CNS grafts of rat choroid plexus protect against cerebral ischemia in adult rats

Borlongan, Cesario V.; Skinner, S. J. M.; Geaney, Marilyn S.; Vasconcellos, Alfred V.; Elliott, Robert B.; Emerich, Dwaine F.

doi:10.1097/01.wnr.0000133298.84901.cf

Cited by 56 publications

(39 citation statements)

References 22 publications

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“…However, recent studies show that ependymal cell of the lateral ventricles can be activated to generate neuroblasts in the ischemic brain (Carlen et al, 2009). In addition, cellular therapy using ependymal cells could represent a new opportunity since it has been shown that animals transplanted with encapsulated choroid plexus displayed a reduction in both functional deficit and lesion size after stroke (Borlongan et al, 2004a).…”

Section: Discussionmentioning

confidence: 99%

Time-dependent contribution of non neuronal cells to BDNF production after ischemic stroke in rats

Béjot

Prigent‐Tessier

Cachia

et al. 2011

Neurochemistry International

125

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Although brain-derived neurotrophic factor (BDNF) plays a central role in recovery after cerebral ischemia, little is known about cells involved in BDNF production after stroke.The present study testes the hypothesis that neurons are not the unique source of neosynthesized BDNF after stroke and that non neuronal-BDNF producing cells differ according to the delay after stroke induction. For this purpose, cellular localization of BDNF and BDNF content of each hemisphere were analysed in parallel before and after (4h, 24h and 8d) ischemic stroke in rats. Stroke of different severities was induced by embolization of the brain with variable number of calibrated microspheres allowing us to explore the association between BDNF production and neuronal death severity. The main results are that a) unilateral stroke increased BDNF production in both hemispheres with a more intense and long-lasting effect in the lesioned hemisphere, b) BDNF levels either of the lesioned or unlesioned hemispheres were not inversely correlated to neuronal death severity whatever the delay after stroke onset, c) in the unlesioned hemisphere, stroke resulted in increased BDNF staining in neurons and ependymal cells (at 4h and 24h), d) in the lesioned hemisphere, beside neurons and ependymal cells, microglial cells (at 24h), endothelial cells of cerebral arterioles (at 4h and 24h) and astrocytes (at 8d) exhibited a robust BDNF staining as well. Taken together, overall data suggest that non neuronal cells are able to produce substantial amount of BDNF after ischemic stroke and that more attention should be given to these cells in the design of strategies aimed at improving stroke recovery through BDNFrelated mechanisms.

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Section: Discussionmentioning

confidence: 99%

Time-dependent contribution of non neuronal cells to BDNF production after ischemic stroke in rats

Béjot

Prigent‐Tessier

Cachia

et al. 2011

Neurochemistry International

125

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“…If this is the case, the age-related overwhelming levels of IL-4 at the CP have a negative outcome for the functioning brain, not only because of induction of CCL11 but also because of dysregulation of BDNF and possibly other CPderived neurotrophic factors. Notably, the CP produces BDNF following CNS trauma (45) and chronic stress (46).…”

