Long-term neuroblast migration along blood vessels in an area with transient angiogenesis and increased vascularization after stroke
(2007) In Stroke: a journal of cerebral circulation 38(11). p.3032-3039- Abstract
- Background and Purpose - Stroke induced by middle cerebral artery occlusion (MCAO) causes long-term formation of new striatal neurons from stem/progenitor cells in the subventricular zone (SVZ). We explored whether MCAO leads to hypoxia, changes in vessel density, and angiogenesis in the ipsilateral SVZ and adjacent striatum, and determined the relation between the migrating neuroblasts and the vasculature. Methods - Adult rats were subjected to 2 hours of MCAO. Hypoxia was studied by injecting Hypoxyprobe-1 during MCAO or 6 weeks later. Vessel density and length was estimated using stereology. New cells were labeled with 5'-bromo-2' deoxyuridine (BrdU) during weeks 1 and 2 or 7 and 8 after MCAO, and angiogenesis was assessed... (More)
- Background and Purpose - Stroke induced by middle cerebral artery occlusion (MCAO) causes long-term formation of new striatal neurons from stem/progenitor cells in the subventricular zone (SVZ). We explored whether MCAO leads to hypoxia, changes in vessel density, and angiogenesis in the ipsilateral SVZ and adjacent striatum, and determined the relation between the migrating neuroblasts and the vasculature. Methods - Adult rats were subjected to 2 hours of MCAO. Hypoxia was studied by injecting Hypoxyprobe-1 during MCAO or 6 weeks later. Vessel density and length was estimated using stereology. New cells were labeled with 5'-bromo-2' deoxyuridine (BrdU) during weeks 1 and 2 or 7 and 8 after MCAO, and angiogenesis was assessed immunohistochemically with antibodies against BrdU and endothelial cell markers. Distance from neuroblasts to nearest vessel was measured using confocal microscopy. Results - The ischemic insult caused transient hypoxia and early, low-grade angiogenesis, but no damage or increase of vascular density in the SVZ. Angiogenesis was detected during the first 2 weeks in the dorsomedial striatum adjacent to the SVZ, which also showed long-lasting increase of vascularization. At 2, 6, and 16 weeks after MCAO, the majority of neuroblasts migrated through this area toward the damage, closely associated with blood vessels. Conclusions - The vasculature plays an important role for long-term striatal neurogenesis after stroke. During several months, neuroblasts migrate close to blood vessels through an area exhibiting early vascular remodeling and persistently increased vessel density. Optimizing vascularization should be an important strategy to promote neurogenesis and repair after stroke. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/651766
- author
- Thored, Pär
LU
; Wood, James
LU
; Arvidsson, Andreas
LU
; Cammenga, Jörg
LU
; Kokaia, Zaal
LU
and Lindvall, Olle LU
- organization
- publishing date
- 2007
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- hypoxia, neurogenesis, angiogenesis, stroke
- in
- Stroke: a journal of cerebral circulation
- volume
- 38
- issue
- 11
- pages
- 3032 - 3039
- publisher
- American Heart Association
- external identifiers
-
- wos:000250518300026
- scopus:35648934511
- ISSN
- 1524-4628
- DOI
- 10.1161/STROKEAHA.107.488445
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Restorative Neurology (0131000160), Molecular Medicine and Gene Therapy (0131000135), Stem Cell Center (013041110), Faculty of Medicine (000022000), Neurology, Lund (013027000)
- id
- 5b379330-b79e-40fc-9f31-d14930ae402b (old id 651766)
- date added to LUP
- 2016-04-01 16:22:23
- date last changed
- 2022-08-22 20:07:17
@article{5b379330-b79e-40fc-9f31-d14930ae402b, abstract = {{Background and Purpose - Stroke induced by middle cerebral artery occlusion (MCAO) causes long-term formation of new striatal neurons from stem/progenitor cells in the subventricular zone (SVZ). We explored whether MCAO leads to hypoxia, changes in vessel density, and angiogenesis in the ipsilateral SVZ and adjacent striatum, and determined the relation between the migrating neuroblasts and the vasculature. Methods - Adult rats were subjected to 2 hours of MCAO. Hypoxia was studied by injecting Hypoxyprobe-1 during MCAO or 6 weeks later. Vessel density and length was estimated using stereology. New cells were labeled with 5'-bromo-2' deoxyuridine (BrdU) during weeks 1 and 2 or 7 and 8 after MCAO, and angiogenesis was assessed immunohistochemically with antibodies against BrdU and endothelial cell markers. Distance from neuroblasts to nearest vessel was measured using confocal microscopy. Results - The ischemic insult caused transient hypoxia and early, low-grade angiogenesis, but no damage or increase of vascular density in the SVZ. Angiogenesis was detected during the first 2 weeks in the dorsomedial striatum adjacent to the SVZ, which also showed long-lasting increase of vascularization. At 2, 6, and 16 weeks after MCAO, the majority of neuroblasts migrated through this area toward the damage, closely associated with blood vessels. Conclusions - The vasculature plays an important role for long-term striatal neurogenesis after stroke. During several months, neuroblasts migrate close to blood vessels through an area exhibiting early vascular remodeling and persistently increased vessel density. Optimizing vascularization should be an important strategy to promote neurogenesis and repair after stroke.}}, author = {{Thored, Pär and Wood, James and Arvidsson, Andreas and Cammenga, Jörg and Kokaia, Zaal and Lindvall, Olle}}, issn = {{1524-4628}}, keywords = {{hypoxia; neurogenesis; angiogenesis; stroke}}, language = {{eng}}, number = {{11}}, pages = {{3032--3039}}, publisher = {{American Heart Association}}, series = {{Stroke: a journal of cerebral circulation}}, title = {{Long-term neuroblast migration along blood vessels in an area with transient angiogenesis and increased vascularization after stroke}}, url = {{http://dx.doi.org/10.1161/STROKEAHA.107.488445}}, doi = {{10.1161/STROKEAHA.107.488445}}, volume = {{38}}, year = {{2007}}, }