Formation of microparticles in the injured brain of patients with severe isolated traumatic brain injury
The potential pathophysiological role of circulating microparticles (MPs) has been recognized in various conditions, such as cardiovascular and thrombotic diseases. Traumatic brain injury (TBI) has a complex pathophysiology that involves coagulopathy and inflammation. We investigated endothelial-, p...
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| Veröffentlicht in: | Journal of neurotrauma 2014-12, Vol.31 (23), p.1927-1933 |
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| creator | Nekludov, Michael Mobarrez, Fariborz Gryth, Dan Bellander, Bo-Michael Wallen, Håkan |
| description | The potential pathophysiological role of circulating microparticles (MPs) has been recognized in various conditions, such as cardiovascular and thrombotic diseases. Traumatic brain injury (TBI) has a complex pathophysiology that involves coagulopathy and inflammation. We investigated endothelial-, platelet-, and leukocyte-derived microparticles (EMPs, PMPs, and LMPs, respectively) in 16 patients with severe isolated TBI. Arterial and cerebrovenous samples were taken repeatedly, during 1-72 h after injury. Subpopulations of MPs, exposing tissue factor (TF) and P-selection, were also studied. MP counts in cerebrovenous samples, irrespective of cellular origin, were higher in TBI cases, compared to healthy controls (peak levels of EMPs were approximately 7 times higher, PMPs 1.4 times higher, and LMPs 2 times higher, respectively; p |
| doi_str_mv | 10.1089/neu.2013.3168 |
| format | Article |
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Traumatic brain injury (TBI) has a complex pathophysiology that involves coagulopathy and inflammation. We investigated endothelial-, platelet-, and leukocyte-derived microparticles (EMPs, PMPs, and LMPs, respectively) in 16 patients with severe isolated TBI. Arterial and cerebrovenous samples were taken repeatedly, during 1-72 h after injury. Subpopulations of MPs, exposing tissue factor (TF) and P-selection, were also studied. MP counts in cerebrovenous samples, irrespective of cellular origin, were higher in TBI cases, compared to healthy controls (peak levels of EMPs were approximately 7 times higher, PMPs 1.4 times higher, and LMPs 2 times higher, respectively; p<0.001 for all). MP counts declined sharply from high levels shortly after the trauma toward slightly elevated levels 72 h later. EMPs and PMPs exposing TF, as well as PMPs exposing P-selection, showed a transcranial gradient with higher concentration in cerebrovenous, compared to arterial, samples. In contrast, LMPs exposing TF were higher in arterial samples, suggesting accumulation of LMPs in the brain. We conclude that the pattern of circulating MPs is altered after TBI. PMPs exposing P-selection and EMPs exposing TF seem to be generated in the injured brain, whereas LMPs exposing TF are accumulated. The pathophysiological significance of these changes in MP pattern in TBI should be further investigated. Including MPs exposing brain-specific antigens in the assessment of brain injury would give further information of origin and likely give additional information of the size of the injury, given that the MP phenotypes investigated in the present study are not brain-specific markers.</description><identifier>ISSN: 0897-7151</identifier><identifier>EISSN: 1557-9042</identifier><identifier>DOI: 10.1089/neu.2013.3168</identifier><identifier>PMID: 24956150</identifier><language>eng</language><publisher>United States: Mary Ann Liebert, Inc</publisher><subject>Adult ; Aged ; Atoms & subatomic particles ; Brain - metabolism ; Brain - pathology ; Brain damage ; Brain Injuries - metabolism ; Brain Injuries - pathology ; Cell-Derived Microparticles - metabolism ; Cell-Derived Microparticles - pathology ; Female ; Humans ; Male ; Middle Aged ; P-Selectin - metabolism ; Patients ; Thromboplastin - metabolism ; Young Adult</subject><ispartof>Journal of neurotrauma, 2014-12, Vol.31 (23), p.1927-1933</ispartof><rights>(©) Copyright 2014, Mary Ann Liebert, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c392t-9e53772985fd3ceb460f9e6959b1f78114b9fca9faefe438d507d8bd139571893</citedby><cites>FETCH-LOGICAL-c392t-9e53772985fd3ceb460f9e6959b1f78114b9fca9faefe438d507d8bd139571893</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24956150$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:130106742$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Nekludov, Michael</creatorcontrib><creatorcontrib>Mobarrez, Fariborz</creatorcontrib><creatorcontrib>Gryth, Dan</creatorcontrib><creatorcontrib>Bellander, Bo-Michael</creatorcontrib><creatorcontrib>Wallen, Håkan</creatorcontrib><title>Formation