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Article ; Online: Role of thyroid hormones in craniofacial development.

Leitch, Victoria D / Bassett, J H Duncan / Williams, Graham R

2020 Volume 16, Issue 3, Page(s) 147–164

Abstract: The development of the craniofacial skeleton relies on complex temporospatial organization of diverse cell types by key signalling molecules. Even minor disruptions to these processes can result in deleterious consequences for the structure and function ... ...

Abstract	The development of the craniofacial skeleton relies on complex temporospatial organization of diverse cell types by key signalling molecules. Even minor disruptions to these processes can result in deleterious consequences for the structure and function of the skull. Thyroid hormone deficiency causes delayed craniofacial and tooth development, dysplastic facial features and delayed development of the ossicles in the middle ear. Thyroid hormone excess, by contrast, accelerates development of the skull and, in severe cases, might lead to craniosynostosis with neurological sequelae and facial hypoplasia. The pathogenesis of these important abnormalities remains poorly understood and underinvestigated. The orchestration of craniofacial development and regulation of suture and synchondrosis growth is dependent on several critical signalling pathways. The underlying mechanisms by which these key pathways regulate craniofacial growth and maturation are largely unclear, but studies of single-gene disorders resulting in craniofacial malformations have identified a number of critical signalling molecules and receptors. The craniofacial consequences resulting from gain-of-function and loss-of-function mutations affecting insulin-like growth factor 1, fibroblast growth factor receptor and WNT signalling are similar to the effects of altered thyroid status and mutations affecting thyroid hormone action, suggesting that these critical pathways interact in the regulation of craniofacial development.
MeSH term(s)	Animals ; Craniofacial Abnormalities/metabolism ; Craniosynostoses/metabolism ; Humans ; Signal Transduction/physiology ; Skull/metabolism ; Thyroid Hormones/metabolism
Chemical Substances	Thyroid Hormones
Language	English
Publishing date	2020-01-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2489381-X
ISSN	1759-5037 ; 1759-5029
ISSN (online)	1759-5037
ISSN	1759-5029
DOI	10.1038/s41574-019-0304-5
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Article ; Online: Hypochondroplasia gain-of-function mutation in FGFR3 causes defective bone mineralization in mice.

Loisay, Léa / Komla-Ebri, Davide / Morice, Anne / Heuzé, Yann / Viaut, Camille / de La Seiglière, Amélie / Kaci, Nabil / Chan, Danny / Lamouroux, Audrey / Baujat, Geneviève / Bassett, J H Duncan / Williams, Graham R / Legeai-Mallet, Laurence

JCI insight

2023 Volume 8, Issue 12

Abstract: Hypochondroplasia (HCH) is a mild dwarfism caused by missense mutations in fibroblast growth factor receptor 3 (FGFR3), with the majority of cases resulting from a heterozygous p.Asn540Lys gain-of-function mutation. Here, we report the generation and ... ...

Abstract	Hypochondroplasia (HCH) is a mild dwarfism caused by missense mutations in fibroblast growth factor receptor 3 (FGFR3), with the majority of cases resulting from a heterozygous p.Asn540Lys gain-of-function mutation. Here, we report the generation and characterization of the first mouse model (Fgfr3Asn534Lys/+) of HCH to our knowledge. Fgfr3Asn534Lys/+ mice exhibited progressive dwarfism and impairment of the synchondroses of the cranial base, resulting in defective formation of the foramen magnum. The appendicular and axial skeletons were both severely affected and we demonstrated an important role of FGFR3 in regulation of cortical and trabecular bone structure. Trabecular bone mineral density (BMD) of long bones and vertebral bodies was decreased, but cortical BMD increased with age in both tibiae and femurs. These results demonstrate that bones in Fgfr3Asn534Lys/+ mice, due to FGFR3 activation, exhibit some characteristics of osteoporosis. The present findings emphasize the detrimental effect of gain-of-function mutations in the Fgfr3 gene on long bone modeling during both developmental and aging processes, with potential implications for the management of elderly patients with hypochondroplasia and osteoporosis.
MeSH term(s)	Animals ; Mice ; Calcification, Physiologic ; Dwarfism/genetics ; Gain of Function Mutation ; Osteoporosis ; Receptor, Fibroblast Growth Factor, Type 3/genetics
Chemical Substances	Receptor, Fibroblast Growth Factor, Type 3 (EC 2.7.10.1) ; Fgfr3 protein, mouse (EC 2.7.10.1)
Language	English
Publishing date	2023-06-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.168796
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Article ; Online: Role of Thyroid Hormones in Skeletal Development and Bone Maintenance.

