Fig. 7

NRG-1 attenuates mortality associated with ECM through ErbB4/STAT3/AKT signaling. Protein lysates from different brain regions including the cortex and hippocampus of ECM mice subjected to exogenously infused NRG-1 were probed with antibodies against phosphorylated STAT3, total STAT3, phosphorylated ErbB4 (Tyr1284), total ErbB4 (tErbB4), phosphorylated AKT, and total AKT as indicated. a pErbB4 levels increased in PbA-infected mice treated with NRG-1 and ARM individually in brain cortex. b Exogenous treatment of NRG-1 and/or ARM inhibited activation of STAT3 and increased activation of pAKT in the brain cortex. Beneath the Western blot is the densitometric analysis of the bands performed with the ImageQuant program. The data are expressed as the fold stimulation relative to appropriate controls and are the mean ± SE of duplicated samples performed in three independent experiments. (*p < 0.05, **p < 0.01, compared to infected sample at first column). c pErbB4 levels increased in PbA-infected mice treated with NRG-1 and ARM individually, while there was a robust increase when treated with both NRG-1 and ARM (NRG-1/ARM) in pooled samples prepared from hippocampal tissues. d Exogenous treatment of NRG-1 and/or ARM inhibited activation of STAT3 and increased activation of pAKT in brain hippocampus. Beneath the Western blot is the densitometric analysis of the bands performed with the ImageQuant program. The data are expressed as the fold stimulation relative to appropriate controls and are the mean ± SE of duplicated samples performed in three independent experiments. (*p < 0.05, **p < 0.01, compared to infected sample at first column). All the data represent one of three independent experiments with similar results