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

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 recepto...

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Published inJournal of neuroinflammation Vol. 19; no. 1; pp. 46 - 21
Main Authors Zou, Zhimin, Li, Li, Li, Qin, Zhao, Peng, Zhang, Kun, Liu, Chengyong, Cai, Daozhang, Maegele, Marc, Gu, Zhengtao, Huang, Qiaobing
Format Journal Article
LanguageEnglish
Published England BioMed Central Ltd 11.02.2022
BioMed Central
BMC
Subjects
ADAM17
ADAM17 Protein - metabolism
Animal models
Animals
Astrocytes
Blood-brain barrier
Blood-Brain Barrier - metabolism
Brain
Brain Injuries, Traumatic - metabolism
Capillary Permeability
Endothelial cells
Endothelial Cells - metabolism
Endothelial glycocalyx
Glycocalyx
Glycocalyx - metabolism
Health aspects
Immunofluorescence
Injuries
Laboratory animals
Lungs
Pathogens
Permeability
Rats
Rodents
S100 Calcium Binding Protein beta Subunit - metabolism
S100b protein
S100B/RAGE
Secondary injury
Signal transduction
Syndecan
Trauma
Traumatic brain injury
Tumor necrosis factor
Tumor necrosis factor-TNF
China
United States > US
S100B/RAGE
Secondary injury
Endothelial glycocalyx
ADAM17
Traumatic brain injury
Blood–brain barrier
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Abstract 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. 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 cells and medium, were detected by western blot. The distribution of relative molecules was observed with immunofluorescence. We found that TBI could activate the release of S100B, mostly from astrocytes, and S100B and RAGE could mutually regulate their expression and activation. Most importantly, present study revealed an obvious increase of syndecan-1 in rat serum or in endothelial cultured medium after injury, and a significant decrease in tissue and in cultured endothelial cells, indicating TBI-induced shedding of endothelial glycocalyx. The data further proved that the activation of S100B/RAGE signaling could promote the shedding of endothelial glycocalyx by enhancing the expression, translocation and activity of ADAM17, an important sheddase, in endothelial cells. The damage of endothelial glycocalyx consequently aggravated blood brain barrier (BBB) dysfunction and systemic vascular hyper-permeability, overall resulting in secondary brain and lung injury. TBI triggers the activation of S100B/RAGE signal pathway. The regulation S100B/RAGE on ADAM17 expression, translocation and activation further promotes the shedding of endothelial glycocalyx, aggravates the dysfunction of BBB, and increases the vascular permeability, leading to secondary brain and lung injury. Present study may open a new corridor for the more in-depth understanding of the molecular processes responsible for cerebral and systemic vascular barrier impairment and secondary injury after TBI.
AbstractList 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.BACKGROUNDTraumatic 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.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 cells and medium, were detected by western blot. The distribution of relative molecules was observed with immunofluorescence.METHODSThis 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 cells and medium, were detected by western blot. The distribution of relative molecules was observed with immunofluorescence.We found that TBI could activate the release of S100B, mostly from astrocytes, and S100B and RAGE could mutually regulate their expression and activation. Most importantly, present study revealed an obvious increase of syndecan-1 in rat serum or in endothelial cultured medium after injury, and a significant decrease in tissue and in cultured endothelial cells, indicating TBI-induced shedding of endothelial glycocalyx. The data further proved that the activation of S100B/RAGE signaling could promote the shedding of endothelial glycocalyx by enhancing the expression, translocation and activity of ADAM17, an important sheddase, in endothelial cells. The damage of endothelial glycocalyx consequently aggravated blood brain barrier (BBB) dysfunction and systemic vascular hyper-permeability, overall resulting in secondary brain and lung injury.RESULTSWe found that TBI could activate the release of S100B, mostly from astrocytes, and S100B and RAGE could mutually regulate their expression and activation. Most importantly, present study revealed an obvious increase of syndecan-1 in rat serum or in endothelial cultured medium after injury, and a significant decrease in tissue and in cultured endothelial cells, indicating TBI-induced shedding of endothelial glycocalyx. The data further proved that the activation of S100B/RAGE signaling could promote the shedding of endothelial glycocalyx by enhancing the expression, translocation and activity of ADAM17, an important sheddase, in endothelial cells. The damage of endothelial glycocalyx consequently aggravated blood brain barrier (BBB) dysfunction and systemic vascular hyper-permeability, overall resulting in secondary brain and lung injury.TBI triggers the activation of S100B/RAGE signal pathway. The regulation S100B/RAGE on ADAM17 expression, translocation and activation further promotes the shedding of endothelial glycocalyx, aggravates the dysfunction of BBB, and increases the vascular permeability, leading to secondary brain and lung injury. Present study may open a new corridor for the more in-depth understanding of the molecular processes responsible for cerebral and systemic vascular barrier impairment and secondary injury after TBI.CONCLUSIONSTBI triggers the activation of S100B/RAGE signal pathway. The regulation S100B/RAGE on ADAM17 expression, translocation and activation further promotes the shedding of endothelial glycocalyx, aggravates the dysfunction of BBB, and increases the vascular permeability, leading to secondary brain and lung injury. Present study may open a new corridor for the more in-depth understanding of the molecular processes responsible for cerebral and systemic vascular barrier impairment and secondary injury after TBI.
