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Common genes and pathways involved in the response to stressful stimuli by astrocytes: A meta-analysis of genome-wide expression studies

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posted on 2021-02-02, 10:29 authored by Yeimy González-Giraldo, Diego A. Forero, George E. Barreto, Andrés Felipe Aristizábal-Pachón
Astrocytes play pivotal roles in the brain and they become reactive under stress conditions. Here, we carried out, for the first time, an integrative meta-analysis of genome-wide expression profiling of astrocytes from human and mouse exposed to different stressful stimuli (hypoxia, infections by virus and bacteria, cytokines, ethanol, among others). We identified common differentially expressed genes and pathways in human and murine astrocytes. Our results showed that astrocytes induce expression of genes associated with stress response and immune system regulation when they are exposed to stressful stimuli, whereas genes related to neurogenesis are found as downregulated. Several of the identified genes showed to be important hubs in the protein-protein interaction analysis (TRAF2, CDC37 and PAX6). This work demonstrates that despite astrocytes are highly heterogeneous and complex, there are common gene expression signatures that can be triggered under distinct detrimental stimuli, which opens an opportunity for exploring other possible markers of reactivity.

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Publication

Genomics;113(2), pp. 669-680

Publisher

Elsevier

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peer-reviewed The full text of this article will not be available in ULIR until the embargo expires on 21/01/2022

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Colciencias

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This is the author’s version of a work that was accepted for publication in Genomics. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Genomics, Vol. 113(2), pp. 669-680 https://doi.org/10.1016/j.ygeno.2021.01.008

Language

English

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