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Erschienen in: Metabolic Brain Disease 2/2020

14.11.2019 | Original Article

IFNG/IFNG-AS1 expression level balance: implications for autism spectrum disorder

verfasst von: Hamid Fallah, Arezou Sayad, Fatemeh Ranjbaran, Fatemeh Talebian, Soudeh Ghafouri-Fard, Mohammad Taheri

Erschienen in: Metabolic Brain Disease | Ausgabe 2/2020

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Abstract

Autism spectrum disorder (ASD) is a neurodevelopmental disorder associated with different epidemiological, genetic, epigenetic, and environmental factors. Although its etiology is not fully understood, immune dysfunction is implicated in this disease. Recently, a large number of genes encoding long noncoding RNAs (lncRNAs) were discovered which act as positive or negative regulators of neighboring target genes. The lncRNA, Interferon gamma-antisense RNA (IFNG-AS1), regulates expression levels of the Interferon gamma (IFNG) gene. In the present study, we investigated expression of IFNG and IFNG-AS1 in 50 children with ASD (15 females and 35 males, mean age: 6 ± 1.4 years) and 50 healthy controls (14 females and 36 males, mean age: 6 ± 1.74 years) by real time PCR technique. The results showed significant up-regulation of IFNG and down-regulation of IFNG-AS1 expression in children with ASD compared to controls (Fold change = 1.5, P < 0.0001; Fold change = −0.143, P = 0.013, respectively). The IFNG expression level increase was more pronounced in male ASD children (Fold change = 1.621; p < 0.0001). Our data reveal a functional disruption in the interactive network of IFNG/IFNG-AS1 regulation, which could be a contributing factor in the chronic inflammatory aspect of ASD. Our findings can help understanding the underlying contributors to ASD pathogenesis and find novel treatment options for children with ASD.
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Metadaten
Titel
IFNG/IFNG-AS1 expression level balance: implications for autism spectrum disorder
verfasst von
Hamid Fallah
Arezou Sayad
Fatemeh Ranjbaran
Fatemeh Talebian
Soudeh Ghafouri-Fard
Mohammad Taheri
Publikationsdatum
14.11.2019
Verlag
Springer US
Erschienen in
Metabolic Brain Disease / Ausgabe 2/2020
Print ISSN: 0885-7490
Elektronische ISSN: 1573-7365
DOI
https://doi.org/10.1007/s11011-019-00510-4

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