Involvement of wound-associated factors in rat brain astrocyte migratory response to axonal injury: in vitro simulation.

Faber-Elman, A; Solomon, Arieh S.; Abraham, Judith A.; Marikovsky, Moshe; Schwartz, Michal

doi:10.1172/jci118385

Cited by 130 publications

(81 citation statements)

References 84 publications

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“…To this end, we used an in vitro model of neuronal reaction to injury. The model we utilized here was first introduced by Yu et al (50) and has been widely used since to analyze neural reactions to lesions (51,52). Experimental lesions were made by scratching of clones CB, C22, and CE, and the expression of C/EBP␤ was explored at different times after scratching by Western blot and immunofluorescence analyses.…”

Section: Resultsmentioning

confidence: 99%

Microarray Analysis Supports a Role for CCAAT/Enhancer-binding Protein-β in Brain Injury

Cortes‐Canteli

Wagner

Ansorge

et al. 2004

Journal of Biological Chemistry

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CCAAT/enhancer-binding protein-␤ (C/EBP␤) is a transcription factor that plays an important role in regulating cell growth and differentiation. This protein plays a central role in lymphocyte and adipocyte differentiation and hepatic regeneration and in the control of inflammation and immunity in the liver and in cells of the myelomonocytic lineage. Our previous studies suggested that this protein could also have important functions in the brain. Therefore, we were interested in the identification of downstream targets of this transcription factor in cells of neural origin. We performed cDNA microarray analysis and found that a total of 48 genes were up-regulated in C/EBP␤-overexpressing neuronal cells. Of the genes that displayed significant changes in expression, several were involved in inflammatory processes and brain injury. Northern blot analysis confirmed the up-regulation of ornithine decarboxylase, 24p3/LCN2, GRO1/KC, spermidine/spermine N 1 -acetyltransferase, xanthine dehydrogenase, histidine decarboxylase, decorin, and TM4SF1/L6. Using promoter-luciferase reporter transfection assays, we showed the ornithine decarboxylase and 24p3 genes to be biological downstream targets of C/EBP␤ in neuroblastoma cells. Moreover, the levels of C/EBP␤ protein were significantly induced after neuronal injury, which was accompanied by increased levels of cyclooxygenase-2 enzyme. This strongly supports the concept that C/EBP␤ may play an important role in brain injury.

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Section: Resultsmentioning

confidence: 99%

Microarray Analysis Supports a Role for CCAAT/Enhancer-binding Protein-β in Brain Injury

Cortes‐Canteli

Wagner

Ansorge

et al. 2004

Journal of Biological Chemistry

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“…Alternatively, HB-EGF might inhibit cell migration after MCAO by a direct effect on proliferating neurons. HB-EGF exerts not only mitogenic, but also chemoattractant effects on a variety of non-neuronal cell types (Faber-Elman et al, 1996), and HB-EGFinduced cell migration appears to depend on two HB-EGF receptors: EGFR/ErbB1 and NRDc (Nishi et al, 2001). We found previously that both of these receptors (but not another HB-EGF receptor, ErbB4) are expressed on cells in the SVZ (Jin et al, 2002), where they would be in a position to mediate these responses.…”

Section: Hb-egf Modifies Migration Of Svz Cells Toward Hypoxic Corticmentioning

confidence: 99%

Post-ischemic Administration of Heparin-Binding Epidermal Growth Factor-like Growth Factor (HB-EGF) Reduces Infarct Size and Modifies Neurogenesis after Focal Cerebral Ischemia in the Rat

