Abstract
AIM: Stressful events during pregnancy may influence respiratory system development, resulting in long-term effects in the offspring. However, little is known on its long-lasting effects upon the expression of important genes in the lungs. Thus, we aimed to evaluate the effect of two different prenatal stress paradigms on lung glucocorticoid receptor (GR) expression in adulthood.METHODS: Pregnant BALB/c mice were divided into 3 groups: control (CON), prenatal stress from the second week of pregnancy (PNS1) and prenatal stress on the last week of pregnancy (PNS2). In both groups (PNS1 and PNS2), restraint stress was used. When adults, male and female offspring were submitted to 30 min of restraint stress. Lung gene expression of GR was evaluated.RESULTS: There was a significant increase in GR expression in males (PNS1), under basal conditions. Restraint stress during adulthood significantly reduced GR expression in PNS1 and PNS2 males as compared to controls. No significant differences were found for females.CONCLUSION: Results indicate that prenatal stress from the second week of gestation modulates adult male mice GR expression in the lungs. Thus, fetal exposure to maternal stress from the second week of gestation seems to modulate mechanisms responsible for pulmonary development in a sex-dependent manner.
Highlights
The gestational period is well recognized for its plasticity and sensibility
Adverse events during gestation can generate longlasting programming effects that remain throughout life, several mechanisms involving the action of peripheral glucocorticoids are still not well elucidated [16]
Our results demonstrate that prenatal stress 1 (PNS1) males had a higher expression of glucocorticoid receptor (GR) in the lungs under basal conditions
Summary
The gestational period is well recognized for its plasticity and sensibility. Stressful events during pregnancy can influence fetal development, resulting in long-term effects in the offspring [1, 2]. During the respiratory system development in utero, glucocorticoids are key factors for fetal development, such as alveolar maturation and production of surfactant [5, 6]. Disturbances during this period may modulate lung development. Mechanisms related to lung glucocorticoid exposure of the offspring during gestation have not yet been well elucidated, it is well known that glucocorticoid receptors (GR) function is fundamental for the maintenance of several physiological effects [6, 12]
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