Fig. 3: Gene expression profiles of iPSC-derived astrocytes in response to treatment with EtOH, acamprosate or naltrexone. | Translational Psychiatry

Fig. 3: Gene expression profiles of iPSC-derived astrocytes in response to treatment with EtOH, acamprosate or naltrexone.

From: Molecular mechanisms involved in alcohol craving, IRF3, and endoplasmic reticulum stress: a multi-omics study

Fig. 3

A The volcano plots show differential gene expression profiles after exposure to EtOH (25 mM), acamprosate (5 µM) or naltrexone (30 nM) for 7 days, respectively, as compared to vehicle treatment. RNA-seq was performed using iPSC-derived astrocytes from six AUD subjects. Two biological replicates were performed for each sample. B Effects of EtOH, acamprosate or naltrexone in iPSC-derived astrocytes on expression of genes encoding inflammatory mediators, as determined by RNA-seq. *FDR < 0.05. C Left panel: Venn diagram showing the 1836 genes with expression that was affected by both EtOH and acamprosate as determined by RNA-seq (FDR < 0.05). Right panel: Heatmap showing expression profiles for the 1836 genes were affected by both EtOH and acamprosate. Note that the expression of these genes was “anti-correlated” when results after EtOH and acamprosate treatment were compared. D Left panel: Venn diagram showing expression profiles for the 1376 genes with expression that could be affected by EtOH, acamprosate, and naltrexone as determined by RNA-seq (FDR < 0.05). Right panel: Heatmap showing expression profiles for the 1376 genes affected by EtOH, acamprosate and naltrexone. Note that the expression of these genes was “anti-correlated” when comparing results after EtOH and after anti-craving drug exposure.

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