Prenatal THC exposure and the gut microbiota
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB71402 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR12791300.fastq.gz | Fastqsanger.gz | |||
| ERR12791301.fastq.gz | Fastqsanger.gz | |||
| ERR12791302.fastq.gz | Fastqsanger.gz | |||
| ERR12791303.fastq.gz | Fastqsanger.gz | |||
| ERR12791304.fastq.gz | Fastqsanger.gz |
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Project description:Drug exposure during critical periods of development is known to have lasting effects, increasing one’s risk for developing mental health disorders. Emerging evidence has also indicated the possibility for drug exposure to even impact subsequent generations. Our previous work demonstrated that adolescent exposure to Δ9-tetrahydrocannabinol (THC), the main psychoactive component of marijuana (Cannabis sativa), in a Long-Evans rat model affects reward-related behavior and gene regulation in the subsequent (F1) generation unexposed to the drug. Questions, however, remained regarding potential epigenetic consequences. In the current study, using the same rat model, we employed Enhanced Reduced Representation Bisulfite Sequencing to interrogate the epigenome of the nucleus accumbens, a key brain area involved in reward processing. This analysis compared 16 animals with parental-THC exposure and 16 without to characterize relevant systems-level changes in DNA methylation. We identified 1,027 differentially methylated regions (DMRs) associated with parental THC exposure in F1 adults, each represented by multiple CpGs. These DMRs fell predominantly within introns, exons, and intergenic intervals, while showing a significant depletion in gene promoters. From these, we identified a network of DMR-associated genes involved in glutamatergic synaptic regulation, which also exhibited altered mRNA expression in the nucleus accumbens. These data provide novel insight into drug-related cross-generational epigenetic effects, and serve as a useful resource for investigators to explore novel neurobiological systems underlying drug abuse vulnerability. Study consisted of a total of 32 F1 individuals (Long-Evan rats); 16 animals (8 female, 8 male) were offspring from THC-exposed parents, and the remaining 16 animals (8 female, 8 male) were offspring from saline-exposed parents ("controls"; "VEH-exposed").
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Project description:Cannabis is commonly used in pregnancy for symptoms of nausea and pain, especially in the first trimester. Cannabis remains a federally illicit drug in the United States, but local legalization trends have resulted in increased availability and a decreased perception of harm. Unfortunately, limited scientifically rigorous information exists to inform decisions on use. Delta-9-tetrahydrocannabinol (THC, the main psychoactive component of cannabis) can cross the placenta and bind to cannabinoid receptor 1 (CB1) on the fetus. Because CB1 receptors are expressed in cardiomyocytes and endothelial cells, this suggests that THC exposure may impact fetal cardiovascular development. To understand this impact, our group used an established rhesus macaque model of chronic edible THC use during pregnancy. Animals were slowly titrated to a heavy THC dose (2.5mg/7kg/day) for 4 months preconception. Dams continued this daily THC dose throughout pregnancy with c-section delivery near term. Our model showed a decreased heart-to-body weight ratio from THC exposure. We examined the underlying changes in this selective fetal growth restriction of the cardiovascular system through tissue, protein, and gene expression analyses. H istological analysis of coronal sections of the heart and cross sections of the aorta showed no changes in collagen expression or maturity. Western blot analysis of collagen III expression showed no changes in left or right ventricle. Elastin expression was also unchanged in the aorta. To assess transcriptional changes, we performed bulk RNA-sequencing of vascular cells in the fetal aorta, umbilical vein, and umbilical artery, which revealed differentially expressed genes involved in metabolism and inflammation. These results suggest potential cardiovascular harm from in utero THC exposure by altering endothelial metabolism and inflammation.
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