Regulatory Interactions between Androgens, Hoxb5, and TGF<b><i>β</i></b>Signaling in Murine Lung Development

Volpe, MaryAnn V.; Ramadurai, Sujatha M.; Mujahid, Sana; Vong, Thanhxuan; Brandão, Márcia Maria dos Anjos; Wang, Karen T.; Pham, Lucia D.; Nielsen, Heber C.

doi:10.1155/2013/320249

Cited by 18 publications

(12 citation statements)

References 51 publications

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“…The expression of the HoxB5 gene began at the earliest stages of lung development, peaked at the end of the pseudoglandular stage, and then its expression was moderated in the saccular stage 33. Regarding histological analysis, it appears that the overexpression of this gene in the fluoxetine treatment group is probably due to the delay in lung development.…”

Section: Resultsmentioning

confidence: 91%

The expression of HoxB5 and SPC in neonatal rat lung at exposure to fluoxetine

Taghizadeh

Taghipour

Karimi

et al. 2016

DDDT

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ObjectiveApproximately 10% of pregnant women suffer from pregnancy-associated depression. Fluoxetine, as a selective serotonin reuptake inhibitor, is being employed as a therapy for depressive disorders. The present study aimed to determine the effects of fluoxetine on neonatal lung development.MethodsThirty pregnant Wistar rats (weighing 200–250 g) were treated daily with 7 mg/kg fluoxetine from gestation day 0 to gestation day 21, via gavage. The control group received a similar volume of distilled water only. Following delivery, the newborns and their lungs were immediately weighed in both of the groups. The right lung was fixed for histological assessments while the left lung was used for evaluation of the expression of SPC and HoxB5 by the real-time polymerase chain reaction method.ResultsResults have indicated that even though the body weight and the number of neonatal rats in both groups were the same, the lung weight of neonates exposed to fluoxetine was significantly different compared to the control group (P<0.05). Expression of both genes was increased, nonetheless, only elevation of HoxB5 was significant (P<0.05). Histological studies demonstrated that lung tissue in the fluoxetine treatment group morphologically appears to be similar to the pseudoglandular phase, whereas the control group lungs experienced more development.ConclusionAccording to the upregulated expression of HoxB5 concerning histological findings, results of the present study showed that fluoxetine can influence lung growth and may in turn lead to delay in lung development. So establishment of studies to identify the effects of antidepressant drugs during pregnancy is deserved.

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Section: Resultsmentioning

confidence: 91%

The expression of HoxB5 and SPC in neonatal rat lung at exposure to fluoxetine

Taghizadeh

Taghipour

Karimi

et al. 2016

DDDT

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“…The AR is expressed in both male and female lung epithelial cells and can bind to DNA sequences to regulate the expression of cell differentiation genes [ 78 , 79 ]. Studies have also shown that the AR can mediate androgen-induced delays in fetal lung maturation [ 80 , 81 , 82 ]. For example, maternal treatment with dihydrotestosterone inhibits surfactant phospholipid production in the fetal lung, while treatment with the AR-selective antagonist flutamide enhances surfactant phospholipid production [ 83 ].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA Signatures Associated with Bronchopulmonary Dysplasia Severity in Tracheal Aspirates of Preterm Infants

et al. 2021

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Bronchopulmonary dysplasia (BPD) is a form of chronic lung disease that develops in neonates as a consequence of preterm birth, arrested fetal lung development, and inflammation. The incidence of BPD remains on the rise as a result of increasing survival of extremely preterm infants. Severe BPD contributes to significant health care costs and is associated with prolonged hospitalizations, respiratory infections, and neurodevelopmental deficits. In this study, we aimed to detect novel biomarkers of BPD severity. We collected tracheal aspirates (TAs) from preterm babies with mild/moderate (n = 8) and severe (n = 17) BPD, and we profiled the expression of 1048 miRNAs using a PCR array. Associations with biological pathways were determined with the Ingenuity Pathway Analysis (IPA) software. We found 31 miRNAs differentially expressed between the two disease groups (2-fold change, false discovery rate (FDR) < 0.05). Of these, 4 miRNAs displayed significantly higher expression levels, and 27 miRNAs had significantly lower expression levels in the severe BPD group when compared to the mild/moderate BPD group. IPA identified cell signaling and inflammation pathways associated with miRNA signatures. We conclude that TAs of extremely premature infants contain miRNA signatures associated with severe BPD. These may serve as potential biomarkers of disease severity in infants with BPD.

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“…The AR is expressed in both male and female lung epithelial cells and can bind to DNA sequences to regulate the expression of cell differentiation genes [69,70]. Studies have also shown that the AR can mediate androgen-induced delays in fetal lung maturation [71][72][73]. For example, maternal treatment with dihydrotestosterone inhibits surfactant phospholipid production in the fetal lung, while treatment with the AR selective antagonist flutamide enhances surfactant phospholipid production [74].…”

Section: Discussionmentioning

confidence: 99%

Tracheal Aspirate miRNA Signatures in Preterm Infants with Severe Bronchopulmonary Dysplasia

Siddaiah¹,

Oji‐Mmuo²,

Montes³

et al. 2021

Preprint

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Bronchopulmonary dysplasia (BPD) is a form of chronic lung disease that develops in neonates as a consequence of preterm birth and arrested fetal lung development. The incidence of BPD remains on the rise, as a result of increasing survival of extremely preterm infants. Severe BPD contributes to significant health care costs and is associated with prolonged hospitalizations, respiratory infections, and neurodevelopmental deficits. In this study, we aimed to detect novel biomarkers of severe BPD. We collected tracheal aspirates (TA) from preterm babies with mild/moderate (n = 8) and severe (n = 17) BPD, and we profiled the expression of 1048 miRNAs using a PCR array. Associations with biological pathways were determined with the Ingenuity Pathway Analysis (IPA) software. We found 31 miRNAs differentially expressed between the two disease groups (2-fold change, FDR &lt; 0.05). Of these, 4 miRNAs displayed significantly higher expression levels, and 27 miRNAs had significantly lower expression levels in the severe BPD vs. the mild/moderate BPD group. IPA identified cell signaling and inflammation pathways associated with miRNA signatures. We conclude that TAs of extreme premature infants contain miRNA signatures associated with severe BPD. These signatures may serve as biomarkers of disease severity in infants with BPD.

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Regulatory Interactions between Androgens, Hoxb5, and TGFβSignaling in Murine Lung Development

Cited by 18 publications

References 51 publications

The expression of HoxB5 and SPC in neonatal rat lung at exposure to fluoxetine

The expression of HoxB5 and SPC in neonatal rat lung at exposure to fluoxetine

MicroRNA Signatures Associated with Bronchopulmonary Dysplasia Severity in Tracheal Aspirates of Preterm Infants

Tracheal Aspirate miRNA Signatures in Preterm Infants with Severe Bronchopulmonary Dysplasia

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