Abstract Background 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. Methods 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 cells and medium, were detected by western blot. The distribution of relative molecules was observed with immunofluorescence. Results We found that TBI could activate the release of S100B, mostly from astrocytes, and S100B and RAGE could mutually regulate their expression and activation. Most importantly, present study revealed an obvious increase of syndecan-1 in rat serum or in endothelial cultured medium after injury, and a significant decrease in tissue and in cultured endothelial cells, indicating TBI-induced shedding of endothelial glycocalyx. The data further proved that the activation of S100B/RAGE signaling could promote the shedding of endothelial glycocalyx by enhancing the expression, translocation and activity of ADAM17, an important sheddase, in endothelial cells. The damage of endothelial glycocalyx consequently aggravated blood brain barrier (BBB) dysfunction and systemic vascular hyper-permeability, overall resulting in secondary brain and lung injury. Conclusions TBI triggers the activation of S100B/RAGE signal pathway. The regulation S100B/RAGE on ADAM17 expression, translocation and activation further promotes the shedding of endothelial glycocalyx, aggravates the dysfunction of BBB, and increases the vascular permeability, leading to secondary brain and lung injury. Present study may open a new corridor for the more in-depth understanding of the molecular processes responsible for cerebral and systemic vascular barrier impairment and secondary injury after TBI.
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. 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 cells and medium, were detected by western blot. The distribution of relative molecules was observed with immunofluorescence. We found that TBI could activate the release of S100B, mostly from astrocytes, and S100B and RAGE could mutually regulate their expression and activation. Most importantly, present study revealed an obvious increase of syndecan-1 in rat serum or in endothelial cultured medium after injury, and a significant decrease in tissue and in cultured endothelial cells, indicating TBI-induced shedding of endothelial glycocalyx. The data further proved that the activation of S100B/RAGE signaling could promote the shedding of endothelial glycocalyx by enhancing the expression, translocation and activity of ADAM17, an important sheddase, in endothelial cells. The damage of endothelial glycocalyx consequently aggravated blood brain barrier (BBB) dysfunction and systemic vascular hyper-permeability, overall resulting in secondary brain and lung injury. TBI triggers the activation of S100B/RAGE signal pathway. The regulation S100B/RAGE on ADAM17 expression, translocation and activation further promotes the shedding of endothelial glycocalyx, aggravates the dysfunction of BBB, and increases the vascular permeability, leading to secondary brain and lung injury. Present study may open a new corridor for the more in-depth understanding of the molecular processes responsible for cerebral and systemic vascular barrier impairment and secondary injury after TBI.
Background 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. Methods 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 cells and medium, were detected by western blot. The distribution of relative molecules was observed with immunofluorescence. Results We found that TBI could activate the release of S100B, mostly from astrocytes, and S100B and RAGE could mutually regulate their expression and activation. Most importantly, present study revealed an obvious increase of syndecan-1 in rat serum or in endothelial cultured medium after injury, and a significant decrease in tissue and in cultured endothelial cells, indicating TBI-induced shedding of endothelial glycocalyx. The data further proved that the activation of S100B/RAGE signaling could promote the shedding of endothelial glycocalyx by enhancing the expression, translocation and activity of ADAM17, an important sheddase, in endothelial cells. The damage of endothelial glycocalyx consequently aggravated blood brain barrier (BBB) dysfunction and systemic vascular hyper-permeability, overall resulting in secondary brain and lung injury. Conclusions TBI triggers the activation of S100B/RAGE signal pathway. The regulation S100B/RAGE on ADAM17 expression, translocation and activation further promotes the shedding of endothelial glycocalyx, aggravates the dysfunction of BBB, and increases the vascular permeability, leading to secondary brain and lung injury. Present study may open a new corridor for the more in-depth understanding of the molecular processes responsible for cerebral and systemic vascular barrier impairment and secondary injury after TBI. Keywords: Traumatic brain injury, Secondary injury, Blood-brain barrier, Endothelial glycocalyx, S100B/RAGE, ADAM17
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. 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 cells and medium, were detected by western blot. The distribution of relative molecules was observed with immunofluorescence. We found that TBI could activate the release of S100B, mostly from astrocytes, and S100B and RAGE could mutually regulate their expression and activation. Most importantly, present study revealed an obvious increase of syndecan-1 in rat serum or in endothelial cultured medium after injury, and a significant decrease in tissue and in cultured endothelial cells, indicating TBI-induced shedding of endothelial glycocalyx. The data further proved that the activation of S100B/RAGE signaling could promote the shedding of endothelial glycocalyx by enhancing the expression, translocation and activity of ADAM17, an important sheddase, in endothelial cells. The damage of endothelial glycocalyx consequently aggravated blood brain barrier (BBB) dysfunction and systemic vascular hyper-permeability, overall resulting in secondary brain and lung injury. TBI triggers the activation of S100B/RAGE signal pathway. The regulation S100B/RAGE on ADAM17 expression, translocation and activation further promotes the shedding of endothelial glycocalyx, aggravates the dysfunction of BBB, and increases the vascular permeability, leading to secondary brain and lung injury. Present study may open a new corridor for the more in-depth understanding of the molecular processes responsible for cerebral and systemic vascular barrier impairment and secondary injury after TBI.
Background 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. Methods 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 cells and medium, were detected by western blot. The distribution of relative molecules was observed with immunofluorescence. Results We found that TBI could activate the release of S100B, mostly from astrocytes, and S100B and RAGE could mutually regulate their expression and activation. Most importantly, present study revealed an obvious increase of syndecan-1 in rat serum or in endothelial cultured medium after injury, and a significant decrease in tissue and in cultured endothelial cells, indicating TBI-induced shedding of endothelial glycocalyx. The data further proved that the activation of S100B/RAGE signaling could promote the shedding of endothelial glycocalyx by enhancing the expression, translocation and activity of ADAM17, an important sheddase, in endothelial cells. The damage of endothelial glycocalyx consequently aggravated blood brain barrier (BBB) dysfunction and systemic vascular hyper-permeability, overall resulting in secondary brain and lung injury. Conclusions TBI triggers the activation of S100B/RAGE signal pathway. The regulation S100B/RAGE on ADAM17 expression, translocation and activation further promotes the shedding of endothelial glycocalyx, aggravates the dysfunction of BBB, and increases the vascular permeability, leading to secondary brain and lung injury. Present study may open a new corridor for the more in-depth understanding of the molecular processes responsible for cerebral and systemic vascular barrier impairment and secondary injury after TBI.
