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Book ; Conference proceedings: Research in arthritis

Hardingham, T. E.

(British journal of rheumatology ; 30, Suppl. 1)

1991

Institution	Mathilda and Terence Kennedy Institute of Rheumatology
Event/congress	Kennedy Institute of Rheumatology 25th Anniversary Symposium (1990, London)
Author's details	Kennedy Institute of Rheumatology 25th Anniversary Symposium, 1990
Series title	British journal of rheumatology ; 30, Suppl. 1
Collection
Keywords	Arthritis / congresses ; Research / congresses
Size	80 S. : Ill., graph. Darst.
Publisher	Baillière Tindall
Publishing place	London
Publishing country	Great Britain
Document type	Book ; Conference proceedings
HBZ-ID	HT003810381
Database	Catalogue ZB MED Medicine, Health

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Article ; Online: Enhanced chondrogenesis from human embryonic stem cells.

Wang, Tao / Nimkingratana, Puwapong / Smith, Christopher A / Cheng, Aixin / Hardingham, Timothy E / Kimber, Susan J

Stem cell research

2019 Volume 39, Page(s) 101497

Abstract: Human embryonic stem cells (hESCs) have great potential for the repair of damaged articular cartilage. We developed a serum-free 14-day protocol for hESC differentiation into chondrocyte progenitors, which surprisingly lacked strong cartilage matrix ... ...

Abstract	Human embryonic stem cells (hESCs) have great potential for the repair of damaged articular cartilage. We developed a serum-free 14-day protocol for hESC differentiation into chondrocyte progenitors, which surprisingly lacked strong cartilage matrix production in in vitro tests. In order to direct these progenitors to a more mature phenotype, we investigated substituting different members of the TGFβ family in the protocol. Initially, we supplemented, or substituted GDF5 (day 11-14), with combinations of BMP7 and TGFβ-1, or -3, but these modifications yielded no improvement in matrix gene expression. However, replacing BMP4 with BMP2 (days 3-10 of the protocol) resulted in a more rapid increase in SOX9 gene expression and increased expression of chondrogenic genes SOX5, ACAN and COL2A1. The replacement of BMP4 with BMP2 also enhanced the formation of chondrogenic cell aggregates, with greater deposition of type II collagen. This change was not accompanied by hypertrophic chondrocyte marker COL10A1 expression. The results demonstrate that BMP2 has greater specificity for the generation of chondrogenic cells from hESCs than BMP4 and this was consistent in two hESC lines (HUES1 and MAN7). hESC-chondrogenic cells derived with either BMP2 or BMP4 were tested in vivo by implanting them in fibrin into osteochondral defects in the femur of RNU rats. Repaired cartilage tissue, positive for Safranin O and type II collagen was detected at 6 and 12 weeks with both cell sources, but the BMP2 cells scored higher for tissue quality (Pineda score). Therefore, BMP2 is more effective at driving chondrogenic differentiation from human pluripotent stem cells than BMP4 and the effect on the resulting chondroprogenitors is sustained in an in vivo setting.
MeSH term(s)	Apoptosis/drug effects ; Blotting, Western ; Bone Morphogenetic Protein 2/pharmacology ; Bone Morphogenetic Protein 4/pharmacology ; Cell Differentiation/drug effects ; Cell Line ; Chondrogenesis/drug effects ; Flow Cytometry ; Fluorescent Antibody Technique ; Human Embryonic Stem Cells/cytology ; Human Embryonic Stem Cells/drug effects ; Human Embryonic Stem Cells/metabolism ; Humans
Chemical Substances	Bone Morphogenetic Protein 2 ; Bone Morphogenetic Protein 4
Language	English
Publishing date	2019-07-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2393143-7
ISSN	1876-7753 ; 1873-5061
ISSN (online)	1876-7753
ISSN	1873-5061
DOI	10.1016/j.scr.2019.101497
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Article: 40 Years of CSF Toxicity Studies in ALS: What Have We Learnt About ALS Pathophysiology?

Ng Kee Kwong, Koy Chong / Harbham, Pratap K / Selvaraj, Bhuvaneish T / Gregory, Jenna M / Pal, Suvankar / Hardingham, Giles E / Chandran, Siddharthan / Mehta, Arpan R

Frontiers in molecular neuroscience

2021 Volume 14, Page(s) 647895

Abstract: Based on early evidence ... ...

