Stem Cell Dynamics in an Experimental Model of Stroke
- Author:
Min Cheol LEE
1
;
Chun Yan JIN
;
Hyung Seok KIM
;
Jae Hyu KIM
;
Myeong Kyu KIM
;
Hyoung Ihl KIM
;
Young Jin LEE
;
Young Jun SON
;
Young Ok KIM
;
Young Jong WOO
Author Information
- Publication Type:Original Article
- Keywords: Stroke; MRI; Neural stem cell; Dynamics
- MeSH: Cold Temperature; Corpus Callosum; Emigration and Immigration; Immunohistochemistry; Intermediate Filament Proteins; Light; Magnetic Resonance Imaging; Models, Theoretical; Motor Cortex; Nerve Tissue Proteins; Neural Stem Cells; Neurons; Rats, Sprague-Dawley; Rose Bengal; Stem Cells; Stroke; Transplants
- From:Chonnam Medical Journal 2011;47(2):90-98
- CountryRepublic of Korea
- Language:English
- Abstract: We investigated the migration of endogenous neural stem cells (NSCs) toward an infarct lesion in a photo-thrombotic stroke model. The lesions produced by using rose bengal dye (20 mg/kg) with cold light in the motor cortex of Sprague-Dawley rats were also evaluated with sequential magnetic resonance imaging (MRI) from 30 minutes through 8 weeks. Migration of NSCs was identified by immunohistochemistry for nestin monoclonal antibody in the lesion cortex, subventricular zone (SVZ), and corpus callosum (CC). The contrast to noncontrast ratio (CNR) on MRI was greatest at 12 hours in DWI and decreased over time. By contrast, T1-weighted and T2-weighted images showed a constant CNR from the beginning through 8 weeks. MRI of the lesional cortex correlated with histopathologic findings, which could be divided into three stages: acute (edema and necrosis) within 24 hours, subacute (acute and chronic inflammatory cell infiltration) at 2 to 7 days, and chronic (gliofibrosis) at 2 to 4 weeks. The volume of the infarct was significantly reduced by reparative gliofibrosis. The number of nestin+ NSCs in the contralateral SVZ was similar to that of the ipsilateral SVZ in each group. However, the number of nestin+ NSCs in the ipsilateral cortex and CC increased at 12 hours to 3 days compared with the contralateral side (p<0.01) and was reduced significantly by 7 days (p<0.01). Active emigration of internal NSCs from the SVZ toward the infarct lesion may also contribute to decreased volume of the infarct lesion, but the self-repair mechanism by endogenous NSCs is insufficient to treat stroke causing extensive neuronal death. Further studies should be focused on amplification technologies of NSCs to enhance the collection of endogenous or transplanted NSCs for the treatment of stroke.
