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Article ; Online: Molecular mechanisms underlying adverse effects of dexamethasone and betamethasone in the developing cardiovascular system.

Garrud, Tessa A C / Teulings, Noor E W D / Niu, Youguo / Skeffington, Katie L / Beck, Christian / Itani, Nozomi / Conlon, Fiona G / Botting, Kimberley J / Nicholas, Lisa M / Tong, Wen / Derks, Jan B / Ozanne, Susan E / Giussani, Dino A

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2023 Volume 37, Issue 6, Page(s) e22887

Abstract: Antenatal glucocorticoids accelerate fetal lung maturation and reduce mortality in preterm babies but can trigger adverse effects on the cardiovascular system. The mechanisms underlying off-target effects of the synthetic glucocorticoids mostly used, ... ...

Abstract	Antenatal glucocorticoids accelerate fetal lung maturation and reduce mortality in preterm babies but can trigger adverse effects on the cardiovascular system. The mechanisms underlying off-target effects of the synthetic glucocorticoids mostly used, Dexamethasone (Dex) and Betamethasone (Beta), are unknown. We investigated effects of Dex and Beta on cardiovascular structure and function, and underlying molecular mechanism using the chicken embryo, an established model system to isolate effects of therapy on the developing heart and vasculature, independent of effects on the mother or placenta. Fertilized eggs were treated with Dex (0.1 mg kg
MeSH term(s)	Chick Embryo ; Female ; Pregnancy ; Animals ; Betamethasone/adverse effects ; Glucocorticoids/adverse effects ; Heart ; Arteries ; Dexamethasone/adverse effects
Chemical Substances	Betamethasone (9842X06Q6M) ; Glucocorticoids ; Dexamethasone (7S5I7G3JQL)
Language	English
Publishing date	2023-05-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202200676RR
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Article: APRIL in B-cell malignancies and autoimmunity.

Kimberley, Fiona C / Medema, Jan Paul / Hahne, Michael

Results and problems in cell differentiation

2009 Volume 49, Page(s) 161–182

Abstract: A Proliferation Inducing Ligand (APRIL) was first identified as a cytokine expressed predominantly by tumour tissues and was not found in most normal tissues. The activity of this new cytokine, in terms of its ability to stimulate tumour cell ... ...

Abstract	A Proliferation Inducing Ligand (APRIL) was first identified as a cytokine expressed predominantly by tumour tissues and was not found in most normal tissues. The activity of this new cytokine, in terms of its ability to stimulate tumour cell proliferation in vivo, determined the catchy acronym of yet another TNF family cytokine: APRIL. Reports showing an association between APRIL and cancer have since been prolific, in particular, those showing a link with B cell malignancies. Evidence is accumulating that APRIL is also a player in several autoimmune diseases, including systemic lupus erythematosus, rheumatoid arthritis, and Sjoegren's syndrome. However, we now know that APRIL also plays an important role in the immune system and in lymphocyte biology. In this chapter we outline the physiological role of APRIL in immunity and describe what is known regarding the role of APRIL in B cell malignancies and autoimmune disease.
MeSH term(s)	Animals ; Autoimmune Diseases/immunology ; Autoimmune Diseases/metabolism ; Autoimmune Diseases/pathology ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; B-Lymphocytes/pathology ; Cell Proliferation ; Gene Expression Regulation, Neoplastic/immunology ; Humans ; Neoplasm Proteins/biosynthesis ; Neoplasm Proteins/immunology ; Neoplasms/immunology ; Neoplasms/metabolism ; Neoplasms/pathology ; Tumor Necrosis Factor Ligand Superfamily Member 13/biosynthesis ; Tumor Necrosis Factor Ligand Superfamily Member 13/immunology
Chemical Substances	Neoplasm Proteins ; TNFSF13 protein, human ; Tumor Necrosis Factor Ligand Superfamily Member 13
Language	English
Publishing date	2009
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	0080-1844
ISSN	0080-1844
DOI	10.1007/400_2008_19
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Article ; Online: "APRIL hath put a spring of youth in everything": Relevance of APRIL for survival.

Kimberley, Fiona C / Hahne, Michael / Medema, Jan Paul

Journal of cellular physiology

2009 Volume 218, Issue 1, Page(s) 1–8

Abstract: A proliferation inducing ligand (APRIL or TALL-2 and TRDL-1) was first discovered as a cytokine over-expressed in many transformed cells and with the capacity to stimulate proliferation. APRIL was shown to bind two different receptors of the TNF receptor ...

