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Effect of intrauterine growth restriction on the H3K4me3, H3K9ac, H3K27ac and H3k9me3 histione modification of microglia in hippocampus

ABSTRACT: Early-life exposures (spanning from the gamete stage to childhood) to adverse environmental factors can exert long-term effects on offspring health through epigenetic modifications, significantly increasing susceptibility to chronic diseases such as neuropsychiatric disorders in adulthood. Previous studies have shown that fetal growth restriction can lead to excessive activation of microglia in the individual's brain, but there is still a lack of research on its epigenetic mechanisms. Our data supplements the gap of changes of H3K4me3, H3K9ac, H3K27ac and H3K9me3 histone modification of microglia in the hippocampus of individuals with fetal growth restriction, and explores the epigenetic basis of microglial activation

ORGANISM(S): Mus musculus

PROVIDER: GSE317929 | GEO | 2026/01/30

REPOSITORIES: GEO

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Project description:Fetal growth restriction (FGR) is a risk factor for obesity in adult life. Importantly, growth-restricted females are more prone to obesity than males. The mechanisms involved in this sexually dimorphic programming are not known. Previously, we have demonstrated that ambient hyperthermia (40° C) led to placental insufficiency and significant FGR, and the perirenal adipose tissue undergoes sexually dimorphic gene expression. We demonstrated that males undergo significant changes in gene expression with growth restriction. This was not the case in females. We have also demonstrated that the isolated preadipocytes from male FGR (MFGR) have reduced differentiation potential compared to control males & females and female FGR (FFGR). Thus, we hypothesized that growth restriction differentially programs gene expression and genetic pathways in perirenal preadipocytes, which reduces their differentiation potential in male fetuses in a sexually dimorphic manner. We created fetal growth restriction by exposing pregnant sheep to ambient hyperthermia. After isolating preadipocytes from perirenal adipose tissue, we differentiated them following published protocols. We examined the gene expression before and after differentiation from control male, control female, MFGR, and FFGR female. We also compared our data with other published studies in mouse and human preadipocytes. Our results demonstrate that a set of 21 genes altered with preadipocyte differentiation to mature adipocytes is common in adipose tissue from both sexes, humans, mice, and sheep, at different organismal ages (embryonic, fetal, and adult) and different sites (subcutaneous inguinal, pancreatic, perirenal). We also demonstrate that female FFGR fetuses demonstrate all these 21 genes altered similar to control males and females; however, MFGR fetuses have six genes (Dgat2, Fabp4, Lipe, Lrrfip1, Spred3, and Thrsp) that are not changed with preadipocyte differentiation to mature adipocyte. These genes may be responsible for reduced differentiation potential and obesity in FGR males compared to FGR females. Another important finding of the present study is that Lrrfip1, known to be associated with obesity, was upregulated with FGR and requires further investigation. Overall, our studies provide several target genes that may play a crucial role in reducing the risk of MFGR for obesity.

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Effect of intrauterine growth restriction on the H3K4me3, H3K9ac, H3K27ac and H3k9me3 histione modification of microglia in hippocampus

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