Exposure to synthetic glucocorticoids during pregnancy alters the expression of p73 gene variants in fetal brains in a sex-specific manner

Abul, Mai; Al‐Bader, Maie; Mouihate, Abdeslam

doi:10.1016/j.brainres.2018.11.030

Cited by 4 publications

(4 citation statements)

References 45 publications

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“…Adult FGR mice exhibit impaired hippocampaldependent learning and memory According to previously reported methods (Abul et al, 2019;Liu et al, 2015), we first established two FGR models in mice: DEX-induced FGR (DEX-FGR) and PR-influenced FGR (PR-FGR). As expected, the body weight and length at post-natal day (PD) 1 of both DEX-FGR and PR-FGR pups were significantly reduced (Figures 1A and 1B;Figures S1A and S1B).…”

Section: Resultsmentioning

confidence: 99%

“…In the investigation of the mechanisms by which FGR predisposes an individual to disease development later in life, several animal models have been developed according to the causes of FGR, in particular, exposure to glucocorticoid (GC) to mimic either maternal chronic stress or excessive administration of therapeutic GC and prenatal protein restriction (PR) to represent maternal undernutrition (Swanson and David, 2015). These two widely used models show similar neuroendocrine and clinical characteristics, for example, an adverse GC environment in utero, disturbance of the hypothalamic-pituitary-adrenal (HPA) axis, and decreases in brain weight, suggesting that the two usual FGR models may induce neurodevelopmental disorders in part by a common mechanism (Lesage et al, 2001;Abul et al, 2019;Liu et al, 2015). In this study, we established FGR mouse models through either prenatal overexposure to dexamethasone (DEX; a synthetic GC analog) or a prenatal PR diet and showed that FGR decreases hippocampal neurogenesis from the early post-natal period to adulthood and impairs the learning and memory abilities in adult offspring in both mouse models.…”

Section: Introductionmentioning

confidence: 99%

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Fetal growth restriction impairs hippocampal neurogenesis and cognition via Tet1 in offspring

et al. 2021

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Fetal growth restriction impairs hippocampal neurogenesis and cognition via Tet1 in offspring

et al. 2021

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“…Overexposure to glucocorticoids, such as BM, decreases cell proliferation and leads to impaired and delayed development (Fowden et al, 2016; Gramsbergen & Mulder, 1998). Moreover, exposure to glucocorticoids is associated with metabolic impairments, intrauterine growth restriction, and decreased body weight gain (Abul et al, 2019; Borges et al, 2016; Iwasa et al, 2014). Therefore, BM exposure during the neonatal period may lead to delayed development and body growth.…”

Section: Discussionmentioning

confidence: 99%

Reproductive outcomes of neonatal exposure to betamethasone in male and female rats

Figueiredo

Barros

Borges

et al. 2022

J of Applied Toxicology

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Betamethasone (BM) is the drug of choice for antenatal corticosteroid therapy for women at risk of preterm delivery because it induces fetal lung maturation and enhances survival after birth. However, our group reported evidence of fetal programming and impaired reproductive development and function in rats exposed during the critical window of genital system development. Therefore, we aimed to investigate the effects of BM on the sexual development of rats in the period that corresponds to antenatal corticosteroid therapy in humans. Male and female rats were exposed subcutaneously to BM at 0.1 μg/g of pups' body weight or to a NaCl 0.9% solution (control) on postnatal days 1–3. It was observed that neonatal exposure to BM decreased body weight and weight gain in male and female rats during treatment. The estrous cycle was deregulated and LH level was decreased in female rats. In male rats, the sperm concentration in the caput–corpus of the epididymis was decreased, whereas the sperm transit time and sperm concentration in the cauda of the epididymis were increased. Our results demonstrated that neonatal exposure to BM impaired body growth of male and female rats, deregulated the estrous cycle of female rats, and altered sperm quality of male rats. Therefore, BM exposure from postnatal days 1 to 3 corroborated results previously observed after prenatal exposure to this drug. Despite the recognized importance of human antenatal corticosteroid therapy, the findings of this study should encourage further studies in order to minimize possible adverse postnatal effects.

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“…The next day, vaginal smears were examined for the presence of sperms. Females with sperm-positive smear were identified as pregnant and designated day 0 of pregnancy as described previously [34]. These rats were weighed and individually housed in Plexiglas cages undisturbed until day 19 or 21 of gestation when they were sacrificed.…”

Section: Methodsmentioning

confidence: 99%

Effects of Cardiac Hypertrophy, Diabetes, Aging, and Pregnancy on the Cardioprotective Effects of Postconditioning in Male and Female Rats

Babiker

Al-Jarallah

Al-Awadi

2019

Cardiology Research and Practice

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Background. Aging, left ventricular hypertrophy (LVH), diabetes mellitus, and pregnancy are well-recognized risk factors that increase the prevalence of cardio-ischemic events and are linked to poor clinical recovery following acute myocardial infarction. The coexistence of these risk factors with ischemic heart disease (IHD) deteriorates disease prognosis and could potentially lead to fatal arrhythmias and heart failure. The objective of this study was to investigate the vulnerability of hearts with aging, LVH, diabetes, and pregnancy to ischemic insult and their response to pacing postconditioning- (PPC-) induced heart protection. Methods. Hearts isolated from aged, spontaneously hypertensive and diabetic male and female rats and hearts from pregnant female rats (n=8 per group) were subjected to coronary occlusion followed by reperfusion using a modified Langendorff system. Hemodynamics data were computed digitally, and cardiac damage was accessed by measurements of infarct size and cardiac enzyme release. Results. There were no significant differences in the vulnerability of all hearts to ischemic insult compared to their respective controls. PPC improved cardiac hemodynamics and reduced infarct size and cardiac enzyme release in hearts isolated from aged and spontaneously hypertensive female rats and female rats with hypertrophied hearts subjected to PPC (P<0.001). Aged or hypertrophied male hearts were not protected by PPC maneuver. Moreover, the protective effects of PPC were lost in diabetic male and female hearts although retained in hearts from pregnant rats. Conclusions. We demonstrate that aging, LVH, diabetes mellitus, and pregnancy do not affect cardiac vulnerability to ischemic insult. Moreover, PPC mediates cardioprotection in a gender-specific manner in aged and spontaneously hypertensive rats. Diabetes mellitus provokes the protective effects of PPC on both genders equally. Finally, we demonstrate that PPC is a new cardioprotective maneuver in hearts from pregnant female rats.

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Exposure to synthetic glucocorticoids during pregnancy alters the expression of p73 gene variants in fetal brains in a sex-specific manner

Cited by 4 publications

References 45 publications

Fetal growth restriction impairs hippocampal neurogenesis and cognition via Tet1 in offspring

Fetal growth restriction impairs hippocampal neurogenesis and cognition via Tet1 in offspring

Reproductive outcomes of neonatal exposure to betamethasone in male and female rats

Effects of Cardiac Hypertrophy, Diabetes, Aging, and Pregnancy on the Cardioprotective Effects of Postconditioning in Male and Female Rats

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