Abstract	A proliferation inducing ligand (APRIL or TALL-2 and TRDL-1) was first discovered as a cytokine over-expressed in many transformed cells and with the capacity to stimulate proliferation. APRIL was shown to bind two different receptors of the TNF receptor superfamily: B cell maturation antigen (BCMA) and transmembrane activator and calcium modulator and cyclophilin ligand interactor (TACI), as well as heparan sulphate proteoglycans (HSPGs). APRIL has since been shown to play a physiological role in B cell biology, in particular the survival of plasma B cells in a specialized APRIL-rich niche. However, aberrant expression of APRIL and the subsequent activation of pro-survival pathways, is potentially the driving force for the survival of several B cell malignancies. APRIL has therefore become an important therapeutic target, but many questions regarding its mechanism of action still remain. It is for instance unclear what the exact physiological implications of the APRIL-HSPG interaction could be. Neither do we know the precise signals elicited by APRIL in normal or in malignant cells, and whether blocking these effects could provide real therapeutic gain in cancer patients. In this review we discuss the specific relevance of APRIL for cell survival, in terms of both its physiological role and its role in tumor biology, and highlight some of the key questions that will undoubtedly form the basis of future research in this field.
MeSH term(s)	Animals ; B-Cell Maturation Antigen/physiology ; B-Lymphocytes/cytology ; B-Lymphocytes/physiology ; Cell Survival/physiology ; Cell Transformation, Neoplastic ; Humans ; Mice ; Models, Biological ; Neoplasms/pathology ; Neoplasms/physiopathology ; Signal Transduction ; Transmembrane Activator and CAML Interactor Protein/physiology ; Tumor Necrosis Factor Ligand Superfamily Member 13/physiology
Chemical Substances	B-Cell Maturation Antigen ; Transmembrane Activator and CAML Interactor Protein ; Tumor Necrosis Factor Ligand Superfamily Member 13
Language	English
Publishing date	2009-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	3116-1
ISSN	1097-4652 ; 0021-9541
ISSN (online)	1097-4652
ISSN	0021-9541
DOI	10.1002/jcp.21561
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Article: Following a TRAIL: update on a ligand and its five receptors.

Kimberley, Fiona C / Screaton, Gavin R

Cell research

2004 Volume 14, Issue 5, Page(s) 359–372

Abstract: Identification of tumour necrosis factor apoptosis inducing ligand (TRAIL), a TNF family ligand, sparked a torrent of research, following an initial observation that it could kill tumour cells, but spare normal cells. Almost a decade after its discovery, ...

Abstract	Identification of tumour necrosis factor apoptosis inducing ligand (TRAIL), a TNF family ligand, sparked a torrent of research, following an initial observation that it could kill tumour cells, but spare normal cells. Almost a decade after its discovery, and with five known receptors, the true physiological role of TRAIL is still debated and its anti-tumorigenic properties limited by potential toxicity. This review takes a comprehensive look at the story of this enigmatic ligand, addressing its remaining potential as a therapeutic and providing an overview of the TRAIL receptors themselves.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Apoptosis/physiology ; Apoptosis Regulatory Proteins ; Humans ; Ligands ; Membrane Glycoproteins/physiology ; Membrane Glycoproteins/therapeutic use ; Models, Biological ; Protein Structure, Tertiary ; Receptors, Tumor Necrosis Factor/physiology ; TNF-Related Apoptosis-Inducing Ligand ; Tumor Necrosis Factor-alpha/physiology ; Tumor Necrosis Factor-alpha/therapeutic use
Chemical Substances	Apoptosis Regulatory Proteins ; Ligands ; Membrane Glycoproteins ; Receptors, Tumor Necrosis Factor ; TNF-Related Apoptosis-Inducing Ligand ; TNFSF10 protein, human ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2004-11-11
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1319303-x
ISSN	1748-7838 ; 1001-0602
ISSN (online)	1748-7838
ISSN	1001-0602
DOI	10.1038/sj.cr.7290236
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Article ; Online: Disease causing mutations in the TNF and TNFR superfamilies: Focus on molecular mechanisms driving disease.