ArticleNumber 46
Audience Academic
Author Maegele, Marc
Li, Li
Zou, Zhimin
Gu, Zhengtao
Li, Qin
Liu, Chengyong
Zhang, Kun
Cai, Daozhang
Huang, Qiaobing
Zhao, Peng
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/35148784$$D View this record in MEDLINE/PubMed
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Cites_doi 10.1016/j.celrep.2017.09.074
10.1681/ASN.2014050477
10.1186/s13049-018-0565-3
10.1016/j.jamcollsurg.2017.05.012
10.1016/j.intimp.2021.107699
10.2147/NDT.S125620
10.1016/j.intimp.2019.106175
10.1089/neu.2014.3764
10.1007/s00701-016-3046-3
10.1089/neu.2020.7257
10.1038/s41598-018-36878-z
10.1111/j.1476-5381.2012.02132.x
10.1007/s10072-019-04238-y
10.1080/09537104.2016.1203396
10.7554/eLife.23968
10.1016/j.ejso.2007.04.009
10.1016/j.imbio.2019.11.022
10.1016/j.neuroscience.2010.07.009
10.1038/jcbfm.2015.165
10.1182/blood-2018-09-874552
10.1152/ajplung.00485.2016
10.3390/ijms22052439
10.1371/journal.pone.0078155
10.1186/1757-7241-21-77
10.1155/2010/656481
10.1186/s12974-021-02192-1
10.1074/jbc.M110.169342
10.1136/gutjnl-2013-305005
10.1080/14737159.2018.1428089
10.3389/fnins.2019.01178
10.1016/j.neurobiolaging.2008.05.017
10.1038/srep35067
10.1016/j.neuint.2016.02.013
10.1016/j.biopha.2019.109005
10.1111/jnc.12790
10.1186/s13036-019-0145-8
10.1007/s11064-017-2321-x
10.3791/55108
10.1002/jcb.28688
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Issue 1
Keywords S100B/RAGE
Secondary injury
Endothelial glycocalyx
ADAM17
Traumatic brain injury
Blood–brain barrier
Language English
License 2022. The Author(s).
Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
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References G Sorci (2412_CR4) 2010; 2010
C Iaccarino (2412_CR1) 2018; 62
D Slavoaca (2412_CR27) 2020; 41
G Esposito (2412_CR30) 2014; 63
L Mi (2412_CR19) 2019; 116
BI Martinez (2412_CR2) 2019; 13
S Sultana (2412_CR20) 2020; 225
H Kolářová (2412_CR31) 2015; 2014
XF Shao (2412_CR42) 2020; 79
A Villarreal (2412_CR28) 2014; 131
M Cavadas (2412_CR33) 2017; 21
S Yamamura (2412_CR18) 2013; 168
D Dreymueller (2412_CR35) 2017; 28
DVS Costa (2412_CR9) 2019; 9
SJ Gladman (2412_CR22) 2010; 171
MR Guilfoyle (2412_CR15) 2015; 32
PJ Hu (2412_CR40) 2017; 313
RE Gonzalez (2412_CR11) 2017; 225
RE Gonzalez (2412_CR32) 2018; 26
Y Ferrer-Acosta (2412_CR21) 2017; 128
B Balança (2412_CR3) 2021; 22
B Chen (2412_CR17) 2013; 21
I Lorenzen (2412_CR34) 2016; 6
NA Kerr (2412_CR41) 2021; 38
R Bianchi (2412_CR8) 2011; 286
A Dadas (2412_CR26) 2018; 14
EP Thelin (2412_CR5) 2017; 159
SE Hoey (2412_CR24) 2013; 8
S Zhang (2412_CR14) 2016; 96
I Salama (2412_CR16) 2008; 34
V Dinet (2412_CR39) 2019; 13
M Sillesen (2412_CR12) 2014; 76
A Bertram (2412_CR38) 2015; 26
R Bianchi (2412_CR7) 2010; 31
SV Kabadi (2412_CR29) 2015; 35
C Shen (2412_CR23) 2017; 42
Z Gu (2412_CR43) 2021; 98
J Streetley (2412_CR37) 2019; 133
Z Zou (2412_CR10) 2021; 18
X Dang (2412_CR13) 2014; 7
AG Grieve (2412_CR36) 2017; 6
KK Wang (2412_CR6) 2018; 18
XX Zhu (2412_CR25) 2019; 120
References_xml – volume: 21
  start-page: 745
  year: 2017
  ident: 2412_CR33
  publication-title: Cell Rep
  doi: 10.1016/j.celrep.2017.09.074
– volume: 62
  start-page: 535
  year: 2018
  ident: 2412_CR1
  publication-title: J Neurosurg Sci
– volume: 26
  start-page: 2860
  year: 2015
  ident: 2412_CR38
  publication-title: J Am Soc Nephrol
  doi: 10.1681/ASN.2014050477
