Anti-inflammatory mechanism of intravascular neural stem cell transplantation in haemorrhagic stroke
Abstract
Neural stem cell (NSC) transplantation has been investigated as a means to reconstitute the damaged brain after stroke. In this study, however, we investigated the effect on acute cerebral and peripheral inflammation after intracerebral haemorrhage (ICH). NSCs (H1 clone) from fetal human brain were injected intravenously (NSCs-iv, 5 million cells) or intracerebrally (NSCs-ic, 1 million cells) at 2 or 24 h after collagenase-induced ICH in a rat model. Only NSCs-iv-2 h resulted in fewer initial neurologic deteriorations and reduced brain oedema formation, inflammatory infiltrations (OX-42, myeloperoxidase) and apoptosis (activated caspase-3, TUNEL) compared to the vehicle-injected control animals. Rat neurosphere-iv-2 h, but not human fibroblast-iv-2 h, also reduced the brain oedema and the initial neurologic deficits. Human NSCs-iv-2 h also attenuated both cerebral and splenic activations of tumour necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and nuclear factor-kappa B (NF-kappaB). However, we observed only a few stem cells in brain sections of the NSCs-iv-2 h group; in the main, they were detected in marginal zone of spleens. To investigate whether NSCs interact with spleen to reduce cerebral inflammation, we performed a splenectomy prior to ICH induction, which eliminated the effect of NSCs-iv-2 h transplantation on brain water content and inflammatory infiltrations. NSCs also inhibited in vitro macrophage activations after lipopolysaccharide stimulation in a cell-to-cell contact dependent manner. In summary, early intravenous NSC injection displayed anti-inflammatory functionality that promoted neuroprotection, mainly by interrupting splenic inflammatory responses after ICH.
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Microvessels and neuroblasts mutually support each other via release of trophic factors, resulting in a tight interplay that stimulates brain remodelling, reduces delayed neuronal degeneration, promotes neuronal plasticity, modulates glial responses, and attenuates brain inflammation.
“Microvessels and neuroblasts mutually support each other via release of trophic factors, resulting in a tight interplay that stimulates brain remodelling processes, reducing delayed neuronal degeneration,14,45 promoting neuronal plasticity,15 modulating glial responses,14,46 and attenuating brain inflammation14,46 (figure 2).”
From Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation (2012) · cites this paper as [46]
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- Authors
- Lee, S.-T., Chu, K., Jung, K.-H., Kim, S.-J., Kim, D.-H., Kang, K.-M., Hong, N. H., Kim, J.-H., Ban, J.-J., Park, H.-K., Kim, S. U., Park, C.-G., Lee, S. K., Kim, M., & Roh, J.-K.
- Affiliations
- Seoul National University (KR)
- University of British Columbia Hospital (CA)
- Centers for Disease Control and Prevention (US)
- ORCID
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2007-12-21
- Volume
- 131
- Issue
- 3
- Pages
- 616-629
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- OpenAlex
- W2116505148
- Cited by
- 424
- References
- 70
- Citations by year
- 2026: 5 · 2025: 9 · 2024: 9 · 2023: 12 · 2022: 20 · 2021: 14 · 2020: 18 · 2019: 16 · 2018: 24 · 2017: 17 · 2016: 23 · 2015: 41 · 2014: 33 · 2013: 42 · 2012: 38
- FWCI
- 14.67
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain (publishedVersion)
- PubMed (publishedVersion)
- Seoul National University Open Repository (Seoul National University) (submittedVersion)
- Topics
- Health Sciences › Medicine › Neurology › Intracerebral and Subarachnoid Hemorrhage Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Keywords
- neural stem cell transplantation, intravenous transplantation, intracerebral hemorrhage, hemorrhagic stroke, neuroinflammation, splenic inflammation, neuroprotection, brain oedema, macrophage activation, cell-cell contact, splenectomy, TNF-α, interleukin-6, NF-κB, apoptosis, neurospheres
- MeSH terms
- Animals, Body Water, Brain, Cells, Cultured, Encephalitis, Humans, Macrophage Activation, Male, Neuronal Plasticity, Splenectomy, Fetal Tissue Transplantation, Brain Tissue Transplantation, Rats, Sprague-Dawley, Apoptosis, Disease Progression, Inflammation Mediators, Coculture Techniques, Intracranial Hemorrhages, Stroke, Stem Cell Transplantation, Rats, Fetal Stem Cells
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