Abstract	Based on early evidence of
Language	English
Publishing date	2021-03-18
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2452967-9
ISSN	1662-5099
ISSN	1662-5099
DOI	10.3389/fnmol.2021.647895
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Article ; Online: High preoperative levels of circulating SFRP5 predict better prognosis in colorectal cancer patients.

Kirana, Chandra / Smith, Eric / Ngo, Doan T / Trochsler, Markus I / Hewett, Peter J / Stubbs, Richard S / Hardingham, Jennifer E / Maddern, Guy J / Hauben, Ehud

Future oncology (London, England)

2020 Volume 16, Issue 31, Page(s) 2499–2509

Abstract: The purpose of this research was to investigate the diagnostic and prognostic value of circulating SFRP5 (cSFRP5) in colorectal cancer (CRC). We evaluated preoperative cSFRP5 levels in CRC patients and controls (n = 208). We found significantly higher ... ...

Abstract	The purpose of this research was to investigate the diagnostic and prognostic value of circulating SFRP5 (cSFRP5) in colorectal cancer (CRC). We evaluated preoperative cSFRP5 levels in CRC patients and controls (n = 208). We found significantly higher cSFRP5 levels in CRC patients compared with non-CRC controls (p < 0.001). Levels of cSFRP5 were significantly lower in CRC patients with either vascular invasion (p = 0.001) or liver metastasis (p = 0.016). High cSFRP5 levels were associated with longer disease-free survival in both univariate (p = 0.024) and multivariate (p = 0.015) analyses. Analysis of an independent tissue cohort from The Cancer Genome Atlas database revealed significantly lower
MeSH term(s)	Adaptor Proteins, Signal Transducing/blood ; Aged ; Aged, 80 and over ; Biomarkers, Tumor ; Colorectal Neoplasms/blood ; Colorectal Neoplasms/diagnosis ; Colorectal Neoplasms/mortality ; Colorectal Neoplasms/surgery ; DNA Methylation ; Enzyme-Linked Immunosorbent Assay ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; Middle Aged ; Neoplasm Metastasis ; Neoplasm Staging ; Preoperative Period ; Prognosis ; Promoter Regions, Genetic ; ROC Curve
Chemical Substances	Adaptor Proteins, Signal Transducing ; Biomarkers, Tumor ; SFRP5 protein, human
Language	English
Publishing date	2020-10-13
Publishing country	England
Document type	Journal Article
ZDB-ID	2274956-1
ISSN	1744-8301 ; 1479-6694
ISSN (online)	1744-8301
ISSN	1479-6694
DOI	10.2217/fon-2020-0356
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Article ; Online: Astrocyte-oligodendrocyte interaction regulates central nervous system regeneration.

Nature communications

2023 Volume 14, Issue 1, Page(s) 3372

Abstract: Failed regeneration of myelin around neuronal axons following central nervous system damage contributes to nerve dysfunction and clinical decline in various neurological conditions, for which there is an unmet therapeutic demand. Here, we show that ... ...

Abstract	Failed regeneration of myelin around neuronal axons following central nervous system damage contributes to nerve dysfunction and clinical decline in various neurological conditions, for which there is an unmet therapeutic demand. Here, we show that interaction between glial cells - astrocytes and mature myelin-forming oligodendrocytes - is a determinant of remyelination. Using in vivo/ ex vivo/ in vitro rodent models, unbiased RNA sequencing, functional manipulation, and human brain lesion analyses, we discover that astrocytes support the survival of regenerating oligodendrocytes, via downregulation of the Nrf2 pathway associated with increased astrocytic cholesterol biosynthesis pathway activation. Remyelination fails following sustained astrocytic Nrf2 activation in focally-lesioned male mice yet is restored by either cholesterol biosynthesis/efflux stimulation, or Nrf2 inhibition using the existing therapeutic Luteolin. We identify that astrocyte-oligodendrocyte interaction regulates remyelination, and reveal a drug strategy for central nervous system regeneration centred on targeting this interaction.
MeSH term(s)	Male ; Mice ; Animals ; Humans ; Astrocytes/metabolism ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; Central Nervous System/metabolism ; Oligodendroglia/metabolism ; Myelin Sheath/metabolism ; Nerve Regeneration/physiology ; Cholesterol/metabolism
Chemical Substances	NF-E2-Related Factor 2 ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2023-06-08
Publishing country	England
Document type	Journal Article ; 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/s41467-023-39046-8
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Article ; Online: Functional brain defects in a mouse model of a chromosomal t(1;11) translocation that disrupts DISC1 and confers increased risk of psychiatric illness.

