Dataset Information

Gene expression profiling of mouse placenta following prenatal cannabis smoke exposure

ABSTRACT: Prenatal cannabis use is increasing, yet the effects of inhaled cannabis smoke on placental molecular function remain poorly defined. The goal of this study was to characterize placental transcriptomic alterations following prenatal cannabis smoke exposure using a physiologically relevant inhalation model. Timed-pregnant CD1 mice were exposed to cannabis cigarette smoke or room air from embryonic day 6.5 to embryonic day 18.5. Placental tissues were collected at embryonic day 18.5 and analyzed using Affymetrix Clariom S Mouse microarrays. The dataset includes 14 placental samples from control and cannabis smoke-exposed pregnancies, with fetal sex included as a biological variable. Differential gene expression was analyzed using linear modeling with false discovery rate correction. Pathway enrichment analyses and gene set variation analyses were performed to identify biological and compartment-associated transcriptomic changes. Select genes were validated by quantitative PCR. Large-scale transcriptomic profiles showed no distinct clustering by exposure; however, 23 genes were significantly altered using a false discovery rate <0.05 and absolute log2 fold change >0.5 threshold. Pathway analyses revealed overall suppression of oxidative phosphorylation, fatty acid metabolism, and transmembrane transport, alongside enrichment of RNA processing and stress-response pathways. Gene set variation analysis demonstrated reduced labyrinth zone-associated signatures and increased junctional zone-associated signatures in exposed placentae. Quantitative PCR confirmed altered expression of multiple transport-related genes. Together, these findings indicate that prenatal cannabis smoke exposure induces subtle yet coordinated placental transcriptomic reprogramming, characterized by impaired metabolic and transport pathways and altered compartment-specific activity. This dataset provides mechanistic insight into how inhaled cannabis exposure may compromise placental function and contribute to adverse pregnancy outcomes.

ORGANISM(S): Mus musculus

PROVIDER: GSE337449 | GEO | 2026/09/28

REPOSITORIES: GEO

ACCESS DATA

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Project description:Background: How prenatal smoke exposure affects DNA methylation leading to atopic disorders remains to be addressed. Epigenetic biomarkers informative of prenatal smoke exposure and atopic disorders are wanting. Since most children suffering from atopic dermatitis (AD) continue to develop asthma later in life, we explored whether prenatal smoke exposure e induces DNA methylation and searched for predictive epigenetic biomarkers for smoke related atopic disorders. Methods: Methylation differences associated with smoke exposure were screened by Illumina methylation panel for children from the Taiwan birth panel study cohort initially. Information about development of atopic dermatitis (AD) and risk factors were collected. Cord blood cotinine levels were measured to represent prenatal smoke exposure. CpG loci that demonstrated a statistically significant difference in methylation were validated by methylation-dependent fragment separation (MDFS). Differential methylation in three genes (TSLP, GSTT1, and CYB5R3) was identified through the screen and their functions were investigated. Results: Among these, only thymic stromal lymphopoietin (TSLP) gene displayed significant difference in promoter methylation percentage after being validated by MDFS (p=0.029). TSLP gene was further investigated in a larger sample of 92 children from the cohort. Methylation status of the TSLP 5′-CpG island (CGI) was found to be significantly associated with prenatal smoke exposure (OR=3.59, 95%CI=1.49-8.64; cotinine level 0.10 ng/ml, sensitivity= 77%; specificity = 61%) and with AD (OR=4.77, 95%CI=1.47-15.53). The degree of TSLP 5′CGI methylation inversely correlated with TSLP protein expression levels (per unit: β=－6.69 ng/ml; 95% CIs, －12.80~－0.59; p=0.032). Conclusions: The effect of prenatal tobacco smoke exposure on the risk for AD may be mediated through DNA methylation. Cord blood methylated TSLP 5′CGI may be a potential epigenetic biomarker for environmentally-related atopic disorders.

Dataset Information

Gene expression profiling of mouse placenta following prenatal cannabis smoke exposure

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets