Gene expression profile of androgen modulated genes in the murine fetal developing lung

Bresson, Eva; Seaborn, Tommy; Côté, Mélissa; Cormier, Geneviève; Provost, Pierre R.; Piedboeuf, Bruno; Tremblay, Yves

doi:10.1186/1477-7827-8-2

Cited by 38 publications

(40 citation statements)

References 61 publications

(65 reference statements)

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“…The concomitant increase in PPAR target genes involved in lipid synthesis (FAS) or transport (FAT) in lungs of female fetuses of diabetic rats fed the 6% olive-oil-or the 6% safflower-oil-supplemented diets indicates that this increase may contribute to the accumulation of triglycerides and to providing lipid substrates needed for the production of surfactant lipids in these experimental groups (Rehan & Torday 2012). The sex differences observed can be explained by the complex effects of estrogens, which induce profound changes in lipid metabolic pathways and regulate PPARs expression, and of androgens, which induce changes in the expression of multiple genes, including several PPAR coactivators and corepressors (Bresson et al 2010, Benz et al 2012, Oosthuyse & Bosch 2012.…”

Section: Discussionmentioning

confidence: 98%

Peroxisome proliferator-activated receptor ligands regulate lipid content, metabolism, and composition in fetal lungs of diabetic rats

Kurtz¹,

Capobianco²,

Careaga³

et al. 2014

Journal of Endocrinology

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Maternal diabetes impairs fetal lung development. Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors relevant in lipid homeostasis and lung development. This study aims to evaluate the effect of in vivo activation of PPARs on lipid homeostasis in fetal lungs of diabetic rats. To this end, we studied lipid concentrations, expression of lipid metabolizing enzymes and fatty acid composition in fetal lungs of control and diabetic rats i) after injections of the fetuses with Leukotriene B 4 (LTB 4 , PPARa ligand) or 15deoxyD 12,14 prostaglandin J 2 (15dPGJ 2 , PPARg ligand) and ii) fed during pregnancy with 6% olive oil-or 6% safflower oil-supplemented diets, enriched with PPAR ligands were studied. Maternal diabetes increased triglyceride concentrations and decreased expression of lipid-oxidizing enzymes in fetal lungs of diabetic rats, an expression further decreased by LTB 4 and partially restored by 15dPGJ 2 in lungs of male fetuses in the diabetic group. In lungs of female fetuses in the diabetic group, maternal diets enriched with olive oil increased triglyceride concentrations and fatty acid synthase expression, while those enriched with safflower oil increased triglyceride concentrations and fatty acid transporter expression. Both olive oil-and safflower oil-supplemented diets decreased cholesterol and cholesteryl ester concentrations and increased the expression of the reverse cholesterol transporter ATP-binding cassette A1 in fetal lungs of female fetuses of diabetic rats. In fetal lungs of control and diabetic rats, the proportion of polyunsaturated fatty acids increased with the maternal diets enriched with olive and safflower oils. Our results revealed important changes in lipid metabolism in fetal lungs of diabetic rats, and in the ability of PPAR ligands to modulate the composition of lipid species relevant in the lung during the perinatal period.

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Section: Discussionmentioning

confidence: 98%

Peroxisome proliferator-activated receptor ligands regulate lipid content, metabolism, and composition in fetal lungs of diabetic rats

Kurtz¹,

Capobianco²,

Careaga³

et al. 2014

Journal of Endocrinology

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“…It is believed that the female fetal lung produces surfactant earlier in gestation than the male fetal lung. The reasons for this finding may be as follows (15)(16)(17)(18). 1-Androgens delay lung fibroblast secretion of fibroblast-pneumocyte factor, which can delay the development of alveolar type II cells and reduce the release of PS.…”

Section: Discussionmentioning

confidence: 99%

High-risk Factors of Respiratory Distress Syndrome in Term Neonates: A Retrospective Case-control Study