– volume: 26
  start-page: 102
  year: 2018
  ident: 2412_CR32
  publication-title: Scand J Trauma Resusc Emerg Med
  doi: 10.1186/s13049-018-0565-3
– volume: 225
  start-page: 419
  year: 2017
  ident: 2412_CR11
  publication-title: J Am Coll Surg
  doi: 10.1016/j.jamcollsurg.2017.05.012
– volume: 98
  start-page: 107699
  year: 2021
  ident: 2412_CR43
  publication-title: Int Immunopharmacol
  doi: 10.1016/j.intimp.2021.107699
– volume: 14
  start-page: 2989
  year: 2018
  ident: 2412_CR26
  publication-title: Neuropsychiatr Dis Treat
  doi: 10.2147/NDT.S125620
– volume: 79
  start-page: 106175
  year: 2020
  ident: 2412_CR42
  publication-title: Int Immunopharmacol
  doi: 10.1016/j.intimp.2019.106175
– volume: 32
  start-page: 1553
  year: 2015
  ident: 2412_CR15
  publication-title: J Neurotrauma
  doi: 10.1089/neu.2014.3764
– volume: 159
  start-page: 209
  year: 2017
  ident: 2412_CR5
  publication-title: Acta Neurochir
  doi: 10.1007/s00701-016-3046-3
– volume: 7
  start-page: 3818
  year: 2014
  ident: 2412_CR13
  publication-title: Int J Clin Exp Pathol
– volume: 38
  start-page: 646
  year: 2021
  ident: 2412_CR41
  publication-title: J Neurotrauma
  doi: 10.1089/neu.2020.7257
– volume: 9
  start-page: 665
  year: 2019
  ident: 2412_CR9
  publication-title: Sci Rep-Uk
  doi: 10.1038/s41598-018-36878-z
– volume: 168
  start-page: 1088
  year: 2013
  ident: 2412_CR18
  publication-title: Br J Pharmacol
  doi: 10.1111/j.1476-5381.2012.02132.x
– volume: 41
  start-page: 2033
  year: 2020
  ident: 2412_CR27
  publication-title: Neurol Sci
  doi: 10.1007/s10072-019-04238-y
– volume: 28
  start-page: 354
  year: 2017
  ident: 2412_CR35
  publication-title: Platelets
  doi: 10.1080/09537104.2016.1203396
– volume: 6
  start-page: e23968
  year: 2017
  ident: 2412_CR36
  publication-title: Elife
  doi: 10.7554/eLife.23968
– volume: 34
  start-page: 357
  year: 2008
  ident: 2412_CR16
  publication-title: Eur J Surg Oncol
  doi: 10.1016/j.ejso.2007.04.009
– volume: 225
  start-page: 151887
  year: 2020
  ident: 2412_CR20
  publication-title: Immunobiology
  doi: 10.1016/j.imbio.2019.11.022
– volume: 171
  start-page: 577
  year: 2010
  ident: 2412_CR22
  publication-title: Neuroscience
  doi: 10.1016/j.neuroscience.2010.07.009
– volume: 35
  start-page: 2010
  year: 2015
  ident: 2412_CR29
  publication-title: J Cereb Blood Flow Metab
  doi: 10.1038/jcbfm.2015.165
– volume: 133
  start-page: 2707
  year: 2019
  ident: 2412_CR37
  publication-title: Blood
  doi: 10.1182/blood-2018-09-874552
– volume: 313
  start-page: L1
  year: 2017
  ident: 2412_CR40
  publication-title: Am J Physiol Lung Cell Mol Physiol
  doi: 10.1152/ajplung.00485.2016
– volume: 22
  start-page: 2439
  year: 2021
  ident: 2412_CR3
  publication-title: Int J Mol Sci
  doi: 10.3390/ijms22052439
– volume: 8
  start-page: e78155
  year: 2013
  ident: 2412_CR24
  publication-title: PLoS ONE
  doi: 10.1371/journal.pone.0078155
– volume: 21
  start-page: 77
  year: 2013
  ident: 2412_CR17
  publication-title: Scand J Trauma Resus
  doi: 10.1186/1757-7241-21-77
– volume: 2010
  year: 2010
  ident: 2412_CR4
  publication-title: Cardiovasc Psychiatry Neurol
  doi: 10.1155/2010/656481
– volume: 18
  start-page: 134
  year: 2021
  ident: 2412_CR10
  publication-title: J Neuroinflamm
  doi: 10.1186/s12974-021-02192-1
– volume: 76
