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Article ; Online: Antidepressants cheer up hepatic B1 B cells: Hope for the treatment of autoimmune liver diseases?

Amendt, Timm / Tybulewicz, Victor L J

2023 Volume 13, Page(s) 1083173

MeSH term(s)	Humans ; Antidepressive Agents ; B-Lymphocytes ; Liver Diseases
Chemical Substances	Antidepressive Agents
Language	English
Publishing date	2023-01-17
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.1083173
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Article ; Online: Affordable optical clearing and immunolabelling in mouse brain slices.

Muza, Phillip M / Pérez, Marta / Noy, Suzanna / Kurosawa, Miyu / Katsouri, Loukia / Tybulewicz, Victor L J / Fisher, Elizabeth M C / West, Steven J

BMC research notes

2023 Volume 16, Issue 1, Page(s) 246

Abstract: Traditional histological analysis is conducted on thin tissue sections, limiting the data capture from large tissue volumes to 2D profiles, and requiring stereological methods for 3D assessment. Recent advances in microscopical and tissue clearing ... ...

Abstract	Traditional histological analysis is conducted on thin tissue sections, limiting the data capture from large tissue volumes to 2D profiles, and requiring stereological methods for 3D assessment. Recent advances in microscopical and tissue clearing methods have facilitated 3D reconstructions of tissue structure. However, staining of large tissue blocks remains a challenge, often requiring specialised and expensive equipment to clear and immunolabel tissue. Here, we present the Affordable Brain Slice Optical Clearing (ABSOC) method: a modified iDISCO protocol which enables clearing and immunolabeling of mouse brain slices up to 1 mm thick using inexpensive reagents and equipment, with no intensive expert training required. We illustrate the use of ABSOC in 1 mm C57BL/6J mouse coronal brain slices sectioned through the dorsal hippocampus and immunolabelled with an anti-calretinin antibody. The ABSOC method can be readily used for histological studies of mouse brain in order to move from the use of very thin tissue sections to large volumes of tissue - giving more representative analysis of biological samples, without the need for sampling of small regions only.
MeSH term(s)	Mice ; Animals ; Mice, Inbred C57BL ; Brain ; Microscopy/methods ; Imaging, Three-Dimensional/methods ; Specimen Handling
Language	English
Publishing date	2023-09-30
Publishing country	England
Document type	Journal Article
ZDB-ID	2413336-X
ISSN	1756-0500 ; 1756-0500
ISSN (online)	1756-0500
ISSN	1756-0500
DOI	10.1186/s13104-023-06511-y
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Article ; Online: Investigating brain alterations in the Dp1Tyb mouse model of Down syndrome.

Serrano, Maria Elisa / Kim, Eugene / Siow, Bernard / Ma, Da / Rojo, Loreto / Simmons, Camilla / Hayward, Darryl / Gibbins, Dorota / Singh, Nisha / Strydom, Andre / Fisher, Elizabeth M C / Tybulewicz, Victor L J / Cash, Diana

Neurobiology of disease

2024 Volume 188, Page(s) 106336

Abstract: Down syndrome (DS) is one of the most common birth defects and the most prevalent genetic form of intellectual disability. DS arises from trisomy of chromosome 21, but its molecular and pathological consequences are not fully understood. In this study, ... ...

Abstract	Down syndrome (DS) is one of the most common birth defects and the most prevalent genetic form of intellectual disability. DS arises from trisomy of chromosome 21, but its molecular and pathological consequences are not fully understood. In this study, we compared Dp1Tyb mice, a DS model, against their wild-type (WT) littermates of both sexes to investigate the impact of DS-related genetic abnormalities on the brain phenotype. We performed
MeSH term(s)	Male ; Female ; Mice ; Animals ; Down Syndrome/pathology ; Trisomy/genetics ; Trisomy/pathology ; Glutamine/metabolism ; Brain/metabolism ; Hippocampus/metabolism ; Disease Models, Animal
Chemical Substances	Glutamine (0RH81L854J)
Language	English
Publishing date	2024-01-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2023.106336
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Article ; Online: Genetic dissection of triplicated chromosome 21 orthologs yields varying skeletal traits in Down syndrome model mice.

Sloan, Kourtney / Thomas, Jared / Blackwell, Matthew / Voisard, Deanna / Lana-Elola, Eva / Watson-Scales, Sheona / Roper, Daniel L / Wallace, Joseph M / Fisher, Elizabeth M C / Tybulewicz, Victor L J / Roper, Randall J

Disease models & mechanisms

2023 Volume 16, Issue 4

Abstract: Down syndrome (DS) phenotypes result from triplicated genes, but the effects of three copy genes are not well known. A mouse mapping panel genetically dissecting human chromosome 21 (Hsa21) syntenic regions was used to investigate the contributions and ... ...

