Transplantation of human mesenchymal stem cells promotes functional improvement and increased expression of neurotrophic factors in a rat focal cerebral ischemia model

Wakabayashi, Kiryo; Nagai, Atsushi; Sheikh, Abdullah Md.; Shiota, Yuri; Narantuya, Dashdemberel; Watanabe, T.; Masuda, Junichi; Kobayashi, Shotai; Kim, Seung Up; Yamaguchi, Shûhei

doi:10.1002/jnr.22279

Cited by 222 publications

(176 citation statements)

References 32 publications

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“…Rats receiving MSC transplantation demonstrated reduction in infarct volume at 7 and 14 days, as well as expression of neurotrophic factors VEGF, EGF, and FGF within 7 days (Wakabayashi et al, 2010). It appears that there is wide potential for MSC delivery to promote functional recovery through activation of endogenous restorative responses in the brain (Wakabayashi et al, 2010).…”

Section: Mesenchymal Stem Cellsmentioning

confidence: 99%

“…For example, bone marrow MSCs deliv ered via intraventricular transplantation, carotid artery transplantation, and internal jugular vein injection have migrated to the brain injury area and cortex, surviving in the infarct area following middle MCAO in rats (Ruan et al, 2013). Rats receiving MSC transplantation demonstrated reduction in infarct volume at 7 and 14 days, as well as expression of neurotrophic factors VEGF, EGF, and FGF within 7 days (Wakabayashi et al, 2010). It appears that there is wide potential for MSC delivery to promote functional recovery through activation of endogenous restorative responses in the brain (Wakabayashi et al, 2010).…”

Section: Mesenchymal Stem Cellsmentioning

confidence: 99%

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Stroke Repair via Biomimicry of the Subventricular Zone

Matta

Gonzalez

2018

Front. Mater.

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Stroke is among the leading causes of death and disability worldwide, 85% of which are ischemic. Current stroke therapies are limited by a narrow effective therapeutic time and fail to effectively complete the recovery of the damaged area. Magnetic resonance imaging of the subventricular zone (SVZ) following infarct/stroke has allowed visualization of new axonal connections and projections being formed, while new immature neurons migrate from the SVZ to the peri-infarct area. Such studies suggest that the SVZ is a primary source of regenerative cells for the repair and regeneration of stroke-damaged neurons and tissue. Therefore, the development of tissue engineered scaffolds that serve as a bioreplicative SVZ niche would support the survival of multiple cell types that reside in the SVZ. Essential to replication of the human SVZ microenvironment is the establishment of microvasculature that regulates both the healthy and stroke-injured blood-brain barrier, which is dysregulated poststroke. In order to reproduce this niche, understanding how cells interact in this environment is critical, in particular neural stem cells, endothelial cells, pericytes, ependymal cells, and microglia. Remodeling and repair of the matrix-rich SVZ niche by endogenous reparative mechanisms may then support functional recovery when enhanced by an artificial niche that supports the survival and proliferation of migrating vascular and neuronal cells. Critical considerations to mimic this area include an understanding of resident cell types, delivery method, and the use of biocompatible materials. Controlling stem cell survival, differentiation, and migration are key factors to consider when transplanting stem cells. Here, we discuss the role of the SVZ architecture and resident cells in the promotion and enhancement of endogenous repair mechanisms. We elucidate the interplay between the extracellular matrix composition and cell interactions prior to and following stroke. Finally, we review current cell and neuronal niche biomimetic materials that allow for a tissue-engineered approach in order to promote structural and functional restoration of neural circuitry. By creating an artificial mimetic SVZ, tissue engineers can strive to facilitate tissue regeneration and functional recovery.

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Section: Mesenchymal Stem Cellsmentioning

confidence: 99%

Section: Mesenchymal Stem Cellsmentioning

confidence: 99%

Stroke Repair via Biomimicry of the Subventricular Zone

Matta

Gonzalez

2018

Front. Mater.

