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Book ; Online ; Thesis: Mechanismen der Proteinaggregation in Neuronen von Patienten der Machado-Joseph Erkrankung

Jungverdorben, Johannes Christopher [Verfasser]

2016

Author's details	Johannes Jungverdorben
Keywords	Biowissenschaften, Biologie ; Life Science, Biology
Subject code	sg570
Language	German
Publisher	Universitäts- und Landesbibliothek Bonn
Publishing place	Bonn
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Article ; Online: Generation of human cerebral organoids with a structured outer subventricular zone.

Walsh, Ryan M / Luongo, Raffaele / Giacomelli, Elisa / Ciceri, Gabriele / Rittenhouse, Chelsea / Verrillo, Antonietta / Galimberti, Maura / Bocchi, Vittoria Dickinson / Wu, Youjun / Xu, Nan / Mosole, Simone / Muller, James / Vezzoli, Elena / Jungverdorben, Johannes / Zhou, Ting / Barker, Roger A / Cattaneo, Elena / Studer, Lorenz / Baggiolini, Arianna

Cell reports

2024 Volume 43, Issue 4, Page(s) 114031

Abstract: Outer radial glia (oRG) emerge as cortical progenitor cells that support the development of an enlarged outer subventricular zone (oSVZ) and the expansion of the neocortex. The in vitro generation of oRG is essential to investigate the underlying ... ...

Abstract	Outer radial glia (oRG) emerge as cortical progenitor cells that support the development of an enlarged outer subventricular zone (oSVZ) and the expansion of the neocortex. The in vitro generation of oRG is essential to investigate the underlying mechanisms of human neocortical development and expansion. By activating the STAT3 signaling pathway using leukemia inhibitory factor (LIF), which is not expressed in guided cortical organoids, we define a cortical organoid differentiation method from human pluripotent stem cells (hPSCs) that recapitulates the expansion of a progenitor pool into the oSVZ. The oSVZ comprises progenitor cells expressing specific oRG markers such as GFAP, LIFR, and HOPX, closely matching human fetal oRG. Finally, incorporating neural crest-derived LIF-producing cortical pericytes into cortical organoids recapitulates the effects of LIF treatment. These data indicate that increasing the cellular complexity of the organoid microenvironment promotes the emergence of oRG and supports a platform to study oRG in hPSC-derived brain organoids routinely.
MeSH term(s)	Humans ; Organoids/metabolism ; Organoids/cytology ; Leukemia Inhibitory Factor/metabolism ; Leukemia Inhibitory Factor/pharmacology ; Cell Differentiation ; Pluripotent Stem Cells/metabolism ; Pluripotent Stem Cells/cytology ; Lateral Ventricles/cytology ; Lateral Ventricles/metabolism ; STAT3 Transcription Factor/metabolism ; Neuroglia/metabolism ; Neuroglia/cytology ; Signal Transduction
Chemical Substances	Leukemia Inhibitory Factor ; STAT3 Transcription Factor
Language	English
Publishing date	2024-04-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2024.114031
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Article ; Online: Induced pluripotent stem cell-based modeling of neurodegenerative diseases: a focus on autophagy.

Jungverdorben, Johannes / Till, Andreas / Brüstle, Oliver

Journal of molecular medicine (Berlin, Germany)

2017 Volume 95, Issue 7, Page(s) 705–718

Abstract: The advent of cell reprogramming has enabled the generation of induced pluripotent stem cells (iPSCs) from patient skin fibroblasts or blood cells and their subsequent differentiation into tissue-specific cells, including neurons and glia. This approach ... ...