Bassett, J H Duncan / Williams, Graham R

Endocrine reviews

2016 Volume 37, Issue 2, Page(s) 135–187

Abstract: The skeleton is an exquisitely sensitive and archetypal T3-target tissue that demonstrates the critical role for thyroid hormones during development, linear growth, and adult bone turnover and maintenance. Thyrotoxicosis is an established cause of ... ...

Abstract	The skeleton is an exquisitely sensitive and archetypal T3-target tissue that demonstrates the critical role for thyroid hormones during development, linear growth, and adult bone turnover and maintenance. Thyrotoxicosis is an established cause of secondary osteoporosis, and abnormal thyroid hormone signaling has recently been identified as a novel risk factor for osteoarthritis. Skeletal phenotypes in genetically modified mice have faithfully reproduced genetic disorders in humans, revealing the complex physiological relationship between centrally regulated thyroid status and the peripheral actions of thyroid hormones. Studies in mutant mice also established the paradigm that T3 exerts anabolic actions during growth and catabolic effects on adult bone. Thus, the skeleton represents an ideal physiological system in which to characterize thyroid hormone transport, metabolism, and action during development and adulthood and in response to injury. Future analysis of T3 action in individual skeletal cell lineages will provide new insights into cell-specific molecular mechanisms and may ultimately identify novel therapeutic targets for chronic degenerative diseases such as osteoporosis and osteoarthritis. This review provides a comprehensive analysis of the current state of the art.
MeSH term(s)	Adult ; Animals ; Bone Development ; Bone Remodeling/physiology ; Bone and Bones/physiology ; Humans ; Mice ; Mice, Transgenic ; Thyroid Hormones/physiology
Chemical Substances	Thyroid Hormones
Language	English
Publishing date	2016-02-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	603096-8
ISSN	1945-7189 ; 0163-769X
ISSN (online)	1945-7189
ISSN	0163-769X
DOI	10.1210/er.2015-1106
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Article ; Online: Quantitative X-Ray Imaging of Mouse Bone by Faxitron.

Butterfield, Natalie C / Logan, John G / Waung, Julian / Williams, Graham R / Bassett, J H Duncan

Methods in molecular biology (Clifton, N.J.)

2019 Volume 1914, Page(s) 559–569

Abstract: This chapter describes the use of point projection digital microradiography for rapid imaging and quantitation of bone mineral content in mice. ...

Abstract	This chapter describes the use of point projection digital microradiography for rapid imaging and quantitation of bone mineral content in mice.
MeSH term(s)	Animals ; Bone Density ; Bone and Bones/diagnostic imaging ; Bone and Bones/physiology ; Image Processing, Computer-Assisted/instrumentation ; Image Processing, Computer-Assisted/methods ; Mice ; Microradiography/instrumentation ; Microradiography/methods ; Models, Animal ; Software
Language	English
Publishing date	2019-01-30
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-8997-3_30
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Article ; Online: Adult mice lacking the type 2 iodothyronine deiodinase have increased subchondral bone but normal articular cartilage.

Waung, Julian A / Bassett, J H Duncan / Williams, Graham R

Thyroid : official journal of the American Thyroid Association

2015 Volume 25, Issue 3, Page(s) 269–277

Abstract: Background: Although osteoarthritis (OA) is the commonest joint disorder and has a rising prevalence as the population ages, no drugs are available that prevent or delay the onset and progression of disease. Recent studies identified the DIO2 gene ... ...

