Keywords

DNA, methylation, WNT7a, Alcohol, mouse, WGBS

Abstract

Excessive drinking during early pregnancy is associated with fetal developmental anomalies [1], particularly affecting heart formation, known as Congenital Heart Disease (CHD). This health concern is underscored by studies that indicate a high incidence of binge drinking among expectant mothers [1]. This research delves into alcohol's role in altering epigenetic patterns across the embryonic cardiac genome, seeking to isolate genes and their specific sites influenced by in utero alcohol exposure.

The theory posits that ethanol-exposed embryonic mouse hearts will exhibit distinctive patterns of methylation in contrast to unexposed controls [2]. To investigate the proposed theory, ethanol was orally delivered to mouse models at a gestational stage critical for heart development, specifically embryonic day 9.5 (E9.5). Subsequently, at embryonic day 11.5 (E11.5)—a pivotal moment in cardiac morphogenesis—the mice were euthanized to harvest the embryonic hearts. The genomic material was then meticulously extracted from these hearts to enable a comprehensive analysis through whole-genome bisulfite sequencing (WGBS).

Preliminary results revealed a marginal shift toward lower methylation levels without broad genomic changes in the ethanol treated samples [7]. Nonetheless, particular genes, like WNT7A gene, have been pinpointed for their suppressed activity following alcohol exposure, guiding further inquiries into aimed methylation changes and epigenetic variations that may illuminate the mechanisms by which maternal alcohol consumption prompts cardiac anomalies in CHD [7]

Thesis Completion Year

2024

Thesis Completion Semester

Spring

Thesis Chair

Steven N. Ebert

College

College of Medicine

Department

Metabolic and cardiovascular division

Thesis Discipline

Medicine

Language

English

Access Status

Campus Access

Length of Campus Access

5 years

Campus Location

Health Sciences Campus

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Rights Statement

In Copyright