Abstract	The advent of cell reprogramming has enabled the generation of induced pluripotent stem cells (iPSCs) from patient skin fibroblasts or blood cells and their subsequent differentiation into tissue-specific cells, including neurons and glia. This approach can be used to recapitulate disease-specific phenotypes in classical cell culture paradigms and thus represents an invaluable asset for disease modeling and drug validation in the framework of personalized medicine. The autophagy pathway is a ubiquitous eukaryotic degradation and recycling system, which relies on lysosomal degradation of unwanted and potentially cytotoxic components. The relevance of autophagy in the pathogenesis of neurodegenerative diseases is underlined by the observation that disease-linked genetic variants of susceptibility factors frequently result in dysregulation of autophagic-lysosomal pathways. In particular, disrupted autophagy is implied in the accumulation of potentially neurotoxic products such as protein aggregates and their precursors and defective turnover of dysfunctional mitochondria. Here, we review the current state of iPSC-based assessment of autophagic dysfunction in the context of neurodegenerative disease modeling. The collected data show that iPSC technology is capable to reveal even subtle alterations in subcellular homeostatic processes, which form the molecular basis for disease manifestation.
MeSH term(s)	Animals ; Autophagy ; Cellular Reprogramming ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Induced Pluripotent Stem Cells/pathology ; Lysosomes/genetics ; Lysosomes/metabolism ; Lysosomes/pathology ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondria/pathology ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/pathology
Language	English
Publishing date	2017-06-07
Publishing country	Germany
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1223802-8
ISSN	1432-1440 ; 0946-2716
ISSN (online)	1432-1440
ISSN	0946-2716
DOI	10.1007/s00109-017-1533-5
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Article: Generation of human cerebral organoids with a structured outer subventricular zone.

Walsh, Ryan / Giacomelli, Elisa / Ciceri, Gabriele / Rittenhouse, Chelsea / Galimberti, Maura / Wu, Youjun / Muller, James / Vezzoli, Elena / Jungverdorben, Johannes / Zhou, Ting / Barker, Roger A / Cattaneo, Elena / Studer, Lorenz / Baggiolini, Arianna

bioRxiv : the preprint server for biology

2023

Abstract: Mammalian outer radial glia (oRG) emerge as cortical progenitor cells that directly support the development of an enlarged outer subventricular zone (oSVZ) and, in turn, the expansion of the neocortex. ... ...

Abstract	Mammalian outer radial glia (oRG) emerge as cortical progenitor cells that directly support the development of an enlarged outer subventricular zone (oSVZ) and, in turn, the expansion of the neocortex. The
Language	English
Publishing date	2023-02-17
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.02.17.528906
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Article ; Online: Multiparametric rapid screening of neuronal process pathology for drug target identification in HSP patient-specific neurons.

Rehbach, Kristina / Kesavan, Jaideep / Hauser, Stefan / Ritzenhofen, Swetlana / Jungverdorben, Johannes / Schüle, Rebecca / Schöls, Ludger / Peitz, Michael / Brüstle, Oliver

Scientific reports

2019 Volume 9, Issue 1, Page(s) 9615

Abstract: Axonal degeneration is a key pathology of neurodegenerative diseases, including hereditary spastic paraplegia (HSP), a disorder characterized by spasticity in the lower limbs. Treatments for HSP and other neurodegenerative diseases are mainly symptomatic. ...

Abstract	Axonal degeneration is a key pathology of neurodegenerative diseases, including hereditary spastic paraplegia (HSP), a disorder characterized by spasticity in the lower limbs. Treatments for HSP and other neurodegenerative diseases are mainly symptomatic. While iPSC-derived neurons are valuable for drug discovery and target identification, these applications require robust differentiation paradigms and rapid phenotypic read-outs ranging between hours and a few days. Using spastic paraplegia type 4 (SPG4, the most frequent HSP subtype) as an exemplar, we here present three rapid phenotypic assays for uncovering neuronal process pathologies in iPSC-derived glutamatergic cortical neurons. Specifically, these assays detected a 51% reduction in neurite outgrowth and a 60% increase in growth cone area already 24 hours after plating; axonal swellings, a hallmark of HSP pathology, was discernible after only 5 days. Remarkably, the identified phenotypes were neuron subtype-specific and not detectable in SPG4-derived GABAergic forebrain neurons. We transferred all three phenotypic assays to a 96-well setup, applied small molecules and found that a liver X receptor (LXR) agonist rescued all three phenotypes in HSP neurons, providing a potential drug target for HSP treatment. We expect this multiparametric and rapid phenotyping approach to accelerate development of therapeutic compounds for HSP and other neurodegenerative diseases.
MeSH term(s)	Biomarkers ; Cell Differentiation ; Cells, Cultured ; Drug Discovery/methods ; Drug Evaluation, Preclinical/methods ; Haploinsufficiency ; Humans ; Induced Pluripotent Stem Cells/cytology ; Induced Pluripotent Stem Cells/drug effects ; Induced Pluripotent Stem Cells/metabolism ; Neural Stem Cells/cytology ; Neural Stem Cells/drug effects ; Neural Stem Cells/metabolism ; Neuronal Outgrowth ; Neurons/drug effects ; Neurons/metabolism ; Phenotype ; Spastic Paraplegia, Hereditary/drug therapy ; Spastic Paraplegia, Hereditary/etiology ; Spastic Paraplegia, Hereditary/metabolism ; Spastin/genetics
Chemical Substances	Biomarkers ; Spastin (EC 3.6.4.3) ; SPAST protein, human (EC 5.6.1.1)
Language	English
Publishing date	2019-07-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-019-45246-4
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Article ; Online: Activation of HERV-K(HML-2) disrupts cortical patterning and neuronal differentiation by increasing NTRK3.

