Nogo‐66 and myelin‐associated glycoprotein (MAG) inhibit the adhesion and migration of Nogo‐66 receptor expressing human glioma cells

Liao, Hong; Duka, Tetyana; Teng, Felicia Yu Hsuan; Lee, Sun; Bu, Wenyu; Ahmed, Sohail; Tang, Bor Luen; Xiao, Zhicheng

doi:10.1111/j.1471-4159.2004.02573.x

Cited by 45 publications

(39 citation statements)

References 15 publications

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“…Liao H et al [9] showed that the substratum adherence and migration of human U87MG glioma cells in culture were significantly attenuated by the extracellular domain of Nogo-A (Nogo-66) and the myelin-associated glycoprotein (MAG). U87MG cells contained large amounts of endogenous Nogo-66 receptors (NgRs).…”

Section: Discussionmentioning

confidence: 99%

“…Liao H et al [9] reported that the substratum adherence and migration of human U87MG glioma cells in the culture were significantly attenuated by the extracellular domains of Nogo-A, indicating that Nogo-A can modulate glioma growth and migration. However, Teng FY et al [14] hypothesized that Nogo isoforms might have the antitumorigenic or tumorsuppressing activity.…”

Section: Introductionmentioning

confidence: 99%

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Negative correlation of Nogo-A with the malignancy of oligodendroglial tumor

et al. 2007

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Objective Nogo-A is an axon regeneration inhibitor, and its function in central nervous system (CNS) is still unknown. The present study is to explore the relationship between the expression of Nogo-A and the malignancy of oligodendroglial tumors in patients. Methods Tumor tissue samples with different malignancy grade were obtained from the hospitals. The samples used for detection had been diagnosed as oligodendroglial tumors (oligodendroglioma or anaplastic oligodendroglioma). The expression of Nogo-A was detected by immunohistochemistry and western-blot analysis. The correlation test between the Nogo-A expression and the morphological changes (the percentages of atypical cells and mitotic cells in the tumors) related to the malignancy of tumor tissues was performed. Results There was significant negative correlation between the Nogo-A expression and the morphological change of tumor tissues according to immunohistochemistry. Western-blot analysis also indicated that the gray value of Nogo-A protein band in the oligodendroglioma group was significantly higher than that in the anaplastic oligodendroglioma group. Conclusion Nogo-A expression was negatively correlated with the malignancy grade of oligodendroglial tumors.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Negative correlation of Nogo-A with the malignancy of oligodendroglial tumor

et al. 2007

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“…Like other members of the reticulon family, Nogo is an endoplasmic reticulum-enriched protein, and interactions with other endoplasmic reticulum, mitochondrial and cytoplasmic proteins may be important for various cellular physiological processes. The fact that Nogo-deficient mice apparently exhibit a normal physiological phenotype could be related to the compensatory roles that other members of the reticulon family might perform in normal physiology [31,32]. …”

Section: Discussionmentioning

confidence: 99%

Expression of Nogo-A Is Decreased with Increasing Gestational Age in the Human Fetal Brain

et al. 2012

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Nogo is a member of the reticulon family. Our understanding of the physiological functions of the Nogo-A protein has grown over the last few years, and this molecule is now recognized as one of the most important axonal regrowth inhibitors present in central nervous system (CNS) myelin. Nogo-A plays other important roles in nervous system development, epilepsy, vascular physiology, muscle pathology, stroke, inflammation, and CNS tumors. Since the exact role of Nogo-A protein in human brain development is still poorly understood, we studied its cellular and regional distribution by immunohistochemistry in the frontal lobe of 30 human fetal brains. Nogo-A was expressed in the following cortical zones: ependyma, ventricular zone, subventricular zone, intermediate zone, subplate, cortical plate, and marginal zone. The number of positive cells decreased significantly with increasing gestational age in the subplate and marginal zone. Using different antibodies, changes in isoform expression and dimerization states could be shown between various cortical zones. The results demonstrate a significant change in the expression of Nogo-A during the development of the human brain. The effects of its time- and region-specific regulation have to be further studied in detail.

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“…For instance, Nogo-A and NgR1 have been implicated in neurosphere cell proliferation (Li et al, 2011), differentiation (Wang and Zhu, 2008;Lööv et al, 2012), and control of tumor malignancy (Liao et al, 2004;Cheung et al, 2009;Xiong et al, 2012). The latter findings point to the participation of Nogo-A/NgR1 signaling in the regulation of other aspects of growth, such as tissue expansion or turnover by cell proliferation.…”

Section: Introductionmentioning

confidence: 99%

“…Here, neural stem cells (NSCs) with astrocytic features generate intermediate progenitors giving rise to neuroblasts that migrate to the olfactory bulb (OB) along the rostral migratory stream (RMS) (Kriegstein and Alvarez-Buylla, 2009;Ihrie and Alvarez-Buylla, 2011). Using pharmacological approaches along with in vitro and in vivo experiments, we found that Nogo-A/NgR1 signaling regulates the pace of neuronal neogeneration by reducing NSC proliferation.…”

Section: Introductionmentioning

confidence: 99%

Distinct Roles of Nogo-A and Nogo Receptor 1 in the Homeostatic Regulation of Adult Neural Stem Cell Function and Neuroblast Migration

et al. 2012

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In the adult mammalian subventricular zone (SVZ), GFAP-positive neural stem cells (NSCs) generate neuroblasts that migrate tangentially along the rostral migratory stream (RMS) toward the olfactory bulb (OB). In the mouse brain, we found that the plasticity inhibitors Nogo-A and Nogo receptor 1 (NgR1) are differentially expressed in the SVZ-OB system, in which Nogo-A identifies immature neuroblasts and NgR1 germinal astrocytes. We therefore examined the role of Nogo-A and NgR1 in the regulation of neurogenesis. Pharmacological experiments show that Nogo-66/NgR1 interaction reduces the proliferation of NSCs. This is consistent with a negative-feedback loop, in which newly generated neurons modulate cell division of SVZ stem cells. Moreover, the Nogo-A-⌬20 domain promotes neuroblast migration toward the OB through activation of the Rho/ROCK (Rho-associated, coiled-coil containing protein kinase) pathway, without the participation of NgR1. Our findings reveal a new unprecedented function for Nogo-A and NgR1 in the homeostatic regulation of the pace of neurogenesis in the adult mouse SVZ and in the migration of neuroblasts along the RMS.

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Nogo‐66 and myelin‐associated glycoprotein (MAG) inhibit the adhesion and migration of Nogo‐66 receptor expressing human glioma cells

Cited by 45 publications

References 15 publications

Negative correlation of Nogo-A with the malignancy of oligodendroglial tumor

Negative correlation of Nogo-A with the malignancy of oligodendroglial tumor

Expression of Nogo-A Is Decreased with Increasing Gestational Age in the Human Fetal Brain

Distinct Roles of Nogo-A and Nogo Receptor 1 in the Homeostatic Regulation of Adult Neural Stem Cell Function and Neuroblast Migration

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