Fig. 4
From: Tau exacerbates excitotoxic brain damage in an animal model of stroke
Excitotoxic seizures and transient MCAO cause similar differential gene regulation in tau−/− mice. a Immediate early gene (IEG) activation for Arc, Fos and Junb in the affected hemisphere (ipsilateral) 1 h after transient MCAO in tau+/+ and tau−/− mice (**p < 0.01; N = 6; Student’s t-test). No gene induction occurred on the contralateral side. b Time course of IEG mRNA induction of Arc, Fos and Junb after PTZ administration in tau+/+ but little to none in tau−/− mice (*p < 0.05; ***p < 0.001; ****p < 0.0001; N = 6 per time point; two-way ANOVA (Holm-Sidak post hoc)). mRNA levels were determined by real-time PCR (rtPCR) using gene-specific primers listed in Supplementary Table 3. c Whole transcriptome sequencing of tau−/− and tau+/+ mice treated with vehicle or PTZ revealed pronounced lack of gene induction/suppression 1 h after treatment in tau−/− mice. Red indicates up- and green down-regulation. Only genes with significant differential regulation are displayed. The displayed gene names are listed in order in Supplementary Data 1. d Quantitative rtPCR confirms differential regulation of selected transcripts from (see c) tau−/− mice (*p < 0.05; ***p < 0.0001; N = 6; Student’s t-test), as well as similar regulation of others (selected from Supplementary Fig. 6 and Supplementary Data 2) in tau−/− and tau+/+ mice. e Quantitative rtPCR showed a similar pattern of differentially regulated genes in the ipsilateral hemisphere after transient MCAO compared to after PTZ (see d) (*p < 0.05; ***p < 0.0001; N = 6; Student’s t-test), while there was no deregulation contralaterally in tau−/− and tau+/+ mice. f DAVID pathway analysis of genes that lacked response to PTZ administration in tau−/− mice (see c) identified pathways that were up- (black) and down-regulated (gray) in tau+/+ mice. All error bars are s.e.m
