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Tumor-associated Reactive Astrocytes Aid the Evolution of Immunosuppressive Environment in Glioblastoma

ABSTRACT: Tumor-associated Reactive Astrocytes Aid the Evolution of Immunosuppressive Environment in Glioblastoma

PROVIDER: PRJNA528024 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8752250_1.fastq.gz	Fastqsanger.gz
	SRR8752260_1.fastq.gz	Fastqsanger.gz
	SRR8752270_1.fastq.gz	Fastqsanger.gz
	SRR8752280_1.fastq.gz	Fastqsanger.gz
	SRR8752251_1.fastq.gz	Fastqsanger.gz

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Tumor-associated Reactive Astrocytes Aid the Evolution of Immunosuppressive Environment in Glioblastoma

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Tumor-associated reactive astrocytes aid the evolution of immunosuppressive environment in glioblastoma.

Project description:Reactive astrocytes evolve after brain injury, inflammatory and degenerative diseases, whereby they undergo transcriptomic re-programming. In malignant brain tumors, their function and crosstalk to other components of the environment is poorly understood. Here we report a distinct transcriptional phenotype of reactive astrocytes from glioblastoma linked to JAK/STAT pathway activation. Subsequently, we investigate the origin of astrocytic transformation by a microglia loss-of-function model in a human organotypic slice model with injected tumor cells. RNA-seq based gene expression analysis of astrocytes reveals a distinct astrocytic phenotype caused by the coexistence of microglia and astrocytes in the tumor environment, which leads to a large release of anti-inflammatory cytokines such as TGFβ, IL10 and G-CSF. Inhibition of the JAK/STAT pathway shifts the balance of pro- and anti-inflammatory cytokines towards a pro-inflammatory environment. The complex interaction of astrocytes and microglia cells promotes an immunosuppressive environment, suggesting that tumor-associated astrocytes contribute to anti-inflammatory responses.

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Exosome-transmitted RVT1 from reactive astrocytes promotes recurrence glioblastoma proliferation

Project description:Glioblastoma (GBM) remains among the most lethal brain tumors despite improvements in treatment. Surgical resection is a universal component of glioma therapy. However, the mechanism underlying postoperative recurrence remains a challenge due to limited information regarding the changes that occur in the postoperative microenvironment. Here, we show that a subtype of proinflammatory reactive astrocytes designated is induced by inflammatory cytokines or injury. We show that reactive astrocytes can secrete the long noncoding RNA (lncRNA) LOC646762 to promotes recurrence glioblastoma proliferation in an exosome-dependent manner.We firstly named this reactive astrocyte associated lnRNA as “lnc-RVT1”.

2018-06-08 | GSE115459 | GEO

Transcriptome analysis of senescent and reactive human fetal astrocytes

Project description:Senescence was recently linked to neurodegeneration. Senescent as well as reactive astrocytes were detected in Parkinson’s disease postmortem brains. This study aimed to determine differences and similarities between senescent and reactive astrocytes. Astrocytes were treated with the stressors hydrogen peroxide or rotenone to induce senescence or with the cytokines TNFa+IL1a or with IL1b to induce reactivity in astrocytes. Comparing the transcriptome of senescent and reactive astrocytes revealed a set of genes specific to senescent astrocytes together with genes regulated in a similar way in both astrocyte states.

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Reactive astrocytes in ALS display dysregulated intron retention

Project description:Reactive astrocytes are implicated in amyotrophic lateral sclerosis (ALS), although the mechanisms controlling reactive transformation are unknown. We show that decreased intron retention (IR) is common to human iPSC-derived astrocytes carrying VCP, C9orf72 and SOD1 ALS-causing mutations as well as astrocytes stimulated to undergo reactive transformation. Notably, transcripts with decreased IR and increased expression are overrepresented in reactivity processes including cell-adhesion, stress-response, and immune-activation. We examined translatome sequencing (TRAP-seq) of astrocytes from a SOD1 mouse model, which revealed that transcripts upregulated in translation significantly overlap with transcripts with decreased IR. Using nucleo-cytoplasmic fractionation of VCP astrocytes coupled with mRNA sequencing and proteomics, we identify that decreased IR in nuclear-detained transcripts is associated with increased cytoplasmic expression of genes and proteins encoding regulators of reactivity - indicating nuclear-to-cytoplasmic translocation and translation of spliced reactivity-related transcripts. Our study provides important insights into the molecular regulation of reactive transformation of ALS astrocytes.

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Exosome-transmitted RVT1 from reactive astrocytes promotes recurrence glioblastoma proliferation

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Reactive astrocytes in ALS models display dysregulated intron retention

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Proteomic profiling of interferon-responsive reactive astrocytes in rodent and human

Project description:Astrocytes are a heterogenous population of glial cells that respond to pathological insults or injury by undergoing a profound transformation called reactivity. Reactive astrocytes exhibit distinct, context-dependent cellular, molecular, and functional states that can either help or hinder tissue homeostasis. We recently identified a subtype of reactive astrocytes in the mouse brain called interferon-responsive reactive astrocytes (IRRAs), defined by interferon-responsive genes like Igtp, Ifit3, Oasl, Mx1, Cxcl10, and Gbp2 . To further this transcriptomic definition of IRRAs, we wanted to define the proteomic changes that occur in this sub-state.

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Transcriptomic profile of reactive astrocytes induced by activation of the JAK2-STAT3 pathway in mouse striatal astrocytes

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