Abstract	Down syndrome (DS) phenotypes result from triplicated genes, but the effects of three copy genes are not well known. A mouse mapping panel genetically dissecting human chromosome 21 (Hsa21) syntenic regions was used to investigate the contributions and interactions of triplicated Hsa21 orthologous genes on mouse chromosome 16 (Mmu16) on skeletal phenotypes. Skeletal structure and mechanical properties were assessed in femurs of male and female Dp9Tyb, Dp2Tyb, Dp3Tyb, Dp4Tyb, Dp5Tyb, Dp6Tyb, Ts1Rhr and Dp1Tyb;Dyrk1a+/+/- mice. Dp1Tyb mice, with the entire Hsa21 homologous region of Mmu16 triplicated, display bone deficits similar to those of humans with DS and served as a baseline for other strains in the panel. Bone phenotypes varied based on triplicated gene content, sex and bone compartment. Three copies of Dyrk1a played a sex-specific, essential role in trabecular deficits and may interact with other genes to influence cortical deficits related to DS. Triplicated genes in Dp9Tyb and Dp2Tyb mice improved some skeletal parameters. As triplicated genes can both improve and worsen bone deficits, it is important to understand the interaction between and molecular mechanisms of skeletal alterations affected by these genes.
MeSH term(s)	Humans ; Mice ; Male ; Female ; Animals ; Down Syndrome/genetics ; Chromosomes, Human, Pair 21 ; Disease Models, Animal ; Phenotype
Language	English
Publishing date	2023-04-26
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2451104-3
ISSN	1754-8411 ; 1754-8403
ISSN (online)	1754-8411
ISSN	1754-8403
DOI	10.1242/dmm.049927
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Article ; Online: Cognitive impairments in a Down syndrome model with abnormal hippocampal and prefrontal dynamics and cytoarchitecture.

Muza, Phillip M / Bush, Daniel / Pérez-González, Marta / Zouhair, Ines / Cleverley, Karen / Sopena, Miriam L / Aoidi, Rifdat / West, Steven J / Good, Mark / Tybulewicz, Victor L J / Walker, Matthew C / Fisher, Elizabeth M C / Chang, Pishan

iScience

2023 Volume 26, Issue 2, Page(s) 106073

Abstract: The Dp(10)2Yey mouse carries a ∼2.3-Mb intra-chromosomal duplication of mouse chromosome 10 (Mmu10) that has homology to human chromosome 21, making it an essential model for aspects of Down syndrome (DS, trisomy 21). In this study, we investigated ... ...

Abstract	The Dp(10)2Yey mouse carries a ∼2.3-Mb intra-chromosomal duplication of mouse chromosome 10 (Mmu10) that has homology to human chromosome 21, making it an essential model for aspects of Down syndrome (DS, trisomy 21). In this study, we investigated neuronal dysfunction in the Dp(10)2Yey mouse and report spatial memory impairment and anxiety-like behavior alongside altered neural activity in the medial prefrontal cortex (mPFC) and hippocampus (HPC). Specifically, Dp(10)2Yey mice showed impaired spatial alternation associated with increased sharp-wave ripple activity in mPFC during a period of memory consolidation, and reduced mobility in a novel environment accompanied by reduced theta-gamma phase-amplitude coupling in HPC. Finally, we found alterations in the number of interneuron subtypes in mPFC and HPC that may contribute to the observed phenotypes and highlight potential approaches to ameliorate the effects of human trisomy 21.
Language	English
Publishing date	2023-01-28
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.106073
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Article ; Online: B cell-intrinsic requirement for WNK1 kinase in antibody responses in mice.

Hayward, Darryl A / Vanes, Lesley / Wissmann, Stefanie / Sivapatham, Sujana / Hartweger, Harald / Biggs O'May, Joshua / de Boer, Leonard L / Mitter, Richard / Köchl, Robert / Stein, Jens V / Tybulewicz, Victor L J

The Journal of experimental medicine

2023 Volume 220, Issue 3

Abstract: Migration and adhesion play critical roles in B cells, regulating recirculation between lymphoid organs, migration within lymphoid tissue, and interaction with CD4+ T cells. However, there is limited knowledge of how B cells integrate chemokine receptor ... ...