Lobito, Adrian A / Gabriel, Tanit L / Medema, Jan Paul / Kimberley, Fiona C

Trends in molecular medicine

2011 Volume 17, Issue 9, Page(s) 494–505

Abstract: The tumor necrosis factor (TNF) and TNF receptor (TNFR) superfamilies comprise multidomain proteins with diverse roles in cell activation, proliferation and cell death. These proteins play pivotal roles in the initiation, maintenance and termination of ... ...

Abstract	The tumor necrosis factor (TNF) and TNF receptor (TNFR) superfamilies comprise multidomain proteins with diverse roles in cell activation, proliferation and cell death. These proteins play pivotal roles in the initiation, maintenance and termination of immune responses and have vital roles outside the immune system. The discovery and analysis of diseases associated with mutations in these families has revealed crucial mechanistic details of their normal functions. This review focuses on mutations causing four different diseases, which represent distinct pathological mechanisms that can exist within these superfamilies: autoimmune lymphoproliferative syndrome (ALPS; FAS mutations), common variable immunodeficiency (CVID; TACI mutations), tumor necrosis factor receptor associated periodic syndrome (TRAPS; TNFR1 mutations) and hypohidrotic ectodermal dysplasia (HED; EDA1/EDAR mutations). In particular, we highlight how mutations have revealed information about normal receptor-ligand function and how such studies might direct new therapeutic approaches.
MeSH term(s)	Autoimmune Lymphoproliferative Syndrome/genetics ; Autoimmune Lymphoproliferative Syndrome/metabolism ; Common Variable Immunodeficiency/genetics ; Common Variable Immunodeficiency/metabolism ; Ectodermal Dysplasia 3, Anhidrotic/genetics ; Ectodermal Dysplasia 3, Anhidrotic/metabolism ; Edar Receptor/genetics ; Fever ; Hereditary Autoinflammatory Diseases/genetics ; Hereditary Autoinflammatory Diseases/metabolism ; Humans ; Multigene Family ; Mutation ; Receptors, Tumor Necrosis Factor/genetics ; Receptors, Tumor Necrosis Factor, Type I/genetics ; Transmembrane Activator and CAML Interactor Protein/genetics ; Tumor Necrosis Factor-alpha/genetics ; fas Receptor/genetics
Chemical Substances	EDAR protein, human ; Edar Receptor ; FAS protein, human ; Receptors, Tumor Necrosis Factor ; Receptors, Tumor Necrosis Factor, Type I ; TNFRSF13B protein, human ; Transmembrane Activator and CAML Interactor Protein ; Tumor Necrosis Factor-alpha ; fas Receptor
Language	English
Publishing date	2011-09
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2036490-8
ISSN	1471-499X ; 1471-4914
ISSN (online)	1471-499X
ISSN	1471-4914
DOI	10.1016/j.molmed.2011.05.006
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Article: Dissecting the Genomic Architecture of Resistance to

Boulton, Kay / Nolan, Matthew J / Wu, Zhiguang / Riggio, Valentina / Matika, Oswald / Harman, Kimberley / Hocking, Paul M / Bumstead, Nat / Hesketh, Pat / Archer, Andrew / Bishop, Stephen C / Kaiser, Pete / Tomley, Fiona M / Hume, David A / Smith, Adrian L / Blake, Damer P / Psifidi, Androniki

Frontiers in genetics

2018 Volume 9, Page(s) 528

Abstract: Coccidiosis in poultry, caused by protozoan parasites of the ... ...

Abstract	Coccidiosis in poultry, caused by protozoan parasites of the genus
Language	English
Publishing date	2018-11-26
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606823-0
ISSN	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2018.00528
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Article: Alternative roles for CD59.

Kimberley, Fiona C / Sivasankar, Baalasubramanian / Paul Morgan, B

Molecular immunology

2007 Volume 44, Issue 1-3, Page(s) 73–81

Abstract: CD59 was first identified as a regulator of the terminal pathway of complement, which acts by binding to the C8/C9 components of the assembling membrane attack complex (MAC), to inhibit formation of the lytic pore. Structurally, CD59 is a small, highly ... ...

