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Effect of maternal obesogenic diet exposure on murine Neurofibromatosis Type 1 optic pathway glioma

ABSTRACT: Effect of maternal obesogenic diet exposure on murine Neurofibromatosis Type 1 optic pathway glioma

PROVIDER: PRJNA1122182 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29348928_1.fastq.gz	Fastqsanger.gz
	SRR29348928_2.fastq.gz	Fastqsanger.gz
	SRR29348929_1.fastq.gz	Fastqsanger.gz
	SRR29348929_2.fastq.gz	Fastqsanger.gz
	SRR29348930_1.fastq.gz	Fastqsanger.gz

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Effect of maternal obesogenic diet exposure on murine Neurofibromatosis Type 1 optic pathway glioma

Project description:Pediatric low-grade glioma incidence has been rising in the U.S., mirroring the rising rates of pediatric and maternal obesity. Recently, children of obese mothers were demonstrated to develop brain tumors at higher rates. Importantly, obesity in the U.S. is largely driven by diet, given the abudnance of high fat and high sugar food choices. We identified that combined maternal and postnatal obesogenic (Ob) diet exposure accelerated glioma formation in murine Neurofibromatosis type 1 (Nf1) optic pathway glioma (OPG)-forming mice, a model of pediatric glioma formation. Postnatal dietary exposure alone could not fully recaptiulate these effects, indicating maternal exposure was critical for this phenotype. To determine how Ob exposure affected gene expression in the optic nerve, we isolated Ob-exposed versus CD-exposed optic nerves and performed RNASeq. Enriched pathways included nervous system development, neuronal signaling and appetite regulation.

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RNA-sequencing of tumor-associated microglia reveals Ccl5 as a stromal chemokine critical for neurofibromatosis-1 glioma growth

Project description:Solid cancers develop within a supportive microenvironment that promotes tumor formation and continued growth through the elaboration of mitogens and chemokines. Within these tumors, monocytes (macrophages and microglia) represent rich sources of these stromal factors. Leveraging a genetically-engineered mouse model of neurofibromatosis type 1 (NF1) low-grade brain tumor (optic glioma), previous studies have demonstrated that microglia are important for glioma formation and maintenance. To identify the tumor-associated microglial factors that support glioma growth (gliomagens), we employed a comprehensive large scale discovery effort using optimized advanced RNA-sequencing methods. Candidate gliomagens were prioritized to identify potential secreted or membrane-bound proteins, which were next validated by quantitative RT-PCR and RNA FISH following minocycline-mediated microglial inactivation in vivo. Using these selection criteria, Ccl5 was identified as a highly expressed chemokine in both genetically engineered Nf1 mouse and human optic gliomas. As a candidate gliomagen, recombinant Ccl5 increased Nf1-deficient optic nerve astrocyte growth in vitro. Importantly, consistent with its critical role in maintaining tumor growth, Ccl5 inhibition with neutralizing antibodies reduced Nf1 mouse optic glioma growth in vivo. Collectively, these findings establish Ccl5 as critical stromal growth factor in low-grade glioma maintenance relevant to future microglia-targeted therapies for brain tumors.

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Temporal, spatial, and genetic constraints contribute to the patterning and penetrance of murine Neurofibromatosis-1 optic glioma

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Project description:The study investigates the role of NF1 mutation and neuronal activity on the initiation of optic pathway glioma, a type of low-grade glioma. the RNAseq dataset investigates mRNA expression profile of human pilocytic astrocytomas (WHO grade I)

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Project description:Individuals with neurofibromatosis type 1 (NF1) are prone to develop optic pathway gliomas that can result in significant visual impairment. To explore the cellular basis for the reduced visual function resulting from optic glioma formation, we used a genetically engineered mouse model of Nf1 optic glioma (Nf1+/-(GFAP)CKO mice). We performed multimodal functional and structural analyses both before and after the appearance of macroscopic tumors. At 6 weeks of age, before obvious glioma formation, Nf1+/-(GFAP)CKO mice had decreased visual-evoked potential amplitudes and increased optic nerve axon calibers. By 3 months of age, Nf1+/-(GFAP)CKO mice exhibited pronounced optic nerve axonopathy and apoptosis of neurons in the retinal ganglion cell layer. Magnetic resonance diffusion tensor imaging showed a progressive increase in radial diffusivity between 6 weeks and 6 months of age in the optic nerve proximal to the tumor indicating ongoing deterioration of axons. These data suggest that optic glioma formation results in early axonal disorganization and damage, which culminates in retinal ganglion cell death. Collectively, this study shows that Nf1+/-(GFAP)CKO mice can provide a useful model for defining mechanisms of visual abnormalities in children with NF1 and lay the foundations for future interventional studies aimed at reducing visual loss.

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