Abstract	Migration and adhesion play critical roles in B cells, regulating recirculation between lymphoid organs, migration within lymphoid tissue, and interaction with CD4+ T cells. However, there is limited knowledge of how B cells integrate chemokine receptor and integrin signaling with B cell activation to generate efficient humoral responses. Here, we show that the WNK1 kinase, a regulator of migration and adhesion, is essential in B cells for T-dependent and -independent antibody responses. We demonstrate that WNK1 transduces signals from the BCR, CXCR5, and CD40, and using intravital imaging, we show that WNK1 regulates migration of naive and activated B cells, and their interactions with T cells. Unexpectedly, we show that WNK1 is required for BCR- and CD40-induced proliferation, acting through the OXSR1 and STK39 kinases, and for efficient B cell-T cell collaboration in vivo. Thus, WNK1 is critical for humoral immune responses, by regulating B cell migration, adhesion, and T cell-dependent activation.
MeSH term(s)	Mice ; Animals ; Antibody Formation ; B-Lymphocytes ; Lymphoid Tissue ; Signal Transduction ; CD4-Positive T-Lymphocytes ; CD40 Antigens/metabolism ; WNK Lysine-Deficient Protein Kinase 1/metabolism
Chemical Substances	CD40 Antigens ; Wnk1 protein, mouse (EC 2.7.11.1) ; WNK Lysine-Deficient Protein Kinase 1 (EC 2.7.11.1)
Language	English
Publishing date	2023-01-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20211827
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Article ; Online: Craniofacial dysmorphology in Down syndrome is caused by increased dosage of Dyrk1a and at least three other genes.

Redhead, Yushi / Gibbins, Dorota / Lana-Elola, Eva / Watson-Scales, Sheona / Dobson, Lisa / Krause, Matthias / Liu, Karen J / Fisher, Elizabeth M C / Green, Jeremy B A / Tybulewicz, Victor L J

Development (Cambridge, England)

2023 Volume 150, Issue 8

Abstract: Down syndrome (DS), trisomy of human chromosome 21 (Hsa21), occurs in 1 in 800 live births and is the most common human aneuploidy. DS results in multiple phenotypes, including craniofacial dysmorphology, which is characterised by midfacial hypoplasia, ... ...

Abstract	Down syndrome (DS), trisomy of human chromosome 21 (Hsa21), occurs in 1 in 800 live births and is the most common human aneuploidy. DS results in multiple phenotypes, including craniofacial dysmorphology, which is characterised by midfacial hypoplasia, brachycephaly and micrognathia. The genetic and developmental causes of this are poorly understood. Using morphometric analysis of the Dp1Tyb mouse model of DS and an associated mouse genetic mapping panel, we demonstrate that four Hsa21-orthologous regions of mouse chromosome 16 contain dosage-sensitive genes that cause the DS craniofacial phenotype, and identify one of these causative genes as Dyrk1a. We show that the earliest and most severe defects in Dp1Tyb skulls are in bones of neural crest (NC) origin, and that mineralisation of the Dp1Tyb skull base synchondroses is aberrant. Furthermore, we show that increased dosage of Dyrk1a results in decreased NC cell proliferation and a decrease in size and cellularity of the NC-derived frontal bone primordia. Thus, DS craniofacial dysmorphology is caused by an increased dosage of Dyrk1a and at least three other genes.
MeSH term(s)	Mice ; Humans ; Animals ; Down Syndrome/genetics ; Skull ; Chromosome Mapping ; Phenotype ; Disease Models, Animal
Language	English
Publishing date	2023-04-26
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	90607-4
ISSN	1477-9129 ; 0950-1991
ISSN (online)	1477-9129
ISSN	0950-1991
DOI	10.1242/dev.201077
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Ub I Zs.183: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 91: Show issues

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Article ; Online: Chloride sensing by WNK1 regulates NLRP3 inflammasome activation and pyroptosis.

Mayes-Hopfinger, Lindsey / Enache, Aura / Xie, Jian / Huang, Chou-Long / Köchl, Robert / Tybulewicz, Victor L J / Fernandes-Alnemri, Teresa / Alnemri, Emad S

Nature communications

2021 Volume 12, Issue 1, Page(s) 4546

Abstract: The NLRP3 inflammasome mediates the production of proinflammatory cytokines and initiates inflammatory cell death. Although NLRP3 is essential for innate immunity, aberrant NLRP3 inflammasome activation contributes to a wide variety of inflammatory ... ...