Nair, Vidya Padmanabhan / Liu, Hengyuan / Ciceri, Gabriele / Jungverdorben, Johannes / Frishman, Goar / Tchieu, Jason / Cederquist, Gustav Y / Rothenaigner, Ina / Schorpp, Kenji / Klepper, Lena / Walsh, Ryan M / Kim, Tae Wan / Cornacchia, Daniela / Ruepp, Andreas / Mayer, Jens / Hadian, Kamyar / Frishman, Dmitrij / Studer, Lorenz / Vincendeau, Michelle

Cell stem cell

2021 Volume 28, Issue 9, Page(s) 1671–1673

Language	English
Publishing date	2021-09-03
Publishing country	United States
Document type	Published Erratum
ZDB-ID	2375354-7
ISSN	1875-9777 ; 1934-5909
ISSN (online)	1875-9777
ISSN	1934-5909
DOI	10.1016/j.stem.2021.05.003
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Article ; Online: Activation of HERV-K(HML-2) disrupts cortical patterning and neuronal differentiation by increasing NTRK3.

Padmanabhan Nair, Vidya / Liu, Hengyuan / Ciceri, Gabriele / Jungverdorben, Johannes / Frishman, Goar / Tchieu, Jason / Cederquist, Gustav Y / Rothenaigner, Ina / Schorpp, Kenji / Klepper, Lena / Walsh, Ryan M / Kim, Tae Wan / Cornacchia, Daniela / Ruepp, Andreas / Mayer, Jens / Hadian, Kamyar / Frishman, Dmitrij / Studer, Lorenz / Vincendeau, Michelle

Cell stem cell

2021 Volume 28, Issue 9, Page(s) 1566–1581.e8

Abstract: The biological function and disease association of human endogenous retroviruses (HERVs) are largely elusive. HERV-K(HML-2) has been associated with neurotoxicity, but there is no clear understanding of its role or mechanistic basis. We addressed the ... ...

Abstract	The biological function and disease association of human endogenous retroviruses (HERVs) are largely elusive. HERV-K(HML-2) has been associated with neurotoxicity, but there is no clear understanding of its role or mechanistic basis. We addressed the physiological functions of HERV-K(HML-2) in neuronal differentiation using CRISPR engineering to activate or repress its expression levels in a human-pluripotent-stem-cell-based system. We found that elevated HERV-K(HML-2) transcription is detrimental for the development and function of cortical neurons. These effects are cell-type-specific, as dopaminergic neurons are unaffected. Moreover, high HERV-K(HML-2) transcription alters cortical layer formation in forebrain organoids. HERV-K(HML-2) transcriptional activation leads to hyperactivation of NTRK3 expression and other neurodegeneration-related genes. Direct activation of NTRK3 phenotypically resembles HERV-K(HML-2) induction, and reducing NTRK3 levels in context of HERV-K(HML-2) induction restores cortical neuron differentiation. Hence, these findings unravel a cell-type-specific role for HERV-K(HML-2) in cortical neuron development.
MeSH term(s)	Cell Differentiation ; Endogenous Retroviruses ; Humans ; Transcriptional Activation
Language	English
Publishing date	2021-05-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2375354-7
ISSN	1875-9777 ; 1934-5909
ISSN (online)	1875-9777
ISSN	1934-5909
DOI	10.1016/j.stem.2021.04.009
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Article ; Online: Altered Levels of Proteins and Phosphoproteins, in the Absence of Early Causative Transcriptional Changes, Shape the Molecular Pathogenesis in the Brain of Young Presymptomatic Ki91 SCA3/MJD Mouse.