Section: Discussionmentioning

confidence: 99%

9. CNS-specific immunity at the choroid plexus shifts toward destructive Th2 inflammation in brain aging

Baruch

Deczkowska

Schwartz

2013

Brain, Behavior, and Immunity

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The adaptive arm of the immune system has been suggested as an important factor in brain function. However, given the fact that interactions of neurons or glial cells with T lymphocytes rarely occur within the healthy CNS parenchyma, the underlying mechanism is still a mystery. Here we found that at the interface between the brain and blood circulation, the epithelial layers of the choroid plexus (CP) are constitutively populated with CD4+ effector memory cells with a T-cell receptor repertoire specific to CNS antigens. With age, whereas CNS specificity in this compartment was largely maintained, the cytokine balance shifted in favor of the T helper type 2 (Th2) response; the Th2-derived cytokine IL-4 was elevated in the CP of old mice, relative to IFN-γ, which decreased. We found this local cytokine shift to critically affect the CP epithelium, triggering it to produce the chemokine CCL11 shown to be associated with cognitive dysfunction. Partial restoration of cognitive ability in aged mice, by lymphopenia-induced homeostasis-driven proliferation of memory T cells, was correlated with restoration of the IL-4:IFN-γ ratio at the CP and modulated the expression of plasticity-related genes at the hippocampus. Our data indicate that the cytokine milieu at the CP epithelium is affected by peripheral immunosenescence, with detrimental consequences to the aged brain. Amenable to immunomodulation, this interface is a unique target for arresting age-related cognitive decline.blood-cerebrospinal fluid barrier | brain senescence | neuroinflammation C irculating immune cells have been repeatedly shown to be essential for central nervous system (CNS) maintenance (1-3). Specifically, T cells that recognize CNS antigens contribute to the functional integrity of the CNS under both normal and pathological conditions (2, 4-6), supporting hippocampus-dependent learning and memory, adult neurogenesis, and neurotrophic factor production (2).Under physiological conditions, T cells are rarely found in the brain parenchyma and are mainly observed at the borders of the CNS: the choroid plexus (CP) of the brain's ventricles, forming the blood-cerebrospinal fluid barrier (BCSFB), the meningeal spaces, and the cerebrospinal fluid (CSF) (7). T cells were shown to accumulate in these compartments in response to signals from the CNS, specifically in the meninges after performance of cognitive tasks (8) and in the CP after exposure to mental stress (9). In the meningeal spaces, these cells were further characterized as producing the cytokine interleukin 4 (IL-4), known for its beneficial role in CNS maintenance and neuroprotection (8,(10)(11)(12)(13). However, the questions of why, where, and how T-cell specificity is needed for brain plasticity remained mysterious.The CP is strategically positioned at the lining between the CNS and the immune system and, in addition to its classically known role in generating the CSF, can enable bidirectional communication between the CNS parenchyma and blood circulation (14). Accordingly, we envisioned that...

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“…Presently, primary culture from choroid plexus tissues is widely used in transplantation in animal models for central nervous system diseases (4)(5)(6)(7)(8)(9)(10)(11). The cellular and molecular mechanisms of nerve regeneration in the central nervous system after choroid plexus transplantation have not been defined.…”

Section: Introductionmentioning

confidence: 99%

Primary Culture of Choroid Plexuses from Neonate Rats Containing Progenitor Cells Capable of Differentiation

Huang

et al. 2013

Balkan Med J

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ReagentsDulbecco's modified Eagle's medium (DMEM, low glucose) and foetal bovine serum (FBS) were purchased from ABSTRACT Background: The choroid plexuses, which could secrete a number of neurotrophins, have recently been used in transplantation in central nervous system diseases.Aims: To study the mechanism of nerve regeneration in the central nervous system by grafting choroid plexus tissues.Study Design: Animal experimentation. Methods:The choroid plexuses from the lateral ventricles of neonatal rats were cultured in adherent culture, and immunocytochemical methods were used to analyse the progenitor cells on days 2, 6, and 10 after seeding.Results: Expression of both nestin and glial fibrillary acidic protein was observed in small cell aggregates on day 2 in primary culture. Most of the nestinpositive cells on day 6 were immunoreactive to glial fibrillary acidic protein antibody. No cells expressing nestin or glial fibrillary acidic protein were seen on day 10. Conclusion:These experimental results indicate that the choroid plexus contains a specific cell population -progenitor cells. Under in vitro experimental conditions, the progenitor cells differentiated into choroid plexus epithelial cells but did not form neurons or astrocytes.

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CNS grafts of rat choroid plexus protect against cerebral ischemia in adult rats

Cited by 56 publications

References 22 publications

Time-dependent contribution of non neuronal cells to BDNF production after ischemic stroke in rats

Time-dependent contribution of non neuronal cells to BDNF production after ischemic stroke in rats

9. CNS-specific immunity at the choroid plexus shifts toward destructive Th2 inflammation in brain aging

Primary Culture of Choroid Plexuses from Neonate Rats Containing Progenitor Cells Capable of Differentiation

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