  start-page: 19
  issue: 12–19
  year: 2014
  ident: 2412_CR12
  publication-title: J Trauma Acute Care Surg
– volume: 286
  start-page: 7214
  year: 2011
  ident: 2412_CR8
  publication-title: J Biol Chem
  doi: 10.1074/jbc.M110.169342
– volume: 63
  start-page: 1300
  year: 2014
  ident: 2412_CR30
  publication-title: Gut
  doi: 10.1136/gutjnl-2013-305005
– volume: 2014
  start-page: 694312
  year: 2015
  ident: 2412_CR31
  publication-title: Mediat Inflamm
– volume: 18
  start-page: 165
  year: 2018
  ident: 2412_CR6
  publication-title: Expert Rev Mol Diagn
  doi: 10.1080/14737159.2018.1428089
– volume: 13
  start-page: 1178
  year: 2019
  ident: 2412_CR39
  publication-title: Front Neurosci
  doi: 10.3389/fnins.2019.01178
– volume: 31
  start-page: 665
  year: 2010
  ident: 2412_CR7
  publication-title: Neurobiol Aging
  doi: 10.1016/j.neurobiolaging.2008.05.017
– volume: 6
  start-page: 35067
  year: 2016
  ident: 2412_CR34
  publication-title: Sci Rep-Uk
  doi: 10.1038/srep35067
– volume: 96
  start-page: 46
  year: 2016
  ident: 2412_CR14
  publication-title: Neurochem Int
  doi: 10.1016/j.neuint.2016.02.013
– volume: 116
  start-page: 109005
  year: 2019
  ident: 2412_CR19
  publication-title: Biomed Pharmacother
  doi: 10.1016/j.biopha.2019.109005
– volume: 131
  start-page: 190
  year: 2014
  ident: 2412_CR28
  publication-title: J Neurochem
  doi: 10.1111/jnc.12790
– volume: 13
  start-page: 16
  year: 2019
  ident: 2412_CR2
  publication-title: J Biol Eng
  doi: 10.1186/s13036-019-0145-8
– volume: 42
  start-page: 2902
  year: 2017
  ident: 2412_CR23
  publication-title: Neurochem Res
  doi: 10.1007/s11064-017-2321-x
– volume: 128
  start-page: 55108
  year: 2017
  ident: 2412_CR21
  publication-title: J Vis Exp
  doi: 10.3791/55108
– volume: 120
  start-page: 14127
  year: 2019
  ident: 2412_CR25
  publication-title: J Cell Biochem
  doi: 10.1002/jcb.28688
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Snippet Traumatic brain injury (TBI) remains one of the main causes for disability and death worldwide. While the primary mechanical injury cannot be avoided, the...
Background Traumatic brain injury (TBI) remains one of the main causes for disability and death worldwide. While the primary mechanical injury cannot be...
Abstract Background Traumatic brain injury (TBI) remains one of the main causes for disability and death worldwide. While the primary mechanical injury cannot...
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StartPage 46
SubjectTerms ADAM17
ADAM17 Protein - metabolism
Animal models
Animals
Astrocytes
Blood-brain barrier
Blood-Brain Barrier - metabolism
Brain
Brain Injuries, Traumatic - metabolism
Capillary Permeability
Endothelial cells
Endothelial Cells - metabolism
Endothelial glycocalyx
Glycocalyx
Glycocalyx - metabolism
Health aspects
Immunofluorescence
Injuries
Laboratory animals
Lungs
Pathogens
Permeability
Rats
Rodents
S100 Calcium Binding Protein beta Subunit - metabolism
S100b protein
S100B/RAGE
Secondary injury
Signal transduction
Syndecan
Trauma
Traumatic brain injury
Tumor necrosis factor
Tumor necrosis factor-TNF
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Title The role of S100B/RAGE-enhanced ADAM17 activation in endothelial glycocalyx shedding after traumatic brain injury
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