Abstract	CD59 was first identified as a regulator of the terminal pathway of complement, which acts by binding to the C8/C9 components of the assembling membrane attack complex (MAC), to inhibit formation of the lytic pore. Structurally, CD59 is a small, highly glycosylated, GPI-linked protein, with a wide expression profile. Functionally, the role of CD59 in complement regulation is well-defined but studies have also shown clear evidence for signalling properties, which are linked to its glycophosphatidyl inositol (GPI) anchor and its location within lipid rafts. Cross-linking of CD59 using specific monoclonal antibodies drives both calcium release and activation of lipid-raft associated signalling molecules such as tyrosine kinases. These observations clearly show that CD59 exhibits roles independent of its function as a complement inhibitor. In this review, we examine the progression of research in this area and explore the alternative functions of CD59 that have recently been defined.
MeSH term(s)	Animals ; B-Lymphocytes/physiology ; Bacterial Proteins/physiology ; Bacteriocins ; CD2 Antigens/physiology ; CD59 Antigens/physiology ; Calreticulin/physiology ; Humans ; Killer Cells, Natural/physiology ; Lipopolysaccharides/pharmacology ; Signal Transduction ; T-Lymphocytes/physiology
Chemical Substances	Bacterial Proteins ; Bacteriocins ; CD2 Antigens ; CD59 Antigens ; Calreticulin ; Lipopolysaccharides ; intermedilysin protein, Streptococcus intermedius
Language	English
Publishing date	2007-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	424427-8
ISSN	1872-9142 ; 0161-5890
ISSN (online)	1872-9142
ISSN	0161-5890
DOI	10.1016/j.molimm.2006.06.019
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Article ; Online: Circulating transcripts in maternal blood reflect a molecular signature of early-onset preeclampsia.

Science translational medicine

2020 Volume 12, Issue 550

Abstract: Circulating RNA (C-RNA) is continually released into the bloodstream from tissues ... to birth. We asked whether C-RNA analysis could robustly detect aberrations in patients diagnosed ... of PE. Furthermore, machine learning identified combinations of 49 C-RNA transcripts that classified ...

Abstract	Circulating RNA (C-RNA) is continually released into the bloodstream from tissues throughout the body, offering an opportunity to noninvasively monitor all aspects of pregnancy health from conception to birth. We asked whether C-RNA analysis could robustly detect aberrations in patients diagnosed with preeclampsia (PE), a prevalent and potentially fatal pregnancy complication. As an initial examination, we sequenced the circulating transcriptome from 40 pregnancies at the time of severe, early-onset PE diagnosis and 73 gestational age-matched controls. Differential expression analysis identified 30 transcripts with gene ontology annotations and tissue expression patterns consistent with the placental dysfunction, impaired fetal development, and maternal immune and cardiovascular system dysregulation characteristic of PE. Furthermore, machine learning identified combinations of 49 C-RNA transcripts that classified an independent cohort of patients (early-onset PE,
MeSH term(s)	Case-Control Studies ; Female ; Gestational Age ; Humans ; Placenta ; Placenta Diseases ; Pre-Eclampsia/diagnosis ; Pre-Eclampsia/genetics ; Pregnancy ; Pregnancy Trimester, Third
Language	English
Publishing date	2020-06-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.aaz0131
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Article ; Online: Isolating adverse effects of glucocorticoids on the embryonic cardiovascular system.

Teulings, Noor E W D / Garrud, Tessa A C / Niu, Youguo / Skeffington, Katie L / Beck, Christian / Itani, Nozomi / Conlon, Fiona G / Botting, Kimberley J / Nicholas, Lisa M / Ashmore, Thomas J / Blackmore, Heather L / Tong, Wen / Camm, Emily J / Derks, Jan B / Logan, Angela / Murphy, Michael P / Ozanne, Susan E / Giussani, Dino A

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2020 Volume 34, Issue 7, Page(s) 9664–9677

Abstract: ... the placenta. Fertilized chicken eggs were incubated and divided randomly into control (C) or dexamethasone ...

