G. Castelo-Branco

Karolinska Institutet Medical Biochemistry and Biophysics

Dr Gonçalo Castelo-Branco is an Associate Professor of Neurobiology at the Department of Medical Biochemistry and Biophysics at Karolinska Institutet, Stockholm, Sweden. Dr. Castelo-Branco received his PhD in Medical Biochemistry in 2005, working on development of dopaminergic neurons and neural stem differentiation. He completed post-doctoral fellowships first at the Karolinska Institutet and then at the University of Cambridge, United Kingdom, working in neural and pluripotent stem cells and chromatin. Dr. Castelo-Branco started his research group in 2012, focusing on the molecular mechanisms defining the epigenetic state of cells of the oligodendrocyte lineage. The main focus of Dr. Castelo-Branco's research group is to investigate how distinct epigenetic states within the oligodendrocyte lineage are established, by identifying key transcription factors, chromatin modifying complexes and non-coding RNAs that are involved in epigenetic transitions, using technologies such as RNA-Seq (single-cell and bulk), quantitative proteomics and epigenomics, among others. The long term aim of his research group to design epigenetic based-therapies to induce regeneration (remyelination) in demyelinating diseases, such as multiple sclerosis. Dr. Castelo-Branco has received many prestigious awards and grants, including the 100 years’ Jubileum Prize of the Swedish Society for Medical Research (SSMF), and research grants from the European Research Council and Knut and Alice Wallenberg Foundation, among others.

Author Of 1 Presentation

Invited Presentations Invited Abstracts

PS14.01 - Oligodendrocyte Heterogeneity in MS

Presentation Number
PS14.01
Presentation Topic
Invited Presentations
Lecture Time
12:45 - 13:00

Abstract

Abstract

Oligodendrocytes are glial cells that mediate myelination of neurons, a process that allows efficient electrical impulse transmission in the central nervous system (CNS). An autoimmune response against myelin triggers demyelination in multiple sclerosis (MS). Oligodendrocyte precursor cells (OPCs) can initially differentiate and promote remyelination in MS, but this process eventually fails in progressive MS. In order to clearly define transcriptional of oligodendrocyte lineage cells in multiple sclerosis, we performed single-cell RNA-Seq in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS and in different kind of CNS lesions from MS patients. We identified disease-specific of oligodendrocytes and OPC populations in EAE, and altered heterogeneity of the oligodendrocyte lineage in MS patients. One of the populations expressed genes involved in antigen processing and presentation and immunoprotection, and presented immunomodulatory properties. We also performed single-cell ATAC-Seq in oligodendroglia from the EAE mouse model of MS and observed transitions in chromatin accessibility correlating with the single-cell transcriptomics data. Thus, our single cell transcriptomics and epigenomics analysis unveiled a transcriptional overhaul during chronic inflammatory demyelination in multiple sclerosis.

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Presenter Of 1 Presentation

Invited Presentations Invited Abstracts

PS14.01 - Oligodendrocyte Heterogeneity in MS

Presentation Number
PS14.01
Presentation Topic
Invited Presentations
Lecture Time
12:45 - 13:00

Abstract

Abstract

Oligodendrocytes are glial cells that mediate myelination of neurons, a process that allows efficient electrical impulse transmission in the central nervous system (CNS). An autoimmune response against myelin triggers demyelination in multiple sclerosis (MS). Oligodendrocyte precursor cells (OPCs) can initially differentiate and promote remyelination in MS, but this process eventually fails in progressive MS. In order to clearly define transcriptional of oligodendrocyte lineage cells in multiple sclerosis, we performed single-cell RNA-Seq in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS and in different kind of CNS lesions from MS patients. We identified disease-specific of oligodendrocytes and OPC populations in EAE, and altered heterogeneity of the oligodendrocyte lineage in MS patients. One of the populations expressed genes involved in antigen processing and presentation and immunoprotection, and presented immunomodulatory properties. We also performed single-cell ATAC-Seq in oligodendroglia from the EAE mouse model of MS and observed transitions in chromatin accessibility correlating with the single-cell transcriptomics data. Thus, our single cell transcriptomics and epigenomics analysis unveiled a transcriptional overhaul during chronic inflammatory demyelination in multiple sclerosis.

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Invited Speaker Of 1 Presentation

Invited Presentations Invited Abstracts

PS14.01 - Oligodendrocyte Heterogeneity in MS

Presentation Number
PS14.01
Presentation Topic
Invited Presentations
Lecture Time
12:45 - 13:00

Abstract

Abstract

Oligodendrocytes are glial cells that mediate myelination of neurons, a process that allows efficient electrical impulse transmission in the central nervous system (CNS). An autoimmune response against myelin triggers demyelination in multiple sclerosis (MS). Oligodendrocyte precursor cells (OPCs) can initially differentiate and promote remyelination in MS, but this process eventually fails in progressive MS. In order to clearly define transcriptional of oligodendrocyte lineage cells in multiple sclerosis, we performed single-cell RNA-Seq in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS and in different kind of CNS lesions from MS patients. We identified disease-specific of oligodendrocytes and OPC populations in EAE, and altered heterogeneity of the oligodendrocyte lineage in MS patients. One of the populations expressed genes involved in antigen processing and presentation and immunoprotection, and presented immunomodulatory properties. We also performed single-cell ATAC-Seq in oligodendroglia from the EAE mouse model of MS and observed transitions in chromatin accessibility correlating with the single-cell transcriptomics data. Thus, our single cell transcriptomics and epigenomics analysis unveiled a transcriptional overhaul during chronic inflammatory demyelination in multiple sclerosis.

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