blood serum decrease of cortisol by 36.9 % (p < 0.01) and increase of triiodothyronine by 35.4 % (p < 0.005) in comparison with the animals with physiological gestation course that proves total hormonal imbalance. At the stage of placentation (60-65 days) the cows with IUGR demonstrated evident deficit of nitric oxide that was proved by the decrease of its stable metabolite concentration (NO 2 + NO 3 ) in blood serum by 23.9 % (p < 0.05) in comparison with the level of t...

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Fetal origins of neonatal lung disease: understanding the pathogenesis of bronchopulmonary dysplasia

Cited by 22 publications

References 27 publications

Gpr177 regulates pulmonary vasculature development

Gpr177 regulates pulmonary vasculature development

Maternal high-fat diet is associated with impaired fetal lung development

Metabolic Status of the Cows Under Intrauterine Growth Retardation of Embryo and Fetus

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