Inflammatory Regulators of Redirected Neural Migration in the Injured Brain

Bye, Nicole; Turnley, Ann M.; Morganti-Kossmann, Maria Cristina

doi:10.1159/000336542

Cited by 14 publications

(14 citation statements)

References 203 publications

(262 reference statements)

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“…57 Both pro-and antiinflammatory cytokines can influence the proliferation and migration of neural progenitors. 58,59 The link between the immune response that occurs after ischemic stroke, neurogenesis, and subsequent functional recovery has not been well established; however, hypotheses regarding both the beneficial 60 and detrimental 61,62 effects of inflammation have been proposed. Some of the beneficial effects have been attributed to the interaction of T cells with microglia, which stimulates proliferation of SGL and SVZ progenitor cells 60 and directs both NPC migration and differentiation in vitro and in vivo.…”

Section: Interaction Between Inflammation and Neurogenesismentioning

confidence: 99%

Neurogenesis and Inflammation after Ischemic Stroke: What is Known and Where We Go from Here

Tobin

Bonds

Minshall

et al. 2014

J Cereb Blood Flow Metab

303

236

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This review covers the pathogenesis of ischemic stroke and future directions regarding therapeutic options after injury. Ischemic stroke is a devastating disease process affecting millions of people worldwide every year. The mechanisms underlying the pathophysiology of stroke are not fully understood but there is increasing evidence demonstrating the contribution of inflammation to the drastic changes after cerebral ischemia. This inflammation not only immediately affects the infarcted tissue but also causes long-term damage in the ischemic penumbra. Furthermore, the interaction between inflammation and subsequent neurogenesis is not well understood but the close relationship between these two processes has garnered significant interest in the last decade or so. Current approved therapy for stroke involving pharmacological thrombolysis is limited in its efficacy and new treatment strategies need to be investigated. Research aimed at new therapies is largely about transplantation of neural stem cells and using endogenous progenitor cells to promote brain repair. By understanding the interaction between inflammation and neurogenesis, new potential therapies could be developed to further establish brain repair mechanisms.

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Section: Interaction Between Inflammation and Neurogenesismentioning

confidence: 99%

Neurogenesis and Inflammation after Ischemic Stroke: What is Known and Where We Go from Here

Tobin

Bonds

Minshall

et al. 2014

J Cereb Blood Flow Metab

303

236

View full text Add to dashboard Cite

show abstract

“…Activated type B stem cells and their progeny (Lacar et al, ), the transitory amplifying type C cells, express epidermal growth factor receptor (EGFR) (Abhold et al, ), and are most strongly associated with vascular cells (Miller and Gauthier‐Fisher, ). Adult qNSCs (type B cells) in the SVZ and subgranular zone (SGZ) share basic properties with embryonic radial glia (RG: Miller and Gauthier‐Fisher, ), and upon transplantation into neurogenic areas of the adult brain (the hippocampus and (OB), these NPCs can differentiate into new neurons in response to local signals released by neurons following CNS insult (Carbajal et al, ; Bye et al, ).…”

Section: Do Npcs Promote Functional Recovery In Neurogenic Areas Follmentioning

confidence: 99%

“…Interestingly, CXCR4 and MMP9 expression can induce both beneficial (Liu et al, ) or detrimental effects in the developing and adult brain (Kim et al, ; Liu et al, 2008) or spinal cord (Pannu et al, ). Since inflammation is detrimental for neurogenesis (Ekdahl et al, ) and IL‐8, CCL‐2, CCR5, leukotriene B4 ‐LTB4‐, and CXCL1‐chemokines or cell adhesion molecules (ICAM, Selectin, CD11/CD18 integrins) induce leukocyte recruitment toward damaged CNS areas (Kim, ; Kang et al, ; Ma et al, ), it is important to elucidate how EPO regulates chemokines to guide NPC migration from the SVZ toward the damaged CNS and promote repair (Bye et al, ). This feature might be important from a therapeutic view point because TPA (the recombinant tissue plasminogen activator; a thrombolytic factor) is currently the only clinical agent approved for stroke therapy (Saver et al, ).…”