Abstract	Background: Although osteoarthritis (OA) is the commonest joint disorder and has a rising prevalence as the population ages, no drugs are available that prevent or delay the onset and progression of disease. Recent studies identified the DIO2 gene encoding type 2 deiodinase (D2) as a susceptibility locus for OA, and further data suggest deiodinase-regulated local availability of triiodothyronine (T3) in the joint plays an important role in cartilage maintenance and repair. To investigate the hypothesis that reduced tissue T3 availability protects joints from development of OA, the joint phenotypes of adult mice lacking D2 (D2KO) or lacking both D1 and D2 (D1D2KO), the only enzymes that catalyze conversion of the prohormone thyroxine to active T3, were determined. Methods: Knee joints were prepared from male 16-week-old adult wild type (WT; n=9), D2KO (n=5), and D1D2KO (n=3) mice. Articular cartilage pathology was scored using the Osteoarthritis Research Society International (OARSI) histopathology scale for murine OA to determine the severity and extent of disease. Digital X-ray microradiography was used to determine the area and mineral content of subchondral bone immediately beneath the articular cartilage surface. Results: There were no differences in maximum and standardized OA scores, cartilage erosion indices, or articular cartilage cellularity among WT, D2KO, and D1D2KO mice. Subchondral bone area did not differ among genotypes, but mineral content was markedly increased in both D2KO and D1D2KO mice compared to WT. Conclusions: Although adult D2KO mice have normal articular cartilage and no other features of spontaneous joint damage, they exhibit increased subchondral bone mineral content.
MeSH term(s)	Animals ; Bone and Bones/metabolism ; Cartilage, Articular/metabolism ; Disease Models, Animal ; Embryonic Stem Cells/cytology ; Genotype ; Iodide Peroxidase/genetics ; Iodide Peroxidase/physiology ; Joints/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Osteoarthritis/genetics ; Osteoarthritis/metabolism ; Phenotype ; Triiodothyronine/metabolism ; Iodothyronine Deiodinase Type II
Chemical Substances	Triiodothyronine (06LU7C9H1V) ; Iodide Peroxidase (EC 1.11.1.8)
Language	English
Publishing date	2015-02-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1086044-7
ISSN	1557-9077 ; 1050-7256
ISSN (online)	1557-9077
ISSN	1050-7256
DOI	10.1089/thy.2014.0476
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Zs.A 3307: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Common signalling pathways in macrophage and osteoclast multinucleation.

Pereira, Marie / Petretto, Enrico / Gordon, Siamon / Bassett, J H Duncan / Williams, Graham R / Behmoaras, Jacques

Journal of cell science

2018 Volume 131, Issue 11

Abstract: Macrophage cell fusion and multinucleation are fundamental processes in the formation of multinucleated giant cells (MGCs) in chronic inflammatory disease and osteoclasts in the regulation of bone mass. However, this basic cell phenomenon is poorly ... ...

Abstract	Macrophage cell fusion and multinucleation are fundamental processes in the formation of multinucleated giant cells (MGCs) in chronic inflammatory disease and osteoclasts in the regulation of bone mass. However, this basic cell phenomenon is poorly understood despite its pathophysiological relevance. Granulomas containing multinucleated giant cells are seen in a wide variety of complex inflammatory disorders, as well as in infectious diseases. Dysregulation of osteoclastic bone resorption underlies the pathogenesis of osteoporosis and malignant osteolytic bone disease. Recent reports have shown that the formation of multinucleated giant cells and osteoclast fusion display a common molecular signature, suggesting shared genetic determinants. In this Review, we describe the background of cell-cell fusion and the similar origin of macrophages and osteoclasts. We specifically focus on the common pathways involved in osteoclast and MGC fusion. We also highlight potential approaches that could help to unravel the core mechanisms underlying bone and granulomatous disorders in humans.
MeSH term(s)	Animals ; Cell Fusion ; Giant Cells/metabolism ; Granuloma ; Humans ; Macrophages/metabolism ; Osteoclasts/metabolism ; Signal Transduction
Language	English
Publishing date	2018-06-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
DOI	10.1242/jcs.216267
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Article ; Online: The Thyroid Hormone Transporter MCT10 Is a Novel Regulator of Trabecular Bone Mass and Bone Turnover in Male Mice.

Lademann, Franziska / Mayerl, Steffen / Tsourdi, Elena / Verrey, Francois / Leitch, Victoria D / Williams, Graham R / Bassett, J H Duncan / Hofbauer, Lorenz C / Heuer, Heike / Rauner, Martina

Endocrinology

2021 Volume 163, Issue 1

Abstract: Thyroid hormones (TH) are essential for skeletal development and adult bone homeostasis. Their bioavailability is determined by specific transporter proteins at the cell surface. The TH-specific transporter monocarboxylate transporter 8 (MCT8) was ... ...