of microparticles in the injured brain of patients with severe isolated traumatic brain injury</title><title>Journal of neurotrauma</title><addtitle>J Neurotrauma</addtitle><description>The potential pathophysiological role of circulating microparticles (MPs) has been recognized in various conditions, such as cardiovascular and thrombotic diseases. Traumatic brain injury (TBI) has a complex pathophysiology that involves coagulopathy and inflammation. We investigated endothelial-, platelet-, and leukocyte-derived microparticles (EMPs, PMPs, and LMPs, respectively) in 16 patients with severe isolated TBI. Arterial and cerebrovenous samples were taken repeatedly, during 1-72 h after injury. Subpopulations of MPs, exposing tissue factor (TF) and P-selection, were also studied. MP counts in cerebrovenous samples, irrespective of cellular origin, were higher in TBI cases, compared to healthy controls (peak levels of EMPs were approximately 7 times higher, PMPs 1.4 times higher, and LMPs 2 times higher, respectively; p<0.001 for all). MP counts declined sharply from high levels shortly after the trauma toward slightly elevated levels 72 h later. EMPs and PMPs exposing TF, as well as PMPs exposing P-selection, showed a transcranial gradient with higher concentration in cerebrovenous, compared to arterial, samples. In contrast, LMPs exposing TF were higher in arterial samples, suggesting accumulation of LMPs in the brain. We conclude that the pattern of circulating MPs is altered after TBI. PMPs exposing P-selection and EMPs exposing TF seem to be generated in the injured brain, whereas LMPs exposing TF are accumulated. The pathophysiological significance of these changes in MP pattern in TBI should be further investigated. 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Traumatic brain injury (TBI) has a complex pathophysiology that involves coagulopathy and inflammation. We investigated endothelial-, platelet-, and leukocyte-derived microparticles (EMPs, PMPs, and LMPs, respectively) in 16 patients with severe isolated TBI. Arterial and cerebrovenous samples were taken repeatedly, during 1-72 h after injury. Subpopulations of MPs, exposing tissue factor (TF) and P-selection, were also studied. MP counts in cerebrovenous samples, irrespective of cellular origin, were higher in TBI cases, compared to healthy controls (peak levels of EMPs were approximately 7 times higher, PMPs 1.4 times higher, and LMPs 2 times higher, respectively; p<0.001 for all). MP counts declined sharply from high levels shortly after the trauma toward slightly elevated levels 72 h later. EMPs and PMPs exposing TF, as well as PMPs exposing P-selection, showed a transcranial gradient with higher concentration in cerebrovenous, compared to arterial, samples. In contrast, LMPs exposing TF were higher in arterial samples, suggesting accumulation of LMPs in the brain. We conclude that the pattern of circulating MPs is altered after TBI. PMPs exposing P-selection and EMPs exposing TF seem to be generated in the injured brain, whereas LMPs exposing TF are accumulated. The pathophysiological significance of these changes in MP pattern in TBI should be further investigated. Including MPs exposing brain-specific antigens in the assessment of brain injury would give further information of origin and likely give additional information of the size of the injury, given that the MP phenotypes investigated in the present study are not brain-specific markers.</abstract><cop>United States</cop><pub>Mary Ann Liebert, Inc</pub><pmid>24956150</pmid><doi>10.1089/neu.2013.3168</doi><tpages>7</tpages></addata></record> |
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| ispartof | Journal of neurotrauma, 2014-12, Vol.31 (23), p.1927-1933 |
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| subjects | Adult Aged Atoms & subatomic particles Brain - metabolism Brain - pathology Brain damage Brain Injuries - metabolism Brain Injuries - pathology Cell-Derived Microparticles - metabolism Cell-Derived Microparticles - pathology Female Humans Male Middle Aged P-Selectin - metabolism Patients Thromboplastin - metabolism Young Adult |
| title | Formation of microparticles in the injured brain of patients with severe isolated traumatic brain injury |
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