{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zou Z"],"funding":["National Nature Science Fund of China","Guangdong International Training Program for Outstanding Young Scientific Talents of University","Scientific Research Staring Foundation for Talent Introduction for Southern Medical University","Guangdong Natural Science Foundation of China","Certificate of China Postdoctoral Science Foundation Grant","Youth Scientific Research Staring Foundation for the Third Affiliated Hospital of Southern Medical University"],"pagination":["46"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8832692"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["19(1)"],"pubmed_abstract":["<h4>Background</h4>Traumatic brain injury (TBI) remains one of the main causes for disability and death worldwide. While the primary mechanical injury cannot be avoided, the prevention of secondary injury is the focus of TBI research. Present study aimed to elucidate the effects and mechanisms of S100B and its receptor RAGE on mediating secondary injury after TBI.<h4>Methods</h4>This study established TBI animal model by fluid percussion injury in rats, cell model by stretch-injured in astrocytes, and endothelial injury model with conditioned medium stimulation. Pharmacological intervention was applied to interfere the activities of S100B/RAGE/ADAM17 signaling pathway, respectively. The expressions or contents of S100B, RAGE, syndecan-1 and ADAM17 in brain and serum, as well as in cultured"],"journal":["Journal of neuroinflammation"],"pubmed_title":["The role of S100B/RAGE-enhanced ADAM17 activation in endothelial glycocalyx shedding after traumatic brain injury."],"pmcid":["PMC8832692"],"funding_grant_id":["NO.2020A1515010092","NO. 2019Q006","NO.81870210","NO.2019A1515010295","NO.81901997","NO.2019M652960","NO.82172139","NO.2019A1515012022","NO.2019M652965"],"pubmed_authors":["Zou Z","Cai D","Zhang K","Maegele M","Zhao P","Li Q","Gu Z","Liu C","Huang Q","Li L"],"additional_accession":[]},"is_claimable":false,"name":"The role of S100B/RAGE-enhanced ADAM17 activation in endothelial glycocalyx shedding after traumatic brain injury.","description":"<h4>Background</h4>Traumatic brain injury (TBI) remains one of the main causes for disability and death worldwide. While the primary mechanical injury cannot be avoided, the prevention of secondary injury is the focus of TBI research. Present study aimed to elucidate the effects and mechanisms of S100B and its receptor RAGE on mediating secondary injury after TBI.<h4>Methods</h4>This study established TBI animal model by fluid percussion injury in rats, cell model by stretch-injured in astrocytes, and endothelial injury model with conditioned medium stimulation. Pharmacological intervention was applied to interfere the activities of S100B/RAGE/ADAM17 signaling pathway, respectively. The expressions or contents of S100B, RAGE, syndecan-1 and ADAM17 in brain and serum, as well as in cultured","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Feb","modification":"2025-04-04T20:22:08.243Z","creation":"2025-04-04T20:22:08.243Z"},"accession":"S-EPMC8832692","cross_references":{"pubmed":["35148784"],"doi":["10.1186/s12974-022-02412-2"]}}