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Titel: Blood transcriptome analysis suggests an indirect molecular association of early life adversities and adult social anxiety disorder by immune-related signal transduction
VerfasserIn: Edelmann, Susanne
Wiegand, Ariane
Hentrich, Thomas
Pasche, Sarah
Schulze-Hentrich, Julia Maria
Munk, Matthias H. J.
Fallgatter, Andreas J.
Kreifelts, Benjamin
Nieratschker, Vanessa
Sprache: Englisch
Titel: Frontiers in Psychiatry
Bandnummer: 14
Verlag/Plattform: Frontiers
Erscheinungsjahr: 2023
Freie Schlagwörter: RNA sequencing
gene expression
social anxiety disorder
early life adversity
transcriptome
immune system
signal transduction
DDC-Sachgruppe: 500 Naturwissenschaften
Dokumenttyp: Journalartikel / Zeitschriftenartikel
Abstract: Social anxiety disorder (SAD) is a psychiatric disorder characterized by severe fear in social situations and avoidance of these. Multiple genetic as well as environmental factors contribute to the etiopathology of SAD. One of the main risk factors for SAD is stress, especially during early periods of life (early life adversity; ELA). ELA leads to structural and regulatory alterations contributing to disease vulnerability. This includes the dysregulation of the immune response. However, the molecular link between ELA and the risk for SAD in adulthood remains largely unclear. Evidence is emerging that long-lasting changes of gene expression patterns play an important role in the biological mechanisms linking ELA and SAD. Therefore, we conducted a transcriptome study of SAD and ELA performing RNA sequencing in peripheral blood samples. Analyzing differential gene expression between individuals suffering from SAD with high or low levels of ELA and healthy individuals with high or low levels of ELA, 13 significantly differentially expressed genes (DEGs) were identified with respect to SAD while no significant differences in expression were identified with respect to ELA. The most significantly expressed gene was MAPK3 (p = 0.003) being upregulated in the SAD group compared to control individuals. In contrary, weighted gene co-expression network analysis (WGCNA) identified only modules significantly associated with ELA (p ≤ 0.05), not with SAD. Furthermore, analyzing interaction networks of the genes from the ELA-associated modules and the SAD-related MAPK3 revealed complex interactions of those genes. Gene functional enrichment analyses indicate a role of signal transduction pathways as well as inflammatory responses supporting an involvement of the immune system in the association of ELA and SAD. In conclusion, we did not identify a direct molecular link between ELA and adult SAD by transcriptional changes. However, our data indicate an indirect association of ELA and SAD mediated by the interaction of genes involved in immune-related signal transduction.
DOI der Erstveröffentlichung: 10.3389/fpsyt.2023.1125553
URL der Erstveröffentlichung: https://doi.org/10.3389/fpsyt.2023.1125553
Link zu diesem Datensatz: urn:nbn:de:bsz:291--ds-427686
hdl:20.500.11880/38355
http://dx.doi.org/10.22028/D291-42768
ISSN: 1664-0640
Datum des Eintrags: 5-Sep-2024
Bezeichnung des in Beziehung stehenden Objekts: Supplementary Material
In Beziehung stehendes Objekt: https://www.frontiersin.org/api/v3/articles/1125553/file/Data_Sheet_1.docx/1125553_supplementary-materials_datasheets_1_docx/1?isPublishedV2=false
https://www.frontiersin.org/api/v3/articles/1125553/file/Data_Sheet_2.xlsx/1125553_supplementary-materials_datasheets_2_xlsx/2?isPublishedV2=false
Fakultät: NT - Naturwissenschaftlich- Technische Fakultät
Fachrichtung: NT - Biowissenschaften
Professur: NT - Prof. Dr. Julia Schulze-Hentrich
Sammlung:SciDok - Der Wissenschaftsserver der Universität des Saarlandes

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