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Fig. 7 | Journal of Neuroinflammation

Fig. 7

From: The role of S100B/RAGE-enhanced ADAM17 activation in endothelial glycocalyx shedding after traumatic brain injury

Fig. 7

Activating S100B/RAGE signaling promotes ADAM17 expression and activation after TBI. A, B Representative blots of pADAM17, mADAM17 in injured brain and mADAM17 in serum of TBI rats, and TBI plus ONO-2506 (A) or FPS-ZM-1 (B). GADPH was used as a soluble loading control (left panel). In addition, quantification (histograms of right panel) of pADAM17, mADAM17 in brain lysates and mADAM17 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. C Representative blots of pADAM17, mADAM17 in RAECs and mADAM17 in cultured medium after stretch injured-conditioned medium or exogenous S100B administration. GADPH was used as a soluble loading control (left panel). In addition, quantification (histograms of right panel) of pADAM17, mADAM17 from representative blots shown in left panel. *p < 0.05 compared with Control group, n = 3. D, E Representative blots of pADAM17, mADAM17 in RAECs and mADAM17 in cultured medium after treatment of stretch injured-conditioned medium or injured medium plus S100B inhibitor ONO-2506 (D) or FPS-ZM-1 (E). GADPH was used as a soluble loading control (left panel). In addition, quantification (histograms of right panel) of pADAM17, mADAM17 in cell lysates and 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. F Representative confocal images showing the subcellular localization of ADAM17 with vWF in the brain tissue of rats treated with TBI, TBI plus ONO-2506 or FPS-ZM-1. Scale bar = 50 μm. The immunofluorescence intensity of ADAM17 in brain tissue from five fields per sample in each group were quantified and reported as relative fluorescence units (RFUs). *p < 0.05 compared with Sham group, #p < 0.05 compared with TBI group, n = 3

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