Bonneau, Marion / Sullivan, Shane T O' / Gonzalez-Lozano, Miguel A / Baxter, Paul / Gautier, Phillippe / Marchisella, Elena / Hardingham, Neil R / Chesters, Robert A / Torrance, Helen / Howard, David M / Jansen, Maurits A / McMillan, Melanie / Singh, Yasmin / Didier, Michel / Koopmans, Frank / Semple, Colin A / McIntosh, Andrew M / Volkmer, Hansjürgen / Loos, Maarten /

Fox, Kevin / Hardingham, Giles E / Vernon, Anthony C / Porteous, David J / Smit, August B / Price, David J / Kirsty Millar, J

Translational psychiatry

2021 Volume 11, Issue 1, Page(s) 135

Abstract: A balanced t(1;11) translocation that directly disrupts DISC1 is linked to schizophrenia and ... for dysregulation of the same genes and molecular pathways as in neuron cultures generated previously from human t(1 ... therefore apparently accounts for a substantial proportion of the effects of the t(1;11) translocation. RNAseq and ...

Abstract	A balanced t(1;11) translocation that directly disrupts DISC1 is linked to schizophrenia and affective disorders. We previously showed that a mutant mouse, named Der1, recapitulates the effect of the translocation upon DISC1 expression. Here, RNAseq analysis of Der1 mouse brain tissue found enrichment for dysregulation of the same genes and molecular pathways as in neuron cultures generated previously from human t(1;11) translocation carriers via the induced pluripotent stem cell route. DISC1 disruption therefore apparently accounts for a substantial proportion of the effects of the t(1;11) translocation. RNAseq and pathway analysis of the mutant mouse predicts multiple Der1-induced alterations converging upon synapse function and plasticity. Synaptosome proteomics confirmed that the Der1 mutation impacts synapse composition, and electrophysiology found reduced AMPA:NMDA ratio in hippocampal neurons, indicating changed excitatory signalling. Moreover, hippocampal parvalbumin-positive interneuron density is increased, suggesting that the Der1 mutation affects inhibitory control of neuronal circuits. These phenotypes predict that neurotransmission is impacted at many levels by DISC1 disruption in human t(1;11) translocation carriers. Notably, genes implicated in schizophrenia, depression and bipolar disorder by large-scale genetic studies are enriched among the Der1-dysregulated genes, just as we previously observed for the t(1;11) translocation carrier-derived neurons. Furthermore, RNAseq analysis predicts that the Der1 mutation primarily targets a subset of cell types, pyramidal neurons and interneurons, previously shown to be vulnerable to the effects of common schizophrenia-associated genetic variants. In conclusion, DISC1 disruption by the t(1;11) translocation may contribute to the psychiatric disorders of translocation carriers through commonly affected pathways and processes in neurotransmission.
MeSH term(s)	Animals ; Brain/metabolism ; Disease Models, Animal ; Humans ; Mice ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Parvalbumins/metabolism ; Schizophrenia/genetics
Chemical Substances	DISC1 protein, human ; Disc1 protein, mouse ; Nerve Tissue Proteins ; Parvalbumins
Language	English
Publishing date	2021-02-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2609311-X
ISSN	2158-3188 ; 2158-3188
ISSN (online)	2158-3188
ISSN	2158-3188
DOI	10.1038/s41398-021-01256-3
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Article ; Online: Mixed-species RNA-seq for elucidation of non-cell-autonomous control of gene transcription.

Qiu, Jing / Dando, Owen / Baxter, Paul S / Hasel, Philip / Heron, Samuel / Simpson, T Ian / Hardingham, Giles E

Nature protocols

2018 Volume 13, Issue 10, Page(s) 2176–2199

Abstract: Transcriptomic changes induced in one cell type by another mediate many biological processes in the brain and elsewhere; however, achieving artifact-free physical separation of cell types to study them is challenging and generally allows for analysis of ... ...

