Contribution of maternal hypertension to autism etiology in a murine model; cerebellar gene expression

Abstract

Aim: To study the contribution of maternal hypertension to autism spectrum disorders’ (ASD) phenotype, and gene expression, in a murine model. Materials & methods: To examine the effects of maternal hypertension, we used a well-described transgenic mouse model lacking functional endothelial nitric oxide synthase (eNOS or NOS3). Behavioral testing was performed on male offspring between 8 and 10 weeks of age. Cerebella underwent shotgun transcriptome RNA sequencing. Differentially expressed genes were examined for Gene Ontology enrichment. 2-way-RM-ANOVA, 1-way-ANOVA and Student's t-test were used for statistical analysis. Results & conclusion: Our findings revealed that a deficit in social behavior, the hallmark of ASD, is differentially present in offspring born to hypertensive mothers. Novel ASD-related genes were differentially expressed in the cerebellum, implicating its possible role in ASD etiology. Condensation: Altered uterine environment resulting from maternal hypertension contributes to ASD phenotype, and modifies expression of novel ASD-related genes in cerebella of eNOS heterozygous offspring.