Immunological regulation of neurogenic niches in the adult brain

González-Pérez, Óscar; Gutiérrez-Fernández, Fernando; Lopez-Virgen, Verónica; Collas-Aguilar, Jorge; Quiñones‐Hinojosa, Alfredo; García‐Verdugo, José Manuel

doi:10.1016/j.neuroscience.2012.08.053

Cited by 79 publications

(76 citation statements)

References 139 publications

(194 reference statements)

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“…Therefore, we extended the areas for statistical analysis by including the entorhinal cortex, which functions as the core of a widespread neuronal network projecting neuronal output to the hippocampal subregions and receiving input from other cortical areas. Cytokines transferred to distinct areas through axonal flow may be a cause of regional damage in the hippocampus because all cell types in the central nervous system, including neurons, are able to produce cytokines during innate immune responses (33,34).…”

Section: Discussionmentioning

confidence: 99%

Mutant Murine Hepatitis Virus-Induced Apoptosis in the Hippocampus

2014

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SUMMARY:The mutant virus Mu-3 was isolated from the soluble receptor-resistant mutant 7 virus (srr7), which is a neuropathogenic strain of the mouse hepatitis virus JHMV, and cloned as a soluble receptor-resistant mutant from the highly neuropathogenic JHMV strain cl-2 virus (cl-2). In order to identify specific characteristcs of Mu-3, the pathology of Mu-3-infected mice was compared with that of srr7-and cl-2-infected mice. The neuropathology after Mu-3 infection exhibited a mixed pattern comparable to that induced by srr7 and cl-2 infections. In addition, Mu-3 infection caused marked apoptotic lesions in the hippocampal region, particularly in the CA2 and CA3 subregions, in the brains of all infected mice. In contrast, in cl-2 infection, 10-20z of the infected mice exhibited apoptosis in the hippocampus, which was primarily observed in the CA1 subregion. Apoptosis also occurred in the pyramidal neurons and CD11b-bearing cells. The apoptotic cells, indicated by caspase 3-activation, were a mixed population of infected and a higher number of uninfected cells. These data indicated that apoptosis observed in Mu-3 infection could be induced by the indirect effects of infection in addition to direct effects of the infected cells occurring in a cell-autonomous manner.

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Section: Discussionmentioning

confidence: 99%

Mutant Murine Hepatitis Virus-Induced Apoptosis in the Hippocampus

2014

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“…Activated blood vessels in peri-infarct tissue secrete stromal-derived factor 1 (SDF-1), a cytokine that is tropic to immature neurons as they migrate to areas of damage after stroke [29,30]. Chemokine (C-C motif) ligand 2, leukemia inhibitory factor, and tumor necrosis factor (TNF)-α are also inflammatory signaling molecules that are released by astrocytes and microglia/ macrophages after stroke, induce distinct stages of normal neurogenesis, and have been implicated in poststroke neurogenesis [27,31,32]. Activated astrocytes and microglia release other cytokines and chemokines that participate in poststroke neurogenesis [27,30,33].…”

Section: Radial Stroke: Triggers For Neural Repairmentioning

confidence: 99%

The 3 Rs of Stroke Biology: Radial, Relayed, and Regenerative

Carmichael

2016

Neurotherapeutics

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Stroke not only causes initial cell death, but also a limited process of repair and recovery. As an overall biological process, stroke has been most often considered from the perspective of early phases of ischemia, how these inter-relate and lead to expansion of the infarct. However, just as the biology of later stages of stroke becomes better understood, the clinical realities of stroke indicate that it is now more a chronic disease than an acute killer. As an overall biological process, it is now more important to understand how early cell death leads to the later, limited recovery so as develop an integrative view of acute to chronic stroke. This progression from death to repair involves sequential stages of primary cell death, secondary injury events, reactive tissue progenitor responses, and formation of new neuronal circuits. This progression is radial: from the tissue that suffers the infarct secondary injury signals, including free radicals and inflammatory cytokines, radiate out from the stroke core to trigger later regenerative events. Injury and repair processes occur not just in the local stroke site, but are also triggered in the connected networks of neurons that had existed in the stroke center: damage signals are relayed throughout a brain network. From these relayed, distributed damage signals, reactive astrocytosis, inflammatory processes, and the formation of new connections occur in distant brain areas. In short, emerging data in stroke cell death studies and the development of the field of stroke neural repair now indicate a continuum in time and in space of progressive events that can be considered as the 3 Rs of stroke biology: radial, relayed, and regenerative.

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“…The major target phenotype of infiltrating lymphocytes in the brain is the microglia and its activation is responsible to drive innate immune response, that leads to the release of interleukin (IL)-1, TNF-a and LIF (leukemia inhibitory factor) [90]. These factors, together with cardiotrophin-1 (CT-1), ciliary neurotrophic factor (CNTF), monocyte chemoattractant protein 1 (MCP-1), IL-6 and IL-18 play an important role during brain inflammation of CNS.…”

Section: Biomarkers Of Cns Involvement In the Leukemiamentioning

confidence: 99%

Central nervous system niche involvement in the leukemia

et al. 2015

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Central nervous system (CNS) impairment is commonly involved in leukemia, as it can be observed upon onset or relapse of the disease. It is associated with poor prognosis and is a challenging clinical problem. The objective of this paper was to provide a characterization of the CNS niche in leukemia, to elucidate the culprits of CNS involvement, including diagnostic micro RNAs (miRs) and early leukemia prognosis. CNS niche is a proper location for homing of leukemic stem cells, thus representing a candidate target in the treatment of leukemia. Recent advances in the study of leukemia hallmarks have enlightened miRs as novel biomarkers for diagnosis and detection of CNS involvement in leukemia, thus providing the opportunity to develop novel therapeutic approaches. Given the importance of prognosis and early diagnosis of CNS involvement in leukemias as well as the severe side effects of current treatments, diagnostic and therapeutic approaches should focus on identification and inhibition of the factors contributing to CNS involvement, including CXCR3, P-selectin glycoprotein ligand-1 and MCP1. MiRs such as miR-221 and miR-222 are emerging as potential tools for an innovative non-invasive therapy of CNS in leukemia affected patients.

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Immunological regulation of neurogenic niches in the adult brain

Cited by 79 publications

References 139 publications

Mutant Murine Hepatitis Virus-Induced Apoptosis in the Hippocampus

Mutant Murine Hepatitis Virus-Induced Apoptosis in the Hippocampus

The 3 Rs of Stroke Biology: Radial, Relayed, and Regenerative

Central nervous system niche involvement in the leukemia

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