Abstract	Transcriptomic changes induced in one cell type by another mediate many biological processes in the brain and elsewhere; however, achieving artifact-free physical separation of cell types to study them is challenging and generally allows for analysis of only a single cell type. We describe an approach using a co-culture of distinct cell types from different species that enables physical cell sorting to be replaced by in silico RNA sequencing (RNA-seq) read sorting, which is possible because of evolutionary divergence of messenger RNA (mRNA) sequences. As an exemplary experiment, we describe the co-culture of purified neurons, astrocytes, and microglia from different species (12-14 d). We describe how to use our Python tool, Sargasso, to separate the reads from conventional RNA-seq according to species and to eliminate any artifacts borne of imperfect genome annotation (10 h). We show how this procedure, which requires no special skills beyond those that might normally be expected of wet lab and bioinformatics researchers, enables the simultaneous transcriptomic profiling of different cell types, revealing the distinct influence of microglia on astrocytic and neuronal transcriptomes under inflammatory conditions.
MeSH term(s)	Animals ; Astrocytes/cytology ; Astrocytes/metabolism ; Base Sequence ; Cells, Cultured ; Coculture Techniques/methods ; Computer Simulation ; Gene Expression Profiling/methods ; Humans ; Mice ; Microglia/cytology ; Microglia/metabolism ; Neurons/cytology ; Neurons/metabolism ; RNA, Messenger/genetics ; Rats ; Sequence Analysis, RNA/methods ; Species Specificity ; Transcription, Genetic ; Transcriptional Activation ; Transcriptome
Chemical Substances	RNA, Messenger
Language	English
Publishing date	2018-09-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2244966-8
ISSN	1750-2799 ; 1754-2189
ISSN (online)	1750-2799
ISSN	1754-2189
DOI	10.1038/s41596-018-0029-2
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Article ; Online: Altered network properties in C9ORF72 repeat expansion cortical neurons are due to synaptic dysfunction.

Perkins, Emma M / Burr, Karen / Banerjee, Poulomi / Mehta, Arpan R / Dando, Owen / Selvaraj, Bhuvaneish T / Suminaite, Daumante / Nanda, Jyoti / Henstridge, Christopher M / Gillingwater, Thomas H / Hardingham, Giles E / Wyllie, David J A / Chandran, Siddharthan / Livesey, Matthew R

Molecular neurodegeneration

2021 Volume 16, Issue 1, Page(s) 13

Abstract: Background: Physiological disturbances in cortical network excitability and plasticity are established and widespread in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) patients, including those harbouring the C9ORF72 repeat ... ...

Abstract	Background: Physiological disturbances in cortical network excitability and plasticity are established and widespread in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) patients, including those harbouring the C9ORF72 repeat expansion (C9ORF72 Methods: To address this we have generated cortical neurons from patient-derived iPSCs harbouring C9ORF72 Results: We find that C9ORF72 Conclusion: These findings suggest synaptic pathophysiology is widespread in ALS-FTD and has an early and fundamental role in driving altered network function that is thought to contribute to neurodegenerative processes in these patients. The overall importance is the identification of previously unidentified defects in pre and postsynaptic compartments affecting synaptic plasticity, synaptic vesicle stores, and network propagation, which directly impact upon cortical function.
MeSH term(s)	Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/metabolism ; C9orf72 Protein/genetics ; C9orf72 Protein/metabolism ; DNA Repeat Expansion/genetics ; Frontotemporal Dementia/genetics ; Frontotemporal Dementia/metabolism ; Humans ; Induced Pluripotent Stem Cells/cytology ; Motor Neurons/metabolism ; Mutation/genetics ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/metabolism
Chemical Substances	C9orf72 Protein ; C9orf72 protein, human
Language	English
Publishing date	2021-03-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2244557-2
ISSN	1750-1326 ; 1750-1326
ISSN (online)	1750-1326
ISSN	1750-1326
DOI	10.1186/s13024-021-00433-8
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Article ; Online: Mitochondrial bioenergetic deficits in C9orf72 amyotrophic lateral sclerosis motor neurons cause dysfunctional axonal homeostasis.

Mehta, Arpan R / Gregory, Jenna M / Dando, Owen / Carter, Roderick N / Burr, Karen / Nanda, Jyoti / Story, David / McDade, Karina / Smith, Colin / Morton, Nicholas M / Mahad, Don J / Hardingham, Giles E / Chandran, Siddharthan / Selvaraj, Bhuvaneish T

Acta neuropathologica

2021 Volume 141, Issue 2, Page(s) 257–279

Abstract: Axonal dysfunction is a common phenotype in neurodegenerative disorders, including in amyotrophic lateral sclerosis (ALS), where the key pathological cell-type, the motor neuron (MN), has an axon extending up to a metre long. The maintenance of axonal ... ...

