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Project description:Vitamin D deficiency is a common micronutrient deficiency worldwide, especially among reproductive-age women, and vitamin D deficiency during pregnancy increases the risks of offspring’s immune-related diseases later in life. The mechanisms of how our body remembers the exposure status of an adverse environment during development have not been fully elucidated yet. Here we show that prenatal vitamin D deficiency exposure alters the immune cell proportion of the offspring at the prenatal and adult stage, which is attributed to transcriptional alterations of vitamin D receptor downstream genes. Further, we assessed the association between maternal vitamin D status and cord blood immune cell profiles from 75 healthy mother and their term baby pairs and found that maternal vitamin D deficiency significantly alters immune cell proportion in cord blood. Our findings demonstrate that prenatal vitamin D deficiency alters the immune cell compositions of offspring by changing the transcriptional properties of stem cells and altering long-term stem cell fate decisions.
2024-09-30 | GSE242042 | GEO
Project description:Vitamin D deficiency is a common micronutrient deficiency worldwide, especially among reproductive-age women, and vitamin D deficiency during pregnancy increases the risks of offspring’s immune-related diseases later in life. The mechanisms of how our body remembers the exposure status of an adverse environment during development have not been fully elucidated yet. Here we show that prenatal vitamin D deficiency exposure alters the immune cell proportion of the offspring at the prenatal and adult stage, which is attributed to transcriptional alterations of vitamin D receptor downstream genes. Further, we assessed the association between maternal vitamin D status and cord blood immune cell profiles from 75 healthy mother and their term baby pairs and found that maternal vitamin D deficiency significantly alters immune cell proportion in cord blood. Our findings demonstrate that prenatal vitamin D deficiency alters the immune cell compositions of offspring by changing the transcriptional properties of stem cells and altering long-term stem cell fate decisions.
2024-09-30 | GSE242041 | GEO
Project description:Vitamin D deficiency is a common deficiency worldwide, particularly among women of reproductive age. During pregnancy, it increases the risk of immune-related diseases in offspring later in life. However, exactly how the body remembers exposure to an adverse environment during development is poorly understood. Herein, we explore the effects of prenatal vitamin D deficiency on immune cell proportions in offspring using vitamin D deficient mice established by dietary manipulation. We show that prenatal vitamin D deficiency alters immune cell proportions in offspring by changing the transcriptional properties of genes downstream of vitamin D receptor signaling in hematopoietic stem and progenitor cells of both the fetus and adults. Further investigations of the associations between maternal vitamin D levels and cord blood immune cell profiles from 75 healthy pregnant women and their term babies also confirm that maternal vitamin D levels significantly affect immune cell proportions in the babies. Thus, lack of prenatal vitamin D, particularly at the time of hematopoietic stem cell migration from the liver to the bone marrow, has long-lasting effects on immune cell proportions. This highlights the importance of providing vitamin D supplementation at specific stages of pregnancy.
| S-EPMC10515841 | biostudies-literature
Project description:Prenatal vitamin D deficiency alters immune cell proportions of offspring in young adult age.
| PRJNA1011255 | ENA
Project description:Prenatal vitamin D deficiency alters immune cell proportions of offspring in young adult age [scRNA-seq]
| PRJNA1011259 | ENA
Project description:Prenatal vitamin D deficiency alters immune cell proportions of offspring in young adult age [RNA-seq]
| PRJNA1011260 | ENA
Project description:The higher risk of adult neuropsychiatric diseases in individuals with low fetal birth weight may be related to brain-derived neurotrophic factor (BDNF) signaling pathway inhibition. Here, we investigated whether prenatal food restriction (PFR) induces neurobehavioral alterations in adult female offspring and explored the underlying intrauterine programming mechanism. Pregnant Wistar rats in the PFR group were fed 50% of the daily food intake of control rats from gestational day (GD) 11 to 20; some pregnant rats were sacrificed at GD20, and the remaining female pups had normal delivery and were fed a post-weaning high-fat diet (HFD) and half of them were exposed to an unpredictable chronic stress (UCS) from postnatal week (PW) 21. All adult female offspring were sacrificed at PW24. At GD20, PFR altered fetal hippocampal structure and function, increased glucocorticoid receptor (GR) expression, and decreased mineralocorticoid receptor (MR), BDNF and synaptic plasticity-related gene expressions. At PW24, PFR induced depression-like behavioral abnormalities in adult rat offspring fed an HFD. These rats exhibited depression- and anxiety-like behavioral changes after HFD/UCS. Furthermore, the hippocampal morphology of the PFR group showed abnormal changes in adult offspring fed an HFD and more serious damage after HFD/UCS. These changes were accompanied by increased serum corticosterone levels, elevated GR expression, and reduced expression of the BDNF signaling pathway and synaptic plasticity-related genes in the hippocampus. In conclusion, PFR may induce neurobehavioral abnormalities in adult offspring, especially those exposed to UCS, through high levels of glucocorticoids, which increase hippocampal GR expression and decrease BDNF expression.