2014

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Respiratory distress syndrome (RDS) is one of the most common causes of neonatal respiratory failure and neonatal death. The underlying pathogenesis of RDS involves developmental immaturity of the lungs, leading to inadequate pulmonary surfactant (PS) production. It was previously believed that RDS mainly occurs in premature infants (1); however, with the application of antenatal corticosteroids and delivery room PS, typical and severe RDS in premature infants is now rarely diagnosed. Greater awareness of RDS has led to a more frequent diagnosis in term neonates (2-5). However, the reasons for the occurrence of RDS in term neonates are different from those in premature infants, and remain unclear. This study aimed to investigate the cause of RDS in full-term neonates by a retrospective case-control study, and thus provide a useful reference for its diagnosis and treatment. MATERIAL AND METHODSThis investigation was approved by the ethics committee of the Beijing Military General Hospital. In this retrospective case-control study, the proportion of the case group (RDS patients) and control group (RDS-free patients) was 1:2. The following information was recorded: mode of delivery, birth asphyxia, premature rupture of membranes (PROM), maternal age at pregnancy, pregnancy hypertension disease, gestational glucose intolerance or diabetes, sex, birth weight, a cord around the neck with compression, oligohydramnios, meconium staining of amniotic fluid, severe fetal distress, and placental abruption.From January 2008 to December 2010, a total of 205 full-term newborns with RDS who were admitted to the Department of Neonatology & Neonatal Intensive Care Unit (NICU) (the largest NICU in the world with 350 beds; there are about 8,000 newborn infants admitted to this NICU within one year) at Bayi Children's Hospital, affiliated with the Beijing Military General Hospital of the Beijing Military Command, were assigned to this study. The diagnosis of term neonatal RDS met the following criteria (2-5): (1) full-term neonates (gestational age ≥37 weeks); (2) acute onset; (3) an acute, explicit perinatal triggering insult, such as severe perinatal acquired infection, severe birth asphyxia, meconium aspiration syndrome, or delivery by selective cesarean section; (4) representative clinical manifestations, including progressive respiratory distress occurring shortly after birth, tachypnea, expiratory grunting, nasal flaring, Background: Respiratory distress syndrome (RDS) is a common critical disease in term neonates, but reasons for the occurrence of RDS remains unclear. Aims: This study aimed to investigate the cause of RDS in full-term neonates by a retrospective case-control study. Study Design: Case-control study. Methods: Among the patients admitted to Bayi Children's Hospital between January 2008 and December 2010, a total of 205 full-term neonates with RDS were assigned to the study group, and 410 full-term neonates without RDS were assigned to the control group. Clinical information, including the presence or absence of ...

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“…Differences in sex hormone metabolism may also play a role in sex-related differences in lung development (34). Knowledge of the molecular basis for the male delay in lung maturation is increasing and candidate genes under the control of androgens, such as those genes controlling transforming growth factor-␤ and the Wnt pathway, have been identified (8,44).…”

Section: Pulmonary Surfactant Compositionmentioning

confidence: 99%

Sex differences in cardiorespiratory transition and surfactant composition following preterm birth in sheep

Ishak

Hanita

Sozo

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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Male preterm infants are at greater risk of respiratory morbidity and mortality than females but mechanisms are poorly understood. Our objective was to identify the basis for the "male disadvantage" following preterm birth using an ovine model of preterm birth in which survival of females is greater than males. At 0.85 of term, fetal sheep underwent surgery (11 female, 10 male) for the implantation of vascular catheters to monitor blood gases and arterial pressure. After cesarean delivery at 0.90 of term, lambs were monitored for 4 h while spontaneously breathing; lambs were then euthanized and static lung compliance measured. We analyzed surfactant phospholipid composition in amniotic fluid and in bronchoalveolar lavage fluid (BALF) taken at necropsy; we also analyzed surfactant protein (SP) expression in lung tissue. Before delivery male fetuses tended to have lower pH (P = 0.052) compared with females. One hour after delivery, males had significantly lower pH and higher arterial partial pressure of CO(2) (Pa(CO(2))), lactate, glucose, and mean arterial pressure than females. Two males died 1 h after birth. Static lung compliance was 37% lower in males than females (P < 0.05). In BALF, males had significantly more protein, a lower percentage of the phosphatidylcholine (PC) 32:0 (dipalmitoylphosphatidylcholine) and higher percentages of PC34:2 and PC36:2. There were no sex-related differences in lung architecture or expression of SP-A, -B, -C, and -D. The lower lung compliance in male preterm lambs compared with females may be due to altered surfactant phospholipid composition and function. These changes may compromise gas exchange and impair respiratory adaptation after male preterm birth.

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Gene expression profile of androgen modulated genes in the murine fetal developing lung

Cited by 38 publications

References 61 publications

Peroxisome proliferator-activated receptor ligands regulate lipid content, metabolism, and composition in fetal lungs of diabetic rats

Peroxisome proliferator-activated receptor ligands regulate lipid content, metabolism, and composition in fetal lungs of diabetic rats

High-risk Factors of Respiratory Distress Syndrome in Term Neonates: A Retrospective Case-control Study

Sex differences in cardiorespiratory transition and surfactant composition following preterm birth in sheep

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