Abstract	Axonal dysfunction is a common phenotype in neurodegenerative disorders, including in amyotrophic lateral sclerosis (ALS), where the key pathological cell-type, the motor neuron (MN), has an axon extending up to a metre long. The maintenance of axonal function is a highly energy-demanding process, raising the question of whether MN cellular energetics is perturbed in ALS, and whether its recovery promotes axonal rescue. To address this, we undertook cellular and molecular interrogation of multiple patient-derived induced pluripotent stem cell lines and patient autopsy samples harbouring the most common ALS causing mutation, C9orf72. Using paired mutant and isogenic expansion-corrected controls, we show that C9orf72 MNs have shorter axons, impaired fast axonal transport of mitochondrial cargo, and altered mitochondrial bioenergetic function. RNAseq revealed reduced gene expression of mitochondrially encoded electron transport chain transcripts, with neuropathological analysis of C9orf72-ALS post-mortem tissue importantly confirming selective dysregulation of the mitochondrially encoded transcripts in ventral horn spinal MNs, but not in corresponding dorsal horn sensory neurons, with findings reflected at the protein level. Mitochondrial DNA copy number was unaltered, both in vitro and in human post-mortem tissue. Genetic manipulation of mitochondrial biogenesis in C9orf72 MNs corrected the bioenergetic deficit and also rescued the axonal length and transport phenotypes. Collectively, our data show that loss of mitochondrial function is a key mediator of axonal dysfunction in C9orf72-ALS, and that boosting MN bioenergetics is sufficient to restore axonal homeostasis, opening new potential therapeutic strategies for ALS that target mitochondrial function.
MeSH term(s)	Adult ; Aged ; Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/metabolism ; Amyotrophic Lateral Sclerosis/pathology ; Axons/metabolism ; C9orf72 Protein/genetics ; Electron Transport/genetics ; Energy Metabolism/genetics ; Female ; Gene Dosage ; Gene Expression Regulation ; Homeostasis ; Humans ; Induced Pluripotent Stem Cells ; Male ; Middle Aged ; Mitochondria/metabolism ; Motor Neurons/metabolism ; Posterior Horn Cells/pathology
Chemical Substances	C9orf72 Protein ; C9orf72 protein, human
Language	English
Publishing date	2021-01-04
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1079-0
ISSN	1432-0533 ; 0001-6322
ISSN (online)	1432-0533
ISSN	0001-6322
DOI	10.1007/s00401-020-02252-5
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Article ; Online: Biology and therapeutic implications of VEGF-A splice isoforms and single-nucleotide polymorphisms in colorectal cancer.

Canavese, Miriam / Ngo, Doan T M / Maddern, Guy J / Hardingham, Jennifer E / Price, Timothy J / Hauben, Ehud

International journal of cancer

2017 Volume 140, Issue 10, Page(s) 2183–2191

Abstract: Tumor growth, dissemination and metastasis are dependent on angiogenesis. The predominant vascular endothelial growth factor (VEGF) isoform that plays a major role in angiogenesis is VEGF-A. Indeed, VEGF-A is implicated in promoting angiogenesis of ... ...

Abstract	Tumor growth, dissemination and metastasis are dependent on angiogenesis. The predominant vascular endothelial growth factor (VEGF) isoform that plays a major role in angiogenesis is VEGF-A. Indeed, VEGF-A is implicated in promoting angiogenesis of numerous solid malignancies, including colorectal cancer (CRC). A large body of preclinical and clinical evidence indicates that the expression of specific VEGF-A isoforms represents a predominant pro-angiogenic factor, which is associated with formation of metastases and poor prognosis in CRC patients. Different isoforms of human VEGF-A have been identified, all of which arise from alternative splicing of the primary transcript of a single gene. Notably, it has been recently demonstrated that expression of type 3 isoform pattern is significantly correlated with venous involvement in CRC as well as in progression to metastatic colorectal cancer (mCRC), although it remains unclear what proportion of CRC tumors express these isoforms. This review highlights the importance of investigating the genetic and the epigenetic variations in VEGF-A pathways in CRC, the functions of different VEGF-A isoforms and their potential application as prognostic markers and/or therapeutic targets. Better understanding of the mechanisms controlling angiogenesis in liver metastases is necessary to address the limitations of current anti-angiogenic therapies.
MeSH term(s)	Alternative Splicing/genetics ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/therapy ; Humans ; Polymorphism, Single Nucleotide/genetics ; Protein Isoforms ; Vascular Endothelial Growth Factor A/genetics
Chemical Substances	Protein Isoforms ; VEGFA protein, human ; Vascular Endothelial Growth Factor A
Language	English
Publishing date	2017-05-15
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	218257-9
ISSN	1097-0215 ; 0020-7136
ISSN (online)	1097-0215
ISSN	0020-7136
DOI	10.1002/ijc.30567
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