Wiatr, Kalina / Piasecki, Piotr / Marczak, Łukasz / Wojciechowski, Paweł / Kurkowiak, Małgorzata / Płoski, Rafał / Rydzanicz, Małgorzata / Handschuh, Luiza / Jungverdorben, Johannes / Brüstle, Oliver / Figlerowicz, Marek / Figiel, Maciej

Molecular neurobiology

2019 Volume 56, Issue 12, Page(s) 8168–8202

Abstract: Spinocerebellar ataxia type 3 (SCA3/MJD) is a polyQ neurodegenerative disease where the presymptomatic phase of pathogenesis is unknown. Therefore, we investigated the molecular network of transcriptomic and proteomic triggers in young presymptomatic ... ...

Abstract	Spinocerebellar ataxia type 3 (SCA3/MJD) is a polyQ neurodegenerative disease where the presymptomatic phase of pathogenesis is unknown. Therefore, we investigated the molecular network of transcriptomic and proteomic triggers in young presymptomatic SCA3/MJD brain from Ki91 knock-in mouse. We found that transcriptional dysregulations resulting from mutant ataxin-3 are not occurring in young Ki91 mice, while old Ki91 mice and also postmitotic patient SCA3 neurons demonstrate the late transcriptomic changes. Unlike the lack of early mRNA changes, we have identified numerous early changes of total proteins and phosphoproteins in 2-month-old Ki91 mouse cortex and cerebellum. We discovered the network of processes in presymptomatic SCA3 with three main groups of disturbed processes comprising altered proteins: (I) modulation of protein levels and DNA damage (Pabpc1, Ddb1, Nedd8), (II) formation of neuronal cellular structures (Tubb3, Nefh, p-Tau), and (III) neuronal function affected by processes following perturbed cytoskeletal formation (Mt-Co3, Stx1b, p-Syn1). Phosphoproteins downregulate in the young Ki91 mouse brain and their phosphosites are associated with kinases that interact with ATXN3 such as casein kinase, Camk2, and kinases controlled by another Atxn3 interactor p21 such as Gsk3, Pka, and Cdk kinases. We conclude that the onset of SCA3 pathology occurs without altered transcript level and is characterized by changed levels of proteins responsible for termination of translation, DNA damage, spliceosome, and protein phosphorylation. This disturbs global cellular processes such as cytoskeleton and transport of vesicles and mitochondria along axons causing energy deficit and neurodegeneration also manifesting in an altered level of transcripts at later ages.
MeSH term(s)	Age Factors ; Animals ; Ataxin-3/genetics ; Ataxin-3/metabolism ; Brain/metabolism ; Brain/pathology ; Cells, Cultured ; Humans ; Machado-Joseph Disease/genetics ; Machado-Joseph Disease/metabolism ; Mice ; Mice, 129 Strain ; Mice, Inbred C57BL ; Mice, Transgenic ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Phosphoproteins/genetics ; Phosphoproteins/metabolism ; Transcription, Genetic/physiology
Chemical Substances	Nerve Tissue Proteins ; Phosphoproteins ; Ataxin-3 (EC 3.4.19.12) ; Atxn3 protein, mouse (EC 3.4.19.12)
Language	English
Publishing date	2019-06-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-019-01643-4
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Article ; Online: Induced pluripotent stem cell-based modeling of mutant LRRK2-associated Parkinson's disease.

Weykopf, Beatrice / Haupt, Simone / Jungverdorben, Johannes / Flitsch, Lea Jessica / Hebisch, Matthias / Liu, Guang-Hui / Suzuki, Keiichiro / Belmonte, Juan Carlos Izpisua / Peitz, Michael / Blaess, Sandra / Till, Andreas / Brüstle, Oliver

The European journal of neuroscience

2019 Volume 49, Issue 4, Page(s) 561–589

Abstract: Recent advances in cell reprogramming have enabled assessment of disease-related cellular traits in patient-derived somatic cells, thus providing a versatile platform for disease modeling and drug development. Given the limited access to vital human ... ...

