Acute Exposure to CNTFin VivoInduces Multiple Components of Reactive Gliosis

Levison, Steven W.; Ducceschi, Melissa H.; Young, Greg M.; Wood, Teresa L.

doi:10.1006/exnr.1996.0160

Cited by 103 publications

(63 citation statements)

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“…Cerebral spinal fluid from a number of CNS and PNS inflammatory diseases contain elevated levels of CNTF protein [157]. Injection of CNTF into the adult rat neocortex stimulates astrogliosis, and more microglia are observed [158], and similar results were obtained by transgenic overexpression of CNTF [154]. Curiously, there appear to be no reports on the course of inflammation in the nervous system of CNTF KO mice.…”

Section: Remarkably Il-11 Also Exertsmentioning

confidence: 93%

Leukemia Inhibitory Factor, Interleukin 6, and Other Cytokines Using the GP130 Transducing Receptor: Roles in Inflammation and Injury

1999

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Inflammation refers to a complex set of mechanisms by which tissues respond to injury and infection. Among the many soluble mediators associated with this process, cytokines are known to be crucial in regulating a variety of cellular and molecular events. Leukemia inhibitory factor (LIF), interleukin 6 (IL-6), IL-11, and possibly other members of this cytokine family are key mediators in various inflammatory processes such as the acute-phase reaction, tissue damage, and infection. These cytokines can act in both pro-inflammatory and anti-inflammatory ways, depending on a number of variables. We emphasize here recent work utilizing knockout mice, which has highlighted the roles of LIF and IL-6, particularly in interactions between the immune and nervous systems.

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Section: Remarkably Il-11 Also Exertsmentioning

confidence: 93%

Leukemia Inhibitory Factor, Interleukin 6, and Other Cytokines Using the GP130 Transducing Receptor: Roles in Inflammation and Injury

1999

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“…Frozen coronal sections (12 m) were cut on a cryostat and mounted on Superfrost Plus microscope slides. Sections at 48 recovery were stained with anti-BrdU (1:10; Cappel, West Chester, PA) as described previously (Levison et al, 1996).…”

Section: Methodsmentioning

confidence: 99%

Neural Stem/Progenitor Cells Participate in the Regenerative Response to Perinatal Hypoxia/Ischemia

Felling¹,

Snyder²,

Romanko³

et al. 2006

J. Neurosci.

174

166

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Perinatal hypoxia/ischemia (H/I) is the leading cause of neurologic injury resulting from birth complications. Recent advances in critical care have dramatically improved the survival rate of infants suffering this insult, but ϳ50% of survivors will develop neurologic sequelae such as cerebral palsy, epilepsy or cognitive deficits. Here we demonstrate that tripotential neural stem/progenitor cells (NSPs) participate in the regenerative response to perinatal H/I as their numbers increase 100% by 3 d and that they alter their intrinsic properties to divide using expansive symmetrical cell divisions. We further show that production of new striatal neurons follows the expansion of NSPs. Increased proliferation within the NSP niche occurs at 2 d after perinatal H/I, and the proliferating cells express nestin. Of those stem-cell related genes that change, the membrane receptors Notch1, gp-130, and the epidermal growth factor receptor, as well as the downstream transcription factor Hes5, which stimulate NSP proliferation and regulate stem cellness are induced before NSP expansion. The mechanisms for the reactive expansion of the NSPs reported here reveal potential therapeutic targets that could be exploited to amplify this response, thus enabling endogenous precursors to restore a normal pattern of brain development after perinatal H/I.

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“…Emerich et al (1996), for instance, have shown a major neuroprotection in the striatum in the absence of a reported glial differentiation after continuous intraventricular CN TF release by encapsulated cells at a rate (15 ng /10 6 cells per 24 hr), which is in the range of that obtained by recombinant adenovirus in culture (Smith et al, 1996) and probably is an order of magnitude superior to the C N TF concentration in the present study. Reciprocally, Winter et al (1995) and Levison et al (1996) have shown so-called "astrogliosis, " and C latterbuck et al (1996) have described more precisely the phenotypic alteration of astrocytes as "gemistocytic" after injections of recombinant CNTF in the vicinity of intraparenchymal injection sites in the first two studies and more widespread, but using a much higher (1 g) very concentrated (0.2 l) amount of C N TF, in the last study.…”

Section: Apparent Low Efficiency Of the Astroglial Differentiating Acmentioning

confidence: 99%

“…Altogether, a low-efficiency C N TF effect on astrocytes, relative to the highly efficient neuroprotective action of the factor, may help to explain why contradictory results have been obtained in experiments looking for a glial effect (Meyer and Unsicker, 1994;Kahn et al, 1995;Winter et al, 1995;Clatterbuck et al, 1996;Levison et al, 1996;Smith et al, 1996) (see references and discussion in Sendtner et al, 1994). This hypothesis adds to, but does not oppose, two other suggestions recently put forward by Smith et al (1996), namely, an effect related to a particular stage of glial differentiation or requiring specific cell-to-cell interaction.…”

Section: Apparent Low Efficiency Of the Astroglial Differentiating Acmentioning

confidence: 99%

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Phenotypic Alteration of Astrocytes Induced by Ciliary Neurotrophic Factor in the Intact Adult Brain, As Revealed by Adenovirus-Mediated Gene Transfer

et al. 1997

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Synthesis of the ciliary neurotrophic factor (CNTF) and its specific receptor (CNTFR␣) is widespread in the intact CNS, but potential biological roles for this system remain elusive. Contradictory results have been obtained concerning a possible effect on the morphological and biochemical phenotype of astrocytes. To reassess this question, we have taken advantage of adenovirus-mediated gene transfer into the rat brain to obtain the local release of CNTF. Stereotaxic administration of CNTF recombinant adenovirus vectors into the striatum led to phenotypic changes in astrocytes located in regions that were related axonally to striatal neurons at the injection site. Astrocytes appeared hypertrophied and displayed an increase in both GFAP and CNTF immunoreactivity. This response was observed up to 5 weeks after injection, the longest time studied. It was not observed after the administration of a control vector. The methodology used in the present study, allowing us to analyze the effect of the factor in areas remote from the injection site, has provided conclusive evidence that CNTF affects the astroglial phenotype in the intact CNS. The characteristics of these effects may explain why contradictory results have been obtained previously, because this signaling system seems to have a low efficiency and therefore requires a high local concentration of the factor close to the target cells. One might speculate as to the involvement of a CNTF astroglioastroglial signaling system in the organized response of a population of astrocytes to changes in CNS homeostasis detected locally, even by a single cell.

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Acute Exposure to CNTFin VivoInduces Multiple Components of Reactive Gliosis

Cited by 103 publications

References 0 publications

Leukemia Inhibitory Factor, Interleukin 6, and Other Cytokines Using the GP130 Transducing Receptor: Roles in Inflammation and Injury

Leukemia Inhibitory Factor, Interleukin 6, and Other Cytokines Using the GP130 Transducing Receptor: Roles in Inflammation and Injury

Neural Stem/Progenitor Cells Participate in the Regenerative Response to Perinatal Hypoxia/Ischemia

Phenotypic Alteration of Astrocytes Induced by Ciliary Neurotrophic Factor in the Intact Adult Brain, As Revealed by Adenovirus-Mediated Gene Transfer

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