Abstract	Antenatal glucocorticoid therapy reduces mortality in the preterm infant, but evidence suggests off-target adverse effects on the developing cardiovascular system. Whether deleterious effects are direct on the offspring or secondary to alterations in uteroplacental physiology is unclear. Here, we isolated direct effects of glucocorticoids using the chicken embryo, a model system in which the effects on the developing heart and circulation of therapy can be investigated, independent of effects on the mother and/or the placenta. Fertilized chicken eggs were incubated and divided randomly into control (C) or dexamethasone (Dex) treatment at day 14 out of the 21-day incubation period. Combining functional experiments at the isolated organ, cellular and molecular levels, embryos were then studied close to term. Chicken embryos exposed to dexamethasone were growth restricted and showed systolic and diastolic dysfunction, with an increase in cardiomyocyte volume but decreased cardiomyocyte nuclear density in the left ventricle. Underlying mechanisms included a premature switch from tissue accretion to differentiation, increased oxidative stress, and activated signaling of cellular senescence. These findings, therefore, demonstrate that dexamethasone treatment can have direct detrimental off-target effects on the cardiovascular system in the developing embryo, which are independent of effects on the mother and/or placenta.
MeSH term(s)	Animals ; Cellular Senescence ; Chick Embryo ; Chickens ; Dexamethasone/toxicity ; Fibrosis/chemically induced ; Fibrosis/pathology ; Glucocorticoids/toxicity ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/pathology ; Oxidative Stress/drug effects
Chemical Substances	Glucocorticoids ; Dexamethasone (7S5I7G3JQL)
Language	English
Publishing date	2020-06-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202000697R
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Article ; Online: Phenotypic and genetic variation in the response of chickens to Eimeria tenella induced coccidiosis.

Boulton, Kay / Nolan, Matthew J / Wu, Zhiguang / Psifidi, Androniki / Riggio, Valentina / Harman, Kimberley / Bishop, Stephen C / Kaiser, Pete / Abrahamsen, Mitchell S / Hawken, Rachel / Watson, Kellie A / Tomley, Fiona M / Blake, Damer P / Hume, David A

Genetics, selection, evolution : GSE

2018 Volume 50, Issue 1, Page(s) 63

Abstract: Background: Coccidiosis is a major contributor to losses in poultry production. With emerging constraints on the use of in-feed prophylactic anticoccidial drugs and the relatively high costs of effective vaccines, there are commercial incentives to ... ...

Abstract	Background: Coccidiosis is a major contributor to losses in poultry production. With emerging constraints on the use of in-feed prophylactic anticoccidial drugs and the relatively high costs of effective vaccines, there are commercial incentives to breed chickens with greater resistance to this important production disease. To identify phenotypic biomarkers that are associated with the production impacts of coccidiosis, and to assess their covariance and heritability, 942 Cobb500 commercial broilers were subjected to a defined challenge with Eimeria tenella (Houghton). Three traits were measured: weight gain (WG) during the period of infection, caecal lesion score (CLS) post mortem, and the level of a serum biomarker of intestinal inflammation, i.e. circulating interleukin 10 (IL-10), measured at the height of the infection. Results: Phenotypic analysis of the challenged chicken cohort revealed a significant positive correlation between CLS and IL-10, with significant negative correlations of both these traits with WG. Eigenanalysis of phenotypic covariances between measured traits revealed three distinct eigenvectors. Trait weightings of the first eigenvector, (EV1, eigenvalue = 59%), were biologically interpreted as representing a response of birds that were susceptible to infection, with low WG, high CLS and high IL-10. Similarly, the second eigenvector represented infection resilience/resistance (EV2, 22%; high WG, low CLS and high IL-10), and the third eigenvector tolerance (EV3, 19%; high WG, high CLS and low IL-10), respectively. Genome-wide association studies (GWAS) identified two SNPs that were associated with WG at the suggestive level. Conclusions: Eigenanalysis separated the phenotypic impact of a defined challenge with E. tenella on WG, caecal inflammation/pathology, and production of IL-10 into three major eigenvectors, indicating that the susceptibility-resistance axis is not a single continuous quantitative trait. The SNPs identified by the GWAS for body weight were located in close proximity to two genes that are involved in innate immunity (FAM96B and RRAD).
MeSH term(s)	Animals ; Body Weight/genetics ; Cecum/pathology ; Chickens/genetics ; Coccidiosis/genetics ; Coccidiosis/veterinary ; Disease Resistance/genetics ; Eimeria tenella/pathogenicity ; Genome-Wide Association Study ; Interleukin-10/blood ; Interleukin-10/genetics ; Phenotype ; Polymorphism, Single Nucleotide ; Poultry Diseases/genetics ; Weight Gain/genetics
Chemical Substances	Interleukin-10 (130068-27-8)
Language	English
Publishing date	2018-11-21
Publishing country	France
Document type	Journal Article
ZDB-ID	1005838-2
ISSN	1297-9686 ; 0754-0264 ; 0999-193X
ISSN (online)	1297-9686
ISSN	0754-0264 ; 0999-193X
DOI	10.1186/s12711-018-0433-7
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