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Integrative and comparative single-cell analysis reveals the transcriptomic difference between tumefactive demyelinating lesion and glioma

ABSTRACT: Integrative and comparative single-cell analysis reveals the transcriptomic difference between tumefactive demyelinating lesion and glioma

PROVIDER: PRJNA834648 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19052053_1.fastq.gz	Fastqsanger.gz
	SRR19052053_2.fastq.gz	Fastqsanger.gz
	SRR19052054_1.fastq.gz	Fastqsanger.gz
	SRR19052054_2.fastq.gz	Fastqsanger.gz
	SRR19052055_1.fastq.gz	Fastqsanger.gz

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Integrative and comparative single-cell analysis reveals the transcriptomic difference between tumefactive demyelinating lesion and glioma

Project description:Tumefactive demyelinating lesion (TDL) is an immune-mediated disease which could appear like glioma. Here, we perform integrative and comparative single-cell RNA sequencing (ScRNA-seq) transcriptomic analysis on TDL and glioma lesions.

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Integrative and comparative single-cell analysis reveals transcriptomic difference between human tumefactive demyelinating lesion and glioma.

Project description:Tumefactive demyelinating lesion (TDL) is an immune-mediated disease which can be misdiagnosed as glioma. At present, there is no study comparing difference between the two disorders at the cellular level. Here, we perform integrative and comparative single-cell RNA sequencing (ScRNA-seq) transcriptomic analysis on TDL and glioma lesions. At single-cell resolution, TDL is comprised primarily of immune cells, which is completely different from glioma. The integrated analysis reveals a TDL-specific microglial subset involving in B cell activation and proliferation. Comparative analysis highlights remyelination function of glial cells and demyelination function of T cells in TDL. Subclustering and pseudotime trajectory analysis of T cells in TDL reveal their heterogeneity and diverse functions involving in TDL pathogenesis and recovery process. Our study identifies substantial differences between TDL and glioma at single-cell resolution. The observed heterogeneity and potentially diverse functions of cells in TDL may be critical in disease progression.

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Proteomic and lipidomic profiling of demyelinating lesions identifies fatty acids as modulators in inflammation resolution

Project description:After demyelinating injury of the central nervous system, resolution of the mounting acute innate inflammation is crucial for the initiation of a regenerative response. To identify factors in lesion recovery after demyelination injury, we used a toxin-induced model, in which a single dose of lysolecithin is injected into the corpus callosum to induce a focal demyelinating lesion. Afterwards, we investigated the proteome of demyelinating lesions at different time points post injection (dpi) in a time resolved manner. Lesion sites were excised analyzed from different mice at 0 dpi, without lysolecithin injection, as well as lysolecithin treated mice at 3 dpi, 7 dpi, and 14 dpi. Overall, immune cell migration, especially infiltration of microglia and macrophages, as well as fatty acid metabolism are playing crucial roles for the immidiate response, repair and finally lesion recovery. Additionally, Using lipidomics and eicosanoidomics, we identified bioactive lipids in the resolution phase of inflammation with a marked induction of n-3 polyunsaturated fatty acids. Using fat-1 transgenic mice, which convert n-6 fatty acids to n-3 fatty acids, we found that reduction of the n-6/n-3 ratio facilitates inflammation resolution. In addition, we observed accelerated inflammation resolution and enhanced generation of oligodendrocytes in aged mice when n-3 fatty acids are shuttled to the brain. Thus, n-3 fatty acids and eicosanoids, their oxidized bioactive products, enhance lesion recovery and may therefore provide the basis for novel pro-regenerative medicines of demyelinating diseases in the central nervous system.

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Myelin antigen capture in the CNS by B cells expressing EBV latent membrane protein 1 leads to demyelinating lesion formation [RNA-Seq]

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Myelin antigen capture in the CNS by B cells expressing EBV latent membrane protein 1 leads to demyelinating lesion formation [BRB-seq]

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