The neuroblast and angioblast chemotaxic factor SDF-1 (CXCL12) expression is briefly up regulated by reactive astrocytes in brain following neonatal hypoxic-ischemic injury.

Hdl Handle:
http://hdl.handle.net/10675.2/112
Title:
The neuroblast and angioblast chemotaxic factor SDF-1 (CXCL12) expression is briefly up regulated by reactive astrocytes in brain following neonatal hypoxic-ischemic injury.
Authors:
Miller, Jason T; Bartley, John H; Wimborne, Hereward J. C.; Walker, Aisha L.; Hess, David C.; Hill, William D; Carroll, James E
Abstract:
BACKGROUND: Stromal cell-derived factor 1 (SDF-1 or CXCL12) is chemotaxic for CXCR4 expressing bone marrow-derived cells. It functions in brain embryonic development and in response to ischemic injury in helping guide neuroblast migration and vasculogenesis. In experimental adult stroke models SDF-1 is expressed perivascularly in the injured region up to 30 days after the injury, suggesting it could be a therapeutic target for tissue repair strategies. We hypothesized that SDF-1 would be expressed in similar temporal and spatial patterns following hypoxic-ischemic (HI) injury in neonatal brain. RESULTS: Twenty-five 7-day-old C57BL/J mice underwent HI injury. SDF-1 expression was up regulated up to 7 days after the injury but not at the later time points. The chief sites of SDF-1 up regulation were astrocytes, their foot processes along blood vessels and endothelial cells. CONCLUSION: The localization of SDF-1 along blood vessels in the HI injury zone suggests that these perivascular areas are where chemotaxic signaling for cellular recruitment originates and that reactive astrocytes are major mediators of this process. The associated endothelium is likely to be the site for vascular attachment and diapedesis of CXCR4 receptor expressing cells to enter the injured tissue. Here we show that, relative to adults, neonates have a significantly smaller window of opportunity for SDF-1 based vascular chemotaxic recruitment of bone marrow-derived cells. Therefore, without modification, following neonatal HI injury there is only a narrow period of time for endogenous SDF-1 mediated chemotaxis and recruitment of reparative cells, including exogenously administered stem/progenitor cells.
Citation:
BMC Neurosci. 2005 Oct 31; 6:63
Issue Date:
2-Dec-2005
URI:
http://hdl.handle.net/10675.2/112
DOI:
10.1186/1471-2202-6-63
PubMed ID:
16259636
PubMed Central ID:
PMC1298306
Type:
Comparative Study; Journal Article
ISSN:
1471-2202
Appears in Collections:
Department of Neurology: Faculty Research and Presentations

Full metadata record

DC FieldValue Language
dc.contributor.authorMiller, Jason Ten_US
dc.contributor.authorBartley, John Hen_US
dc.contributor.authorWimborne, Hereward J. C.en_US
dc.contributor.authorWalker, Aisha L.en_US
dc.contributor.authorHess, David C.en_US
dc.contributor.authorHill, William Den_US
dc.contributor.authorCarroll, James Een_US
dc.date.accessioned2010-09-24T22:03:22Z-
dc.date.available2010-09-24T22:03:22Z-
dc.date.issued2005-12-02en_US
dc.identifier.citationBMC Neurosci. 2005 Oct 31; 6:63en_US
dc.identifier.issn1471-2202en_US
dc.identifier.pmid16259636en_US
dc.identifier.doi10.1186/1471-2202-6-63en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/112-
dc.description.abstractBACKGROUND: Stromal cell-derived factor 1 (SDF-1 or CXCL12) is chemotaxic for CXCR4 expressing bone marrow-derived cells. It functions in brain embryonic development and in response to ischemic injury in helping guide neuroblast migration and vasculogenesis. In experimental adult stroke models SDF-1 is expressed perivascularly in the injured region up to 30 days after the injury, suggesting it could be a therapeutic target for tissue repair strategies. We hypothesized that SDF-1 would be expressed in similar temporal and spatial patterns following hypoxic-ischemic (HI) injury in neonatal brain. RESULTS: Twenty-five 7-day-old C57BL/J mice underwent HI injury. SDF-1 expression was up regulated up to 7 days after the injury but not at the later time points. The chief sites of SDF-1 up regulation were astrocytes, their foot processes along blood vessels and endothelial cells. CONCLUSION: The localization of SDF-1 along blood vessels in the HI injury zone suggests that these perivascular areas are where chemotaxic signaling for cellular recruitment originates and that reactive astrocytes are major mediators of this process. The associated endothelium is likely to be the site for vascular attachment and diapedesis of CXCR4 receptor expressing cells to enter the injured tissue. Here we show that, relative to adults, neonates have a significantly smaller window of opportunity for SDF-1 based vascular chemotaxic recruitment of bone marrow-derived cells. Therefore, without modification, following neonatal HI injury there is only a narrow period of time for endogenous SDF-1 mediated chemotaxis and recruitment of reparative cells, including exogenously administered stem/progenitor cells.en_US
dc.rightsThe PMC Open Access Subset is a relatively small part of the total collection of articles in PMC. Articles in the PMC Open Access Subset are still protected by copyright, but are made available under a Creative Commons or similar license that generally allows more liberal redistribution and reuse than a traditional copyrighted work. Please refer to the license statement in each article for specific terms of use. The license terms are not identical for all articles in this subset.en_US
dc.subject.meshAge Factorsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnimals, Newbornen_US
dc.subject.meshAstrocytes / metabolism / pathologyen_US
dc.subject.meshBrain / metabolismen_US
dc.subject.meshChemokine CXCL12en_US
dc.subject.meshChemokines, CXC / biosynthesis / geneticsen_US
dc.subject.meshChemotaxis / physiologyen_US
dc.subject.meshGene Expression Regulation, Developmental / physiologyen_US
dc.subject.meshHypoxia-Ischemia, Brain / metabolism / pathologyen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred C57BLen_US
dc.subject.meshUp-Regulation / physiologyen_US
dc.titleThe neuroblast and angioblast chemotaxic factor SDF-1 (CXCL12) expression is briefly up regulated by reactive astrocytes in brain following neonatal hypoxic-ischemic injury.en_US
dc.typeComparative Studyen_US
dc.typeJournal Articleen_US
dc.identifier.pmcidPMC1298306en_US
dc.contributor.corporatenameDepartment of Neurologyen_US
dc.contributor.corporatenameDepartment of Pediatricsen_US
dc.contributor.corporatenameDepartment of Cellular Biology and Anatomyen_US

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