Fig. 6

Up-regulation of ADAM17 after TBI contributes to EG damage. A Representative blots of pADAM17, mADAM17 and syndecan-1 in injured brain and in serum of TBI rats, and TBI plus TAPI-1. GADPH was used as a soluble loading control (left panel). In addition, quantification (histograms of right panels) of pADAM17, mADAM17, and syndecan-1 in brain lysates and in serum from representative blots shown in left panel. *p < 0.05 compared with Sham group, ^#p < 0.05 compared with TBI group, n = 6. B Representative blots of pADAM17, mADAM17 and syndecan-1 in RAECs and in cultured medium after treatment of stretch injured-conditioned medium or injured medium plus ADAM17 inhibitor TAPI-1. GADPH was used as a soluble loading control (left panel). In addition, quantification (histograms of right panels) of pADAM17, mADAM17, and syndecan-1 in cell lysates and in medium from representative blots shown in left panel. *p < 0.05 compared with control group, ^#p < 0.05 compared with conditioned medium-treated group, n = 3. C Representative confocal images showing the subcellular localization of syndecan-1 and vWF in the brain tissue of TBI rats treated with TAPI-1. Scale bar = 100 μm. The immunofluorescence intensity of syndecan-1 in brain tissue from five fields per rat in each group. The relative fluorescence intensity was quantified and reported as relative fluorescence units (RFUs). *p < 0.05 compared with Sham group, ^#p < 0.05 compared with TBI group, n = 3. D Representative confocal images showing the expression and distribution of syndecan-1 in RAECs treated with TAPI-1. Scale bar = 50 μm. The immunofluorescence intensity of syndecan-1 in cells from five fields per sample in each group was quantified and reported as relative fluorescence units (RFUs). *p < 0.05 compared with control group, ^#p < 0.05 compared with conditioned medium-treated group, n = 3