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Maternal high-fat diet aggravates the development of atherosclerosis in offspring via epigenetic memory (SMART-Seq)

ABSTRACT: Maternal high-fat diet aggravates the development of atherosclerosis in offspring via epigenetic memory (SMART-Seq)

PROVIDER: PRJNA1156763 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30559102_1.fastq.gz	Fastqsanger.gz
	SRR30559102_2.fastq.gz	Fastqsanger.gz
	SRR30559103_1.fastq.gz	Fastqsanger.gz
	SRR30559103_2.fastq.gz	Fastqsanger.gz
	SRR30559104_1.fastq.gz	Fastqsanger.gz

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Maternal high-fat diet aggravates the development of atherosclerosis in offspring via epigenetic memory (SMART-Seq)

Project description:Maternal exposure to a western-type diet (WD) increases the susceptibility of adult offspring to atherosclerosis. Lining the inner layer of blood vessels, fetus endothelial cells (ECs) become dysfunctional and inflamed in response to risk factors from mother through maternal and fetal blood exchange. However, the mechanism by which maternal WD promotes vascular endothelial dysfunction and atherosclerosis in offspring after adulthood has not been fully clarified. Here, we found that maternal WD exposure sensitized offspring to WD exposure in adulthood of Ldlr-/- mice, significantly increasing atherosclerotic lesions in the aorta and aortic roots, endowed inflammatory memory at the chromatin level and regulated chromatin dynamics by transcription factor AP-1 in mouse aortic ECs. Plasma 27-hydroxycholesterol (27-HC) was significantly increased in maternal blood and transferred into the offspring. Additionally, 27-HC played a crucial role in memory establishment and also acted as a secondary stimulator, amplifying the expression of inflammatory memory factors and enhancing the enrichment of AP-1/p300 and H3K27ac in the binding domain in human ECs. Inhibiting AP-1 binding to chromatin reduced the inflammatory response in human umbilical vein ECs from mother with maternal hypercholesterolemia and the occurrence and development of atherosclerosis in the offspring with maternal WD exposure. Our findings demonstrate that maternal WD aggravating EC dysfunction and atherosclerosis in offspring after adulthood acquires AP-1-associated epigenetic memory to increase chromatin accessibility of inflammatory genes.

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Maternal high-fat diet aggravates the development of atherosclerosis in offspring via epigenetic memory (ATAC-Seq CUT&Tag)

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Maternal high-fat diet aggravates the development of atherosclerosis in offspring via epigenetic memory (ATAC-Seq CUT&Tag)

Project description:Maternal high-fat diet aggravates the development of atherosclerosis in offspring via epigenetic memory (ATAC-Seq CUT&Tag)

| PRJNA1156764 | ENA

Transcription profiling of mouse offspring of crosses between hypercholesterolemic and normocholesterolemic parents LUMC-HKG-ApoE-Atherosclerosis

Project description:Enhanced prenatal fatty streak formation in human fetuses has been associated with maternal hypercholesterolemia. However, the possible roles of maternal genetic background and in utero environment on development of atherosclerosis in adult life have not been unraveled. We generated genetically identical heterozygous apoE-deficient mice offspring with a different maternal background to study the intrauterine effect of maternal genotype and associated hypercholesterolemia on the developing vascular system. As read out for increased atherosclerosis development in adult life, a constrictive collar was placed around the carotid artery to induce lesion formation. A significant increase in endothelial cell activation and damage was detected in the carotid arteries of heterozygous apoE-deficient fetuses with apoE-deficient mothers compared with offspring from wild type mothers, but no fatty streak formation was observed. Postnatally, all carotid arteries revealed normal morphology. In adult offspring with maternal apoE-deficiency, the constrictive collar resulted in severe lesion (9/10) development compared with no to only minor lesions (2/10) in offspring of wild type mothers. Microarray analysis showed no effect of maternal apoE-deficiency on gene expression in adult offspring. We conclude that maternal apoE-deficiency not only affects fetal arteries, but also increases the susceptibility for development of collar-induced atherosclerosis in adult life. Experiment Overall Design: Crossing of hypercholesterolemic female with normocholesterolemic male and vice versa, determination of susceptabilioty to atherosclerosis in offspring

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Mitochondrial signals mediate paternal effects on offspring metabolism (Smart-Seq)

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Alternate high fat diet aggravates atherosclerosis through an IL1b-dependent reprogramming of neutrophil progenitors

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Bioinformation and deep-learning based model reveals norepinephrine inhibiting PRDX1 aggravates atherosclerosis

Project description:The regulation of metabolites comprises the fundamental biological processes of human. More new phenotypes of classic metabolites were revealed, while the devolution of functional targets and mechanisms of them still have many gaps due to diversity in structures and functions. Here, we report a bioinformation and attention mechanism based deep learning model leveraging abundant bioinformation of metabolites for functional target prediction of specific phenotypes. Taking advantage of this model, the potential target database of 3,382 common human metabolites were resourced publicly. Norepinephrine was identified as a selective peroxidase inhibitor of peroxiredoxin 1 (PRDX1) for atherosclerosis aggravation in model validation experiments. Salvianolic acid A (SAA) was screened out as PRDX1 exogenous stabilization compound for rescuing norepinephrine’s aggravation effects in vivo. Besides, bulk RNA-Sequencing analysis indicated norepinephrine aggravates atherosclerosis through activating transcriptional activity of SREBP2 in a ROS dependent manner. Overall, our research provides a new computational regime for metabolites target identification besides experimental chemical proteomics and PRDX1 stabilization was validated a potential druggable target for cardiovascular diseases intervention.

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Maternal Brown Fat Thermogenesis Programs Glucose Tolerance in the Male Offspring

Project description:We tested if minor changes in maternal non-shivering thermogenesis during pregnancy can severely alter the phenotype of the offspring already in the next generation. Therefore, male offspring of dams lacking the uncoupling protein 1 (UCP1-KO) in the thermogenic brown adipose tissue were analysed. Genome-wide expression profiling identified several alterations in the hepatic transcriptomic landscape, demonstrating that even minor differences in the demand for maternal thermogenesis profoundly and permanently alter hepatic gene activity in the adult offspring. Liver gene expression data of offspring from WT and UCP1-KO dams.

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