Section: Erythropoietin (Epo) Regulates Cxcr4 (Cxcl12) Levels Throughmentioning

confidence: 99%

“…Consequently, both endogenous and grafted NPCs can migrate and differentiate into new neurons according to different chemotactic gradients (Li et al, 2013;Liu et al, 2008). The signaling mechanisms by which chemokines regulate differentiation, cell remodeling and self-repair in pathological circumstances in the CNS may potentially promote recovery to some extent (Bye et al, 2012;Gensel et al, 2012;Hassani et al, 2012). Indeed, proliferation is a feature associated with stem cell transplantation during the first week post-lesion in rodent models of global ischemia (Levison et al, 2001;Chen et al, 2001Chen et al, , 2004Bonecchi et al, 2009).…”

Section: Which Signals Induce Npc Migration Toward Damaged Areas Of Tmentioning

confidence: 99%

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CXCR4/CXCR7 Molecular Involvement in Neuronal and Neural Progenitor Migration: Focus in CNS Repair

Merino

Bellver-Landete

Oset-Gasque

et al. 2014

Journal Cellular Physiology

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In the adult brain, neural progenitor cells (NPCs) reside in the subventricular zone (SVZ) of the lateral ventricles, the dentate gyrus and the olfactory bulb. Following CNS insult, NPCs from the SVZ can migrate along the rostral migratory stream (RMS), a migration of NPCs that is directed by proinflammatory cytokines. Cells expressing CXCR4 follow a homing signal that ultimately leads to neuronal integration and CNS repair, although such molecules can also promote NPC quiescence. The ligand, SDF1 alpha (or CXCL12) is one of the chemokines secreted at sites of injury that it is known to attract NSC-derived neuroblasts, cells that express CXCR4. In function of its concentration, CXCL12 can induce different responses, promoting NPC migration at low concentrations while favoring cell adhesion via EGF and the alpha 6 integrin at high CXCL12 concentrations. However, the preclinical effectiveness of chemokines and their relationship with NPC mobilization requires further study, particularly with respect to CNS repair. NPC migration may also be affected by the release of cytokines or chemokines induced by local inflammation, through autocrine or paracrine mechanisms, as well as through erythropoietin (EPO) or nitric oxide (NO) release. CXCL12 activity requires G-coupled proteins and the availability of its ligand may be modulated by its binding to CXCR7, for which it shows a stronger affinity than for CXCR4.

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“…The surviving neurons and glia are actively involved in synaptic remodeling and tissue repair [43,44]. Additionally, a number of growth factors and cytokines are upregulated within the penumbra region that could potentially aid the graft survival and integration [45,46].…”

Section: Placement Of the Graftmentioning

confidence: 99%

Stem Cells: How We Could Restore the Brain Function After Ischemic Damage

Kokaia¹,

Darasalia

2015

Neuroanesthesia and Cerebrospinal Protection

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Ischemic stroke is caused by occlusion of a cerebral artery, which gives rise to focal ischemia with irreversible injury in a core region and partially reversible damage in the surrounding penumbra zone. Stroke leads to neural death and consequently neurological impairments. Therapeutic intervention of stroke comprises thrombolysis and thrombectomy by chemical or surgical means, respectively. If done in time, these treatments may improve stroke outcome. However, many stroke patients cannot get sufficient degree of such treatment due to incompatibility or delay with admission to the clinic and suffer chronic neurological impairments. This has raised the need to develop effective treatments to improve poststroke recovery. Induced brain plasticity and cell replacement using neural stem cells are two promising strategies for therapy for stroke. This review will discuss the potential of such therapy as well as the factors that need to be taken into account for successful development of new therapy. Neural stem cells are multipotent with the capacity to self-renew and generate mature cells of the nervous system. They can be obtained from embryonic, fetal, or adult central nervous system, as well as through genetic reprogramming of somatic cells. Neural stem cell transplantation has proved to be effective in rodent studies. However, to translate these results into the clinical application, the variety of intrinsic and external factors must be carefully evaluated. This includes accurate stroke outcome predictions, choice of neural stem cell sources and evaluation of the risk of malignant transformation, selection of cell implantation paradigms and criteria for suitable patients.

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Inflammatory Regulators of Redirected Neural Migration in the Injured Brain

Cited by 14 publications

References 203 publications

Neurogenesis and Inflammation after Ischemic Stroke: What is Known and Where We Go from Here

Neurogenesis and Inflammation after Ischemic Stroke: What is Known and Where We Go from Here

CXCR4/CXCR7 Molecular Involvement in Neuronal and Neural Progenitor Migration: Focus in CNS Repair

Stem Cells: How We Could Restore the Brain Function After Ischemic Damage

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