Jin

Sun

Xie

et al. 2004

J Cereb Blood Flow Metab

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Summary: Heparin-binding epidermal growth factor-like growth factor (HB-EGF) is a hypoxia-inducible, neuroprotective protein that also stimulates proliferation of neuronal precursor cells. Accordingly, HB-EGF may contribute to recovery from cerebral injury through direct neuroprotective effects, by enhancing neurogenesis, or both. When administered by the intracerebroventricular route 1-3 days after focal cerebral ischemia in adult rats, HB-EGF decreased the volume of the resulting infarcts and reduced post-ischemic neurological deficits. HB-EGF also increased the incorporation of bromodeoxyuridine into cells expressing the immature neuronal marker protein TUC-4 in the dentate subgranular and rostral subventricular zones, consistent with increased proliferation of neuronal precursors. However, HB-EGF decreased the number of newborn neurons that migrated into the ischemic striatum, perhaps partly because reduction of infarct size by HB-EGF also reduced the stimulus to migration. To determine if HB-EGF might also directly inhibit migration of neuronal precursors, we co-cultured subventricular zone (SVZ) explants treated with HB-EGF or vehicle together with hypoxic cerebral cortical explants, and measured cell migration from the former toward the latter. HB-EGF reduced directed migration of SVZ cells toward the cortical explants, possibly due to a local chemoattractant effect on neuronal precursor cells, which may be mediated through the HB-EGF-specific receptor, N-arginine dibasic convertase. The delayed neuroprotective effect of HB-EGF may have implications for efforts to prolong the therapeutic window for intervention in stroke.

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“…5 In wound-healing models of colonic epithelium, EGF, TGF-a, and HB-EGF play critical roles in enhanced migration of epithelial cells and fibroblasts following their binding to EGFR. 6,7 In primary culture, corneal epithelial cells that are stimulated by TGF-a or EGF become highly motile, involving EGFR and laminin-5 as key intracellular molecules for mediating the motility. 8 In neoplasms, TGF-a stimulation induced sustained MAP-kinase activation in human breast cancer cells, which correlated with enhanced cell motility and in vitro invasion.…”

mentioning

confidence: 99%

“…[10][11][12] In addition, heparin-binding EGF-like growth factor (HB-EGF) has been found to be overexpressed in most human glioblastoma tissues. 13 As HB-EGF is known to promote cell-motility in wound-healing models, 7 it is reasonable to hypothesize that gliomaderived HB-EGF also influences EGFR-mediated glioma motility.…”

mentioning

confidence: 99%

Epidermal growth factor receptor-transfected bone marrow stromal cells exhibit enhanced migratory response and therapeutic potential against murine brain tumors

et al. 2005

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We have created a novel cellular vehicle for gene therapy of malignant gliomas by transfection of murine bone marrow stroma cells (MSCs) with a cDNA encoding epidermal growth factor receptor (EGFR). These cells (EGFR-MSCs) demonstrate enhanced migratory responses toward glioma-conditioned media in comparison to primary MSCs in vitro. Enhanced migration of EGFR-MSC was at least partially dependent on EGF-EGFR, PI3-, MAP kinase kinase, and MAP kinases, protein kinase C, and actin polymerization. Unlike primary MSCs, EGFR-MSCs were resistant to FasL-mediated cytotoxicity and were capable of stimulating allogeneic mixed lymphocyte reaction, suggesting EGFR-MSCs possess suitable characteristics as vehicles for brain tumor immuno-gene therapy. Following injection at various sites, including the contralateral hemisphere in the brain of syngeneic mice, EGFR-MSCs were able to migrate toward GL261 gliomas or B16 melanoma in vivo. Finally, intratumoral injection with EGFR-MSC adenovirally engineered to secrete interferon-a to intracranial GL261 resulted in significantly prolonged survival in comparison to controls. These data indicate that EGFR-MSCs may serve as attractive vehicles for infiltrating brain malignancies such as malignant gliomas.

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Involvement of wound-associated factors in rat brain astrocyte migratory response to axonal injury: in vitro simulation.

Cited by 130 publications

References 84 publications

Microarray Analysis Supports a Role for CCAAT/Enhancer-binding Protein-β in Brain Injury

Microarray Analysis Supports a Role for CCAAT/Enhancer-binding Protein-β in Brain Injury

Post-ischemic Administration of Heparin-Binding Epidermal Growth Factor-like Growth Factor (HB-EGF) Reduces Infarct Size and Modifies Neurogenesis after Focal Cerebral Ischemia in the Rat

Epidermal growth factor receptor-transfected bone marrow stromal cells exhibit enhanced migratory response and therapeutic potential against murine brain tumors

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