Abstract	The NLRP3 inflammasome mediates the production of proinflammatory cytokines and initiates inflammatory cell death. Although NLRP3 is essential for innate immunity, aberrant NLRP3 inflammasome activation contributes to a wide variety of inflammatory diseases. Understanding the pathways that control NLRP3 activation will help develop strategies to treat these diseases. Here we identify WNK1 as a negative regulator of the NLRP3 inflammasome. Macrophages deficient in WNK1 protein or kinase activity have increased NLRP3 activation and pyroptosis compared with control macrophages. Mice with conditional knockout of WNK1 in macrophages have increased IL-1β production in response to NLRP3 stimulation compared with control mice. Mechanistically, WNK1 tempers NLRP3 activation by balancing intracellular Cl
MeSH term(s)	Animals ; Caspase 1/metabolism ; Chlorides/metabolism ; Female ; Imidazoles/pharmacology ; Immunity, Innate/drug effects ; Inflammasomes/metabolism ; Interleukin-1beta/metabolism ; L-Lactate Dehydrogenase/metabolism ; Lipopolysaccharides/pharmacology ; Macrophages/drug effects ; Macrophages/metabolism ; Male ; Mice, Inbred C57BL ; Models, Biological ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Neutrophils/drug effects ; Neutrophils/metabolism ; Potassium/metabolism ; Protein Serine-Threonine Kinases/metabolism ; Pyroptosis/drug effects ; Pyrrolidines/pharmacology ; Tamoxifen/pharmacology ; WNK Lysine-Deficient Protein Kinase 1/antagonists & inhibitors ; WNK Lysine-Deficient Protein Kinase 1/metabolism ; Mice
Chemical Substances	Chlorides ; Imidazoles ; Inflammasomes ; Interleukin-1beta ; Lipopolysaccharides ; NLR Family, Pyrin Domain-Containing 3 Protein ; Pyrrolidines ; WNK463 ; Tamoxifen (094ZI81Y45) ; L-Lactate Dehydrogenase (EC 1.1.1.27) ; Stk39 protein, mouse (EC 2.7.1.-) ; OXSR1 protein, mouse (EC 2.7.11.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; WNK Lysine-Deficient Protein Kinase 1 (EC 2.7.11.1) ; Wnk1 protein, mouse (EC 2.7.11.1) ; Caspase 1 (EC 3.4.22.36) ; Potassium (RWP5GA015D)
Language	English
Publishing date	2021-07-27
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-021-24784-4
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Article ; Online: Increased dosage of DYRK1A leads to congenital heart defects in a mouse model of Down syndrome.

Science translational medicine

2024 Volume 16, Issue 731, Page(s) eadd6883

Abstract: Down syndrome (DS) is caused by trisomy of human chromosome 21 (Hsa21). DS is a gene dosage disorder that results in multiple phenotypes including congenital heart defects. This clinically important cardiac pathology is the result of a third copy of one ... ...

Abstract	Down syndrome (DS) is caused by trisomy of human chromosome 21 (Hsa21). DS is a gene dosage disorder that results in multiple phenotypes including congenital heart defects. This clinically important cardiac pathology is the result of a third copy of one or more of the approximately 230 genes on Hsa21, but the identity of the causative dosage-sensitive genes and hence mechanisms underlying this cardiac pathology remain unclear. Here, we show that hearts from human fetuses with DS and embryonic hearts from the Dp1Tyb mouse model of DS show reduced expression of mitochondrial respiration genes and cell proliferation genes. Using systematic genetic mapping, we determined that three copies of the dual-specificity tyrosine phosphorylation-regulated kinase 1A (
MeSH term(s)	Animals ; Humans ; Mice ; Disease Models, Animal ; Down Syndrome/genetics ; Genes, Mitochondrial ; Heart Defects, Congenital/genetics ; Myocytes, Cardiac ; Trisomy
Chemical Substances	Dyrk1a protein, mouse (EC 2.7.1.-)
Language	English
Publishing date	2024-01-24
Publishing country	United States
Document type	Journal Article
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.add6883
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Article ; Online: T cell migration requires ion and water influx to regulate actin polymerization.

de Boer, Leonard L / Vanes, Lesley / Melgrati, Serena / Biggs O'May, Joshua / Hayward, Darryl / Driscoll, Paul C / Day, Jason / Griffiths, Alexander / Magueta, Renata / Morrell, Alexander / MacRae, James I / Köchl, Robert / Tybulewicz, Victor L J

Nature communications

2023 Volume 14, Issue 1, Page(s) 7844

Abstract: Migration of T cells is essential for their ability to mount immune responses. Chemokine-induced T cell migration requires WNK1, a kinase that regulates ion influx into the cell. However, it is not known why ion entry is necessary for T cell movement. ... ...

Abstract	Migration of T cells is essential for their ability to mount immune responses. Chemokine-induced T cell migration requires WNK1, a kinase that regulates ion influx into the cell. However, it is not known why ion entry is necessary for T cell movement. Here we show that signaling from the chemokine receptor CCR7 leads to activation of WNK1 and its downstream pathway at the leading edge of migrating CD4
MeSH term(s)	Actins/metabolism ; Polymerization ; Cell Movement/physiology ; Actin Cytoskeleton/metabolism ; Signal Transduction/physiology
Chemical Substances	Actins
Language	English
Publishing date	2023-12-06
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-43423-8
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