| S-EPMC6060730 | biostudies-literature
Project description:Maternal infection during pregnancy has been associated with increased incidence of schizophrenia in the adult offspring. Mechanistically, this has been partially attributed to neurodevelopmental disruption of the dopamine neurons, as a consequence of exacerbated maternal immunity. In the present study we sought to target hypoferremia, a cytokine-induced reduction of serum non-heme iron, which is common to all types of infections. Adequate iron supply to the fetus is fundamental for the development of the mesencephalic dopamine neurons and disruption of this following maternal infection can affect the offspring's dopamine function. Using a rat model of localized injury induced by turpentine, which triggers the innate immune response and inflammation, we investigated the effects of maternal iron supplementation on the offspring's dopamine function by assessing behavioral responses to acute and repeated administration of the dopamine indirect agonist, amphetamine. In addition we measured protein levels of tyrosine hydroxylase, and tissue levels of dopamine and its metabolites, in ventral tegmental area, susbtantia nigra, nucleus accumbens, dorsal striatum and medial prefrontal cortex. Offspring of turpentine-treated mothers exhibited greater responses to a single amphetamine injection and enhanced behavioral sensitization following repeated exposure to this drug, when compared to control offspring. These behavioral changes were accompanied by increased baseline levels of tyrosine hydroxylase, dopamine and its metabolites, selectively in the nucleus accumbens. Both, the behavioral and neurochemical changes were prevented by maternal iron supplementation. Localized prenatal inflammation induced a deregulation in iron homeostasis, which resulted in fundamental alterations in dopamine function and behavioral alterations in the adult offspring. These changes are characteristic of schizophrenia symptoms in humans.
| S-EPMC2881043 | biostudies-literature
Project description:Effects of maternal aging on the offspring cognitive function remain controversial in population-based investigations, and information available in animal studies is very limited. We investigated the impact of a delayed first natural pregnancy on pregnancy outcomes in the mouse model. Spatial learning capacity in young adult mouse offspring was observed by step-down passive avoidance task and Morris water maze (MWM). Maternal serum ?-klotho was measured by ELISA. Morphological characteristics of fetoplacental unit and offspring brain were identified by H&E and immunohistochemistry. Klotho, VDR and other related genes expression were quantified by real-time-RT-PCR and western blot. We found delayed pregnancy reduced fertility in female mice by three-fold (Young vs. Old: 5.0% vs. 20.7%), and increased adverse pregnant outcomes by eight-fold (Young vs. Old: 3.0% vs. 27.5%). Mice born to old mothers exhibited shorter retention trial latency in passive avoidance task and longer latency to find the platform in MWM, suggesting worse performance on the tests that measure learning and memory. Serum ?-klotho level was lower in old female mice before pregnancy, whereas became comparable after pregnancy. Vitamin D receptor (VDR) expression, both in mRNA and protein, markedly decreased during the early stage of fetoplacental unit in old mice, especially in trophoblast giant cells when compared with that of young mice. Importantly, consistent with fetoplacental unit, VDR expression also declined in hippocampus from offspring born to old mice. These results suggest that young adult offspring from aged mothers exhibited worse cognitive function and the reduced VDR expression during fetoplacental development might play an important role.
| S-EPMC5883138 | biostudies-literature
Project description:Advanced paternal age (APA) at conception has been linked with autism and schizophrenia in offspring, neurodevelopmental disorders that affect social functioning. The current study explored the effects of paternal age on social development in the general population.We used multilevel growth modeling to investigate APA effects on socioemotional development from early childhood until adolescence, as measured by the Strengths and Difficulties Questionnaire (SDQ) in the Twins Early Development Study (TEDS) sample. We also investigated genetic and environmental underpinnings of the paternal age effects on development, using the Additive genetics, Common environment, unique Environment (ACE) and gene-environment (GxE) models.In the general population, both very young and advanced paternal ages were associated with altered trajectory of social development (intercept: p = .01; slope: p = .03). No other behavioral domain was affected by either young or advanced age at fatherhood, suggesting specificity of paternal age effects. Increased importance of genetic factors in social development was recorded in the offspring of older but not very young fathers, suggesting distinct underpinnings of the paternal age effects at these two extremes.Our findings highlight that the APA-related deficits that lead to autism and schizophrenia are likely continuously distributed in the population.
| S-EPMC5409803 | biostudies-other