Abstract	Recent advances in cell reprogramming have enabled assessment of disease-related cellular traits in patient-derived somatic cells, thus providing a versatile platform for disease modeling and drug development. Given the limited access to vital human brain cells, this technology is especially relevant for neurodegenerative disorders such as Parkinson's disease (PD) as a tool to decipher underlying pathomechanisms. Importantly, recent progress in genome-editing technologies has provided an ability to analyze isogenic induced pluripotent stem cell (iPSC) pairs that differ only in a single genetic change, thus allowing a thorough assessment of the molecular and cellular phenotypes that result from monogenetic risk factors. In this review, we summarize the current state of iPSC-based modeling of PD with a focus on leucine-rich repeat kinase 2 (LRRK2), one of the most prominent monogenetic risk factors for PD linked to both familial and idiopathic forms. The LRRK2 protein is a primarily cytosolic multi-domain protein contributing to regulation of several pathways including autophagy, mitochondrial function, vesicle transport, nuclear architecture and cell morphology. We summarize iPSC-based studies that contributed to improving our understanding of the function of LRRK2 and its variants in the context of PD etiopathology. These data, along with results obtained in our own studies, underscore the multifaceted role of LRRK2 in regulating cellular homeostasis on several levels, including proteostasis, mitochondrial dynamics and regulation of the cytoskeleton. Finally, we expound advantages and limitations of reprogramming technologies for disease modeling and drug development and provide an outlook on future challenges and expectations offered by this exciting technology.
MeSH term(s)	Humans ; Induced Pluripotent Stem Cells ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/genetics ; Mitophagy ; Models, Neurological ; Parkinson Disease/genetics ; Parkinson Disease/therapy
Chemical Substances	LRRK2 protein, human (EC 2.7.11.1) ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (EC 2.7.11.1)
Language	English
Publishing date	2019-01-17
Publishing country	France
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	645180-9
ISSN	1460-9568 ; 0953-816X
ISSN (online)	1460-9568
ISSN	0953-816X
DOI	10.1111/ejn.14345
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Article ; Online: Upregulation of miR-370 and miR-543 is associated with reduced expression of heat shock protein 40 in spinocerebellar ataxia type 3.

Evert, Bernd O / Nalavade, Rohit / Jungverdorben, Johannes / Matthes, Frank / Weber, Stephanie / Rajput, Ashish / Bonn, Stefan / Brüstle, Oliver / Peitz, Michael / Krauß, Sybille

PloS one

2018 Volume 13, Issue 8, Page(s) e0201794

Abstract: Molecular chaperones are important regulators of protein folding and proteasomal removal of misfolded proteins. In spinocerebellar ataxia type 3 (SCA3), the co-chaperone DnaJ homology subfamily B member 1 (DNAJB1 or heat shock protein 40) is recruited to ...

Abstract	Molecular chaperones are important regulators of protein folding and proteasomal removal of misfolded proteins. In spinocerebellar ataxia type 3 (SCA3), the co-chaperone DnaJ homology subfamily B member 1 (DNAJB1 or heat shock protein 40) is recruited to protein aggregates formed by the disease-causing mutant polyglutamine (polyQ) protein ataxin-3 (ATXN3). Over-expression of DNAJB1 reduces polyQ protein toxicity. Here, we identified two miRNAs, miR-370 and miR-543, that function in posttranscriptional regulation of DNAJB1 expression. MiRNAs are small endogenously produced RNAs controlling mRNA stability and play a role in polyQ disease pathogenesis. In human neuronal cultures derived from SCA3 patient-specific induced pluripotent stem cell (iPSC) lines, miR-370 and miR-543 levels are upregulated, while DNAJB1 expression is concurrently reduced. These findings suggest that downregulation of DNAJB1 by these two miRNAs is an early event that could contribute to SCA3 pathogenesis. Inhibition of these two miRNAs in turn could stabilize DNAJB1 and thereby be beneficial in SCA3 disease.
MeSH term(s)	Adult ; Aged ; Animals ; Binding Sites ; Disease Models, Animal ; Female ; Gene Expression Regulation ; HSP40 Heat-Shock Proteins/metabolism ; HeLa Cells ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Machado-Joseph Disease/metabolism ; Male ; Mice, Transgenic ; MicroRNAs/metabolism ; Neurons/metabolism ; RNA, Messenger/metabolism ; Rhombencephalon/metabolism ; Young Adult
Chemical Substances	DNAJB1 protein, human ; HSP40 Heat-Shock Proteins ; MIRN370 microRNA, human ; MIRN543 microRNA, human ; MicroRNAs ; RNA, Messenger
Language	English
Publishing date	2018-08-07
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0201794
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