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

Xiong, Nanxiang; Zhao, Hongyang; Zhang, Fangcheng; He, Zhu-Qiang

doi:10.1007/s12264-007-0006-1

Cited by 17 publications

(13 citation statements)

References 14 publications

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“…Furthermore, it was reported previously that Nogo-A expression correlated negatively with the malignancy grade of oligodendrogliomas (73). In this case, a high expression of Nogo-A may restrict vascularization of the oligodendroglioma and thereby limit the tumor growth.…”

Section: Discussionmentioning

confidence: 58%

Nogo-A is a negative regulator of CNS angiogenesis

Wälchli

Pernet

Weinmann

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

104

130

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Nogo-A is an important axonal growth inhibitor in the adult and developing CNS. In vitro, Nogo-A has been shown to inhibit migration and cell spreading of neuronal and nonneuronal cell types. Here, we studied in vivo and in vitro effects of Nogo-A on vascular endothelial cells during angiogenesis of the early postnatal brain and retina in which Nogo-A is expressed by many types of neurons. Genetic ablation or virus-mediated knock down of Nogo-A or neutralization of Nogo-A with an antibody caused a marked increase in the blood vessel density in vivo. In culture, Nogo-A inhibited spreading, migration, and sprouting of primary brain microvascular endothelial cells (MVECs) in a dose-dependent manner and induced the retraction of MVEC lamellipodia and filopodia. Mechanistically, we show that only the Nogo-A–specific Delta 20 domain exerts inhibitory effects on MVECs, but the Nogo-66 fragment, an inhibitory domain common to Nogo-A, -B, and -C, does not. Furthermore, the action of Nogo-A Delta 20 on MVECs required the intracellular activation of the Ras homolog gene family, member A (Rho-A)-associated, coiled-coil containing protein kinase (ROCK)-Myosin II pathway. The inhibitory effects of early postnatal brain membranes or cultured neurons on MVECs were relieved significantly by anti–Nogo-A antibodies. These findings identify Nogo-A as an important negative regulator of developmental angiogenesis in the CNS. They may have important implications in CNS pathologies involving angiogenesis such as stroke, brain tumors, and retinopathies.

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Section: Discussionmentioning

confidence: 58%

Nogo-A is a negative regulator of CNS angiogenesis

Wälchli

Pernet

Weinmann

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

104

130

View full text Add to dashboard Cite

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“…18 RTN4 expression has also been negatively correlated with the malignancy grade of oligodendroglial tumors. 19 NFIB is a transcription factor gene that has been associated with MYB-NFIB Ribosomal protein that is a component of the 60S subunit À2.02 Figure 1 Hierarchical cluster analysis using the most significant differentially expressed genes (y axis) revealed that both actinic keratosis (A) vs normal skin (N) and squamous cell carcinoma (S) vs normal skin (x axis) demonstrated distinct genetic signatures. Downregulated genes are in blue and upregulated genes are in red.…”

Section: Discussionmentioning

confidence: 99%

Molecular discrimination of cutaneous squamous cell carcinoma from actinic keratosis and normal skin

Hui

Binder

2011

Modern Pathology

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Actinic keratosis is widely believed to be a neoplastic lesion and a precursor to invasive squamous cell carcinoma. However, there has been some debate as to whether actinic keratosis is in fact actually squamous cell carcinoma and should be treated as such. As the clinical management and prognosis of patients is widely held to be different for each of these lesions, our goal was to identify unique gene signatures using DNA microarrays to discriminate among normal skin, actinic keratosis, and squamous cell carcinoma, and examine the molecular pathways of carcinogenesis involved in the progression from normal skin to squamous cell carcinoma. Formalin-fixed and paraffin-embedded blocks of skin: five normal skins (pooled), six actinic keratoses, and six squamous cell carcinomas were retrieved. The RNA was extracted and amplified. The labeled targets were hybridized to the Affymetrix human U133plus2.0 array and the acquisition and initial quantification of array images were performed using the GCOS (Affymetrix). The subsequent data analyses were performed using DNA-Chip Analyzer and Partek Genomic Suite 6.4. Significant differential gene expression (42 fold change, Po0.05) was seen with 382 differentially expressed genes between squamous cell carcinoma and normal skin, 423 differentially expressed genes between actinic keratosis and normal skin, and 9 differentially expressed genes between actinic keratosis and squamous cell carcinoma. The differentially expressed genes offer the possibility of using DNA microarrays as a molecular diagnostic tool to distinguish between normal skin, actinic keratosis, and squamous cell carcinoma. In addition, the differentially expressed genes and their molecular pathways could be potentially used as prognostic markers or targets for future therapeutic innovations.

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“…32 Interestingly, Nogo-A expression seems to negatively correlate with the malignancy grade of oligodendrogliomas 42 and to serve as a tool to differentiate between oligodendrogliomas and the more densely vascularized glioblastomas, 43 suggesting that Nogo-A may also be involved in regulation of neo-angiogenesis in brain tumors.…”

Section: Nogo-a Deficiency Augments Vessel Density In Developing Cns mentioning

confidence: 99%

Nogo-A regulates vascular network architecture in the postnatal brain

Wälchli

Ulmann-Schuler

Hintermüller

et al. 2016

J Cereb Blood Flow Metab

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Recently, we discovered a new role for the well-known axonal growth inhibitory molecule Nogo-A as a negative regulator of angiogenesis in the developing central nervous system. However, how Nogo-A affected the three-dimensional (3D) central nervous system (CNS) vascular network architecture remained unknown. Here, using vascular corrosion casting, hierarchical, synchrotron radiation mCT-based network imaging and computer-aided network analysis, we found that genetic ablation of Nogo-A significantly increased the three-dimensional vascular volume fraction in the postnatal day 10 (P10) mouse brain. More detailed analysis of the cerebral cortex revealed that this effect was mainly due to an increased number of capillaries and capillary branchpoints. Interestingly, other vascular parameters such as vessel diameter, -length, -tortuosity, and -volume were comparable between both genotypes for non-capillary vessels and capillaries. Taken together, our three-dimensional data showing more vessel segments and branchpoints at unchanged vessel morphology suggest that stimulated angiogenesis upon Nogo-A gene deletion results in the insertion of complete capillary micro-networks and not just single vessels into existing vascular networks. These findings significantly enhance our understanding of how angiogenesis, vascular remodeling, and three-dimensional vessel network architecture are regulated during central nervous system development. Nogo-A may therefore be a potential novel target for angiogenesis-dependent central nervous system pathologies such as brain tumors or stroke.

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

Cited by 17 publications

References 14 publications

Nogo-A is a negative regulator of CNS angiogenesis

Nogo-A is a negative regulator of CNS angiogenesis

Molecular discrimination of cutaneous squamous cell carcinoma from actinic keratosis and normal skin

Nogo-A regulates vascular network architecture in the postnatal brain

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