Abstract	Thyroid hormones (TH) are essential for skeletal development and adult bone homeostasis. Their bioavailability is determined by specific transporter proteins at the cell surface. The TH-specific transporter monocarboxylate transporter 8 (MCT8) was recently reported as a regulator of bone mass in mice. Given that high systemic triiodothyronine (T3) levels in Mct8 knockout (KO) mice are still able to cause trabecular bone loss, alternative TH transporters must substitute for MCT8 function in bone. In this study, we analyzed the skeletal phenotypes of male Oatp1c1 KO and Mct10 KO mice, which are euthyroid, and male Mct8/Oatp1c1 and Mct8/Mct10 double KO mice, which have elevated circulating T3 levels, to unravel the role of TH transport in bone. MicroCT analysis showed no significant trabecular bone changes in Oatp1c1 KO mice at 4 weeks and 16 weeks of age compared with wild-type littermate controls, whereas 16-week-old Mct8/Oatp1c1 double KO animals displayed trabecular bone loss. At 12 weeks, Mct10 KO mice, but not Mct8/Mct10 double KO mice, had decreased trabecular femoral bone volume with reduced osteoblast numbers. By contrast, lack of Mct10 in 24-week-old mice led to trabecular bone gain at the femur with increased osteoblast numbers and decreased osteoclast numbers whereas Mct8/Mct10 double KO did not alter bone mass. Neither Mct10 nor Mct8/Mct10 deletion affected vertebral bone structures at both ages. In vitro, osteoblast differentiation and activity were impaired by Mct10 and Mct8/Mct10-deficiency. These data demonstrate that MCT10, but not OATP1C1, is a site- and age-dependent regulator of bone mass and turnover in male mice.
MeSH term(s)	Amino Acid Transport Systems, Neutral/metabolism ; Animals ; Biological Transport ; Biomechanical Phenomena ; Bone and Bones/metabolism ; Cancellous Bone/metabolism ; Cell Differentiation ; Femur/physiology ; Homeostasis ; Male ; Mice ; Mice, Knockout ; Organic Cation Transport Proteins/metabolism ; Osteoblasts/cytology ; Osteoblasts/metabolism ; Osteoclasts/metabolism ; Osteocytes/cytology ; Phenotype ; Symporters/metabolism ; Thyroid Gland/metabolism ; Thyroid Hormones/metabolism ; Triiodothyronine/metabolism ; X-Ray Microtomography
Chemical Substances	Amino Acid Transport Systems, Neutral ; Oatp2 protein, mouse ; Organic Cation Transport Proteins ; Slc16a10 protein, mouse ; Symporters ; Thyroid Hormones ; Triiodothyronine (06LU7C9H1V)
Language	English
Publishing date	2021-10-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/endocr/bqab218
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Article: Mechanisms of action of thyroid hormones in the skeleton.

Wojcicka, Anna / Bassett, J H Duncan / Williams, Graham R

Biochimica et biophysica acta

2012 Volume 1830, Issue 7, Page(s) 3979–3986

Abstract: Background: Thyroid hormones regulate skeletal development, acquisition of peak bone mass and adult bone maintenance. Abnormal thyroid status during childhood disrupts bone maturation and linear growth, while in adulthood it results in altered bone ... ...

