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Article: Bone marrow-derived endothelial progenitor cells protect postischemic axons after traumatic brain injury

TitleBone marrow-derived endothelial progenitor cells protect postischemic axons after traumatic brain injury
Authors
Issue Date2014
Citation
Journal of Cerebral Blood Flow and Metabolism, 2014, v. 34, n. 2, p. 357-366 How to Cite?
AbstractWhite matter sparing after traumatic brain injury (TBI) is an important predictor of survival and outcome. Blood vessels and axons are intimately associated anatomically and developmentally. Neural input is required for appropriate vascular patterning, and vascular signaling is important for neuron development and axon growth. Owing to this codependence between endothelial cells and axons during development and the contribution of endothelial progenitor cells (EPCs) in ischemic injury, we hypothesized that EPCs are important in axonal survival after TBI. We examined the effects of allogenic-cultured EPCs on white matter protection and microvascular maintenance after midline fluid percussion injury in adult Sprague-Dawley rats. We used two in vitro models of injury, mechanical stretch and oxygen-glucose deprivation (OGD), to examine the effects of EPCs on the mechanical and ischemic components of brain trauma, respectively. Our results indicate that EPCs improve the white matter integrity and decrease capillary breakdown after injury. Cultured cortical neurons exposed to OGD had less axon degeneration when treated with EPC-conditioned media, whereas no effect was seen in axons injured by mechanical stretch. The results indicate that EPCs are important for the protection of the white matter after trauma and represent a potential avenue for therapy.
Persistent Identifierhttp://hdl.handle.net/10722/205804
ISSN
2015 Impact Factor: 4.929
2015 SCImago Journal Rankings: 3.004
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorPark, Katya J.-
dc.contributor.authorPark, Eugene-
dc.contributor.authorLiu, Elaine-
dc.contributor.authorBaker, Andrew J.-
dc.date.accessioned2014-10-06T08:02:23Z-
dc.date.available2014-10-06T08:02:23Z-
dc.date.issued2014-
dc.identifier.citationJournal of Cerebral Blood Flow and Metabolism, 2014, v. 34, n. 2, p. 357-366-
dc.identifier.issn0271-678X-
dc.identifier.urihttp://hdl.handle.net/10722/205804-
dc.description.abstractWhite matter sparing after traumatic brain injury (TBI) is an important predictor of survival and outcome. Blood vessels and axons are intimately associated anatomically and developmentally. Neural input is required for appropriate vascular patterning, and vascular signaling is important for neuron development and axon growth. Owing to this codependence between endothelial cells and axons during development and the contribution of endothelial progenitor cells (EPCs) in ischemic injury, we hypothesized that EPCs are important in axonal survival after TBI. We examined the effects of allogenic-cultured EPCs on white matter protection and microvascular maintenance after midline fluid percussion injury in adult Sprague-Dawley rats. We used two in vitro models of injury, mechanical stretch and oxygen-glucose deprivation (OGD), to examine the effects of EPCs on the mechanical and ischemic components of brain trauma, respectively. Our results indicate that EPCs improve the white matter integrity and decrease capillary breakdown after injury. Cultured cortical neurons exposed to OGD had less axon degeneration when treated with EPC-conditioned media, whereas no effect was seen in axons injured by mechanical stretch. The results indicate that EPCs are important for the protection of the white matter after trauma and represent a potential avenue for therapy.-
dc.languageeng-
dc.relation.ispartofJournal of Cerebral Blood Flow and Metabolism-
dc.titleBone marrow-derived endothelial progenitor cells protect postischemic axons after traumatic brain injury-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/jcbfm.2013.216-
dc.identifier.pmid24301295-
dc.identifier.scopuseid_2-s2.0-84895068181-
dc.identifier.volume34-
dc.identifier.issue2-
dc.identifier.spage357-
dc.identifier.epage366-
dc.identifier.eissn1559-7016-
dc.identifier.isiWOS:000330748200022-

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