Contribution of maternal hypertension to autism etiology in a murine model; cerebellar gene expression. (February 2017)

• Record Type: Journal Article
• Authors: Moussa, Hind N; Sibai, Baha M; Blackwell, Sean C; Leon, Mateo G; Hylin, Michael J; Redell, John B; Liu, Yin; Dash, Pramod K; Longo, Monica
• Is Part Of: Future neurology. Volume 12:Number 1(2017)
• Page Start: 21
• Page End: 33
• Publication Date: 2017-02
• Subjects: autism spectrum disorders -- behavior -- cerebellum -- eNOS -- genes -- maternal hypertension -- offspring; Neurology -- Research -- Periodicals; 611.8005
• DOI: 10.2217/fnl-2016-0011
• Languages: English
• ISSNs: 1479-6708

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.