Abstract	Background: Thyroid hormones regulate skeletal development, acquisition of peak bone mass and adult bone maintenance. Abnormal thyroid status during childhood disrupts bone maturation and linear growth, while in adulthood it results in altered bone remodeling and an increased risk of fracture Scope of review: This review considers the cellular effects and molecular mechanisms of thyroid hormone action in the skeleton. Human clinical and population data are discussed in relation to the skeletal phenotypes of a series of genetically modified mouse models of disrupted thyroid hormone signaling. Major conclusions: Euthyroid status is essential for normal bone development and maintenance. Major thyroid hormone actions in skeletal cells are mediated by thyroid hormone receptor α (TRα) and result in anabolic responses during growth and development but catabolic effects in adulthood. These homeostatic responses to thyroid hormone are locally regulated in individual skeletal cell types by the relative activities of the type 2 and 3 iodothyronine deiodinases, which control the supply of the active thyroid hormone 3,5,3'-L-triiodothyronine (T3) to its receptor. General significance: Population studies indicate that both thyroid hormone deficiency and excess are associated with an increased risk of fracture. Understanding the cellular and molecular basis of T3 action in skeletal cells will lead to the identification of new targets to regulate bone turnover and mineralization in the prevention and treatment of osteoporosis. This article is part of a Special Issue entitled Thyroid hormone signaling.
MeSH term(s)	Animals ; Bone Development/genetics ; Bone Development/physiology ; Bone and Bones/metabolism ; Bone and Bones/physiology ; Humans ; Signal Transduction ; Thyroid Hormone Receptors alpha/genetics ; Thyroid Hormone Receptors alpha/metabolism ; Thyroid Hormone Receptors alpha/physiology ; Thyroid Hormones/genetics ; Thyroid Hormones/metabolism ; Thyroid Hormones/physiology
Chemical Substances	Thyroid Hormone Receptors alpha ; Thyroid Hormones
Language	English
Publishing date	2012-05-25
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbagen.2012.05.005
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Article ; Online: Rapid phenotyping of knockout mice to identify genetic determinants of bone strength.

Freudenthal, Bernard / Logan, John / Croucher, Peter I / Williams, Graham R / Bassett, J H Duncan

The Journal of endocrinology

2016 Volume 231, Issue 1, Page(s) R31–46

Abstract: The genetic determinants of osteoporosis remain poorly understood, and there is a large unmet need for new treatments in our ageing society. Thus, new approaches for gene discovery in skeletal disease are required to complement the current genome-wide ... ...

Abstract	The genetic determinants of osteoporosis remain poorly understood, and there is a large unmet need for new treatments in our ageing society. Thus, new approaches for gene discovery in skeletal disease are required to complement the current genome-wide association studies in human populations. The International Knockout Mouse Consortium (IKMC) and the International Mouse Phenotyping Consortium (IMPC) provide such an opportunity. The IKMC generates knockout mice representing each of the known protein-coding genes in C57BL/6 mice and, as part of the IMPC initiative, the Origins of Bone and Cartilage Disease project identifies mutants with significant outlier skeletal phenotypes. This initiative will add value to data from large human cohorts and provide a new understanding of bone and cartilage pathophysiology, ultimately leading to the identification of novel drug targets for the treatment of skeletal disease.
MeSH term(s)	Animals ; Bone Diseases/genetics ; Bone Diseases/physiopathology ; Bone and Bones/physiopathology ; Cartilage Diseases/genetics ; Cartilage Diseases/physiopathology ; Genetic Predisposition to Disease ; Mice ; Mice, Inbred C57BL ; Mice, Knockout/genetics ; Phenotype
Language	English
Publishing date	2016-08-17
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	3028-4
ISSN	1479-6805 ; 0022-0795
ISSN (online)	1479-6805
ISSN	0022-0795
DOI	10.1530/JOE-16-0258
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Article: Frequent falls and confusion: recurrent hypoglycemia in a patient with tuberous sclerosis complex.

Comninos, Alexander N / Yang, Lisa / Abbara, Ali / Dhillo, Waljit S / Bassett, J H Duncan / Todd, Jeannie F

Clinical case reports

2018 Volume 6, Issue 5, Page(s) 904–909

Abstract: Recurrent hypoglycemia is common, but its presentation is often insidious resulting in delays in diagnosis and significant morbidity. We describe a case of an insulinoma presenting with falls and confusion in a patient with tuberous sclerosis, ... ...

Abstract	Recurrent hypoglycemia is common, but its presentation is often insidious resulting in delays in diagnosis and significant morbidity. We describe a case of an insulinoma presenting with falls and confusion in a patient with tuberous sclerosis, demonstrating the importance of early hypoglycemia identification and a potential shared molecular pathogenesis.
Language	English
Publishing date	2018-03-24
Publishing country	England
Document type	Case Reports
ZDB-ID	2740234-4
ISSN	2050-0904
ISSN	2050-0904
DOI	10.1002/ccr3.1483
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