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Fig. 1 | Cell Communication and Signaling

Fig. 1

From: Egr-1 is a key regulator of the blood-brain barrier damage induced by meningitic Escherichia coli

Fig. 1

Meningitic E. coli infection massively increases Egr-1 activation in vitro and in vivo. A Plate array analysis of 96 TFs in hBMEC infected without or with meningitic E. coli. After 3 h of infection, the cells were subjected to nuclear extraction for the TF activation plate assay. Graph of gene array shows the activation or inhibition of 96 TFs in infected hBMEC compared with control hBMEC. B Real-time PCR determination of Egr-1 transcription in hBMEC upon infection. The transcription of β-actin was used as the internal reference. Data were presented as the mean ± SD from three independent experiments. *p < 0.05, ***p < 0.001. C Western blot analysis revealed increased expression of Egr-1 in hBMEC in response to infection. β-actin was used as the loading control, and densitometry was performed to analyze the differences. D Real-time PCR determination of Egr-1 transcription in microvessels isolated from the brains of bacterium-challenged mice at various time points. The transcription of β-actin was used as the internal reference. Data were presented as the mean ± SD from three independent experiments. *p < 0.05, **p < 0.01, and ***p < 0.001. E Microvessels isolated from the brains of bacterium-challenged mice at different time points were subjected to western blot analysis for expression of Egr-1. β-actin expression was used as the loading control, and densitometry of the bands was performed to compare differences

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