Bone marrow-derived mesenchymal stem cells for the treatment of ischemic stroke

Dharmasaroja, Permphan

doi:10.1016/j.jocn.2008.05.006

Cited by 138 publications

(127 citation statements)

References 67 publications

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“…4,5,15 Janowski et al, 4 reviewing studies up to 2006, reported numerous useful findings, but combined results across many types of stem cells and neurologic disorders. Lees et al 5 provided key insights and focused on ischemic stroke, but also combined results across many different cell therapies, as well as cell engineering.…”

Section: Resultsmentioning

confidence: 99%

“…The current review, by focusing on one specific cellular therapy for one specific clinical indication, builds on prior meta-analyses that took a broader approach to stem cell therapy. 4,5,15 First, in accordance with recent Stroke Therapy Academic Industry Roundtable (STAIR) recommendations 16 and a recent NIH workshop, 17 the quality of the studies was reviewed. Second, the effect size of MSCs was determined for the most frequently used behavioral and histologic outcomes.…”

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confidence: 99%

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Meta-analysis of preclinical studies of mesenchymal stromal cells for ischemic stroke

et al. 2014

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Objectives:To evaluate the quality of preclinical evidence for mesenchymal stromal cell (MSC) treatment of ischemic stroke, determine effect size of MSC therapy, and identify clinical measures that correlate with differences in MSC effects.Methods: A literature search identified studies of MSCs in animal models of cerebral ischemia. For each, a Quality Score was derived, and effect size of MSCs was determined for the most common behavioral and histologic endpoints.Results: Of 46 studies, 44 reported that MSCs significantly improved outcome. The median Quality Score was 5.5 (of 10). The median effect size was 1.78 for modified Neurological Severity Score, 1.73 for the adhesive removal test, 1.02 for the rotarod test, and 0.93 for infarct volume reduction. Quality Score correlated significantly and positively with effect size for the modified Neurological Severity Score. Effect sizes varied significantly with clinical measures such as administration route (intracerebral . intra-arterial . IV, although effect size for IV was nonetheless very large at 1.55) and species receiving MSCs (primate . rat . mouse). Because many MSC mechanisms are restorative, analyses were repeated examining only the 36 preclinical studies administering MSCs $24 hours poststroke; results were overall very similar. Conclusions:In preclinical studies, MSCs have consistently improved multiple outcome measures, with very large effect sizes. Results were robust across species studied, administration route, species of MSC origin, timing, degree of immunogenicity, and dose, and in the presence of comorbidities. In contrast to meta-analyses of preclinical data for other stroke therapies, higher-quality MSC preclinical studies were associated with larger behavioral gains. These findings support the utility of further studies to translate MSCs in the treatment of ischemic stroke in humans.

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Section: Resultsmentioning

confidence: 99%

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confidence: 99%

Meta-analysis of preclinical studies of mesenchymal stromal cells for ischemic stroke

et al. 2014

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“…Therefore, the severity of the cerebral hypoxia is dependent on the neuron survival and improved neurological outcome. During the past decade, administration of BMSC has been shown to be a potential cell therapy in brain ischemia [34,35]. Perrasso L. also showed that intravenous administration of BMSCs after global cerebral ischemia decreases hippocampal neural damage, suggesting that BMSCs increase neuron survival by intravenous infusion [3].…”

Section: Discussionmentioning

confidence: 99%

Hypoxia-Inducible Factor 1-α-AA-Modified Bone Marrow Stem Cells Protect PC12 Cells from Hypoxia-Induced Apoptosis, Partially Through VEGF/PI3K/Akt/FoxO1 Pathway

Zhong

Zhou

et al. 2012

Stem Cells and Development

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“…16 Initially identified in bone marrow (BM), MSC or MSC-like cells have meanwhile been described in most tissues. They are recruited to sites of tissue damage, have beneficial effects on tissue regeneration, for example, after myocardial infarction or stroke, 17,18 and thus may serve as a regenerative reservoir. Although the mechanisms are still a matter of debate, paracrine effects via secretion of a vast array of chemokines, cytokines, growth factors and other factors affecting angiogenesis, apoptosis, migration, proliferation, differentiation and extracellular matrix remodeling appear to have a central role, whereas direct tissue replacement by local engraftment and differentiation or even transdifferentiation of MSC seem uncommon.…”

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confidence: 99%

Necrotic cell-derived high mobility group box 1 attracts antigen-presenting cells but inhibits hepatocyte growth factor-mediated tropism of mesenchymal stem cells for apoptotic cell death

et al. 2015

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Tissue damage due to apoptotic or necrotic cell death typically initiates distinct cellular responses, leading either directly to tissue repair and regeneration or to immunological processes first, to clear the site, for example, of potentially damage-inducing agents. Mesenchymal stem cells (MSC) as well as immature dendritic cells (iDC) and monocytes migrate to injured tissues. MSC have regenerative capacity, whereas monocytes and iDC have a critical role in inflammation and induction of immune responses, including autoimmunity after tissue damage. Here, we investigated the influence of apoptotic and necrotic cell death on recruitment of MSC, monocytes and iDC, and identified hepatocyte growth factor (HGF) and the alarmin high mobility group box 1 (HMGB1) as key factors differentially regulating these migratory responses. MSC, but not monocytes or iDC, were attracted by apoptotic cardiomyocytic and neuronal cells, whereas necrosis induced migration of monocytes and iDC, but not of MSC. Only apoptotic cell death resulted in HGF production and HGF-mediated migration of MSC towards the apoptotic targets. In contrast, HMGB1 was predominantly released by the necrotic cells and mediated recruitment of monocytes and iDC via the receptor of advanced glycation end products. Moreover, necrotic cardiomyocytic and neuronal cells caused an HMGB1/toll-like receptor-4-dependent inhibition of MSC migration towards apoptosis or HGF, while recruitment of monocytes and iDC by necrosis or HMGB1 was not affected by apoptotic cells or HGF. Thus, the type of cell death differentially regulates recruitment of either MSC or monocytes and iDC through HGF and HMGB1, respectively, with a dominant, HMGB1-mediated role of necrosis in determining tropism after tissue injury.

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Bone marrow-derived mesenchymal stem cells for the treatment of ischemic stroke

Cited by 138 publications

References 67 publications

Meta-analysis of preclinical studies of mesenchymal stromal cells for ischemic stroke

Meta-analysis of preclinical studies of mesenchymal stromal cells for ischemic stroke

Hypoxia-Inducible Factor 1-α-AA-Modified Bone Marrow Stem Cells Protect PC12 Cells from Hypoxia-Induced Apoptosis, Partially Through VEGF/PI3K/Akt/FoxO1 Pathway

Necrotic cell-derived high mobility group box 1 attracts antigen-presenting cells but inhibits hepatocyte growth factor-mediated tropism of mesenchymal stem cells for apoptotic cell death

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