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“…The development of GLP-1 receptor agonists, such as Geniposide or Extendin-4, which harbor the same neuro-protective and neuro-stimulatory properties as GLP-1 (159), but have longer half-lives (153,157,160,161), may provide effective and standardized long-term options for treating brain insulin resistance diseases such as AD. Finally, a future approach could be to genetically modify mesenchymal or stem cells to provide sustained delivery of neuro-stimulatory and neuroprotective agonists (162)(163)(164), including GLP-1 (165).…”

Section: Targeting Insulin Deficiencymentioning

confidence: 99%

Therapeutic targets of brain insulin resistance in sporadic Alzheimer s disease

Monte

2012

Front Biosci

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Growing evidence supports roles for brain insulin and insulin-like growth factor (IGF) resistance and metabolic dysfunction in the pathogenesis of Alzheimer's disease (AD). Whether the underlying problem stems from a primary disorder of central nervous system (CNS) neurons and glia, or secondary effects of systemic diseases such as obesity, Type 2 diabetes, or metabolic syndrome, the end-results include impaired glucose utilization, mitochondrial dysfunction, increased oxidative stress, neuroinflammation, and the propagation of cascades that result in the accumulation of neurotoxic misfolded, aggregated, and ubiquitinated fibrillar proteins. This article reviews the roles of impaired insulin and IGF signaling to AD-associated neuronal loss, synaptic disconnection, tau hyperphosphorylation, amyloid-beta accumulation, and impaired energy metabolism, and discusses therapeutic strategies and lifestyle approaches that could be used to prevent, delay the onset, or reduce the severity of AD. Finally, it is critical to recognize that AD is heterogeneous and has a clinical course that fully develops over a period of several decades. Therefore, early and multi-modal preventive and treatment approaches should be regarded as essential. KeywordsAmyloid; Anti-oxidants; Brain diabetes; Brain insulin resistance; Incretins; Insulin; Insulin sensitizers; Liver-Brain-Axis; Metal Chelation; Neuroprotection; Nitrosamine; Oxidative Stress; Polyphenols; Statins; Streptozotocin; Tau; Type 3 diabetes INTRODUCTIONThe gold standard for definitively diagnosing AD is to perform a postmortem examination of the brain, with the objective of demonstrating beyond-normal aging associated densities of neurofibrillary tangles, neuritic plaques, and amyloid-beta 40-42 kD fragments of amyloid beta precursor protein (AβPP-Aβ) deposits in corticolimbic structures, bearing in mind that neurodegeneration frequently involves multiple other cortical regions as well. The common thread among these characteristic lesions is that they harbor insoluble aggregates of abnormally phosphorylated and ubiquitinated tau, and neurotoxic AβPP-Aβ in the form of Send correspondence to: Suzanne M. de la Monte, Rhode Island Hospital, 55 Claverick Street, Room 419, Providence, RI. 02903, Tel: 401-444-7364, Fax: 401-444-2939, Suzanne_DeLaMonte_MD@Brown.edu. HHS Public Access Author manuscriptFront Biosci (Elite Ed). Author manuscript; available in PMC 2015 August 26. Published in final edited form as:Front Biosci (Elite Ed). ; 4: 1582-1605. Author Manuscript Author ManuscriptAuthor ManuscriptAuthor Manuscript oligomers, fibrillar aggregates, or extracellular plaques. Secreted AβPP-Aβ oligomers have been demonstrated to be neurotoxic and to inhibit hippocampal long-term potentiation, i.e. synaptic plasticity (1).To improve diagnosis and treatment, we must learn to connect the development and progression of neurodegeneration with molecular, biochemical, physiological, neuroimaging, and clinical abnormalities in AD. Several strategies could be taken to advance this proc...

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“…These cells have also shown positive effects in experimental stroke models when delivered intravenously (Honma et al, 2006;Wakabayashi et al, 2010). A critical aspect with these cells is that they should not lose their MSC phenotype upon modification.…”

Section: Genetically Modified Cellsmentioning

confidence: 99%