The effect of carbamazepine on bone structure and strength in control and osteogenesis imperfecta (<i>Col1a2<sup>+/p.G610C</sup></i>) mice

Blank, Martha; McGregor, Narelle E; Rowley, Lynn; Kung, Louise H. W.; Crimeen‐Irwin, Blessing; Poulton, Ingrid J; Walker, Emma C; Gooi, Julian; Lamandé, Shireen R.; Sims, Natalie A; Bateman, John F.

doi:10.1111/jcmm.17437

J Cellular Molecular Medi

2022

DOI: 10.1111/jcmm.17437

|View full text |Cite

The effect of carbamazepine on bone structure and strength in control and osteogenesis imperfecta (Col1a2^+/p.G610C) mice

Martha Blank

Narelle E McGregor

Lynn Rowley

et al.

Abstract: The inherited brittle bone disease osteogenesis imperfecta (OI) is commonly caused by mutations that compromise the biosynthesis or structure of type I collagen, the predominant organic structural component of bone. The two collagen I α-chain subunits, α1(I) and α2(I), which form the [α1(I)] 2 α2(I) collagen protein trimers are encoded by COL1A1 and COL1A2. Autosomal dominant mutations in these genes cause more than 85% of OI cases 1,2 and fall into two broad functional groups. Mutations that reduce collagen I

Help me understand this report

View preprint versions

Search citation statements

Order By: Relevance

Paper Sections

Select...

Citation Types

Supporting

Mentioning

Contrasting

Year Published

2022

2024

Publication Types

Select...

Article5

Relationship

Self Cite1

Independent4

Authors

Journals

Cited by 5 publications

References 43 publications

(120 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

The effect of carbamazepine on bone structure and strength in control and osteogenesis imperfecta (Col1a2^+/p.G610C) mice

Blank

McGregor

Rowley

et al. 2022

J Cellular Molecular Medi

Self Cite

View full text Add to dashboard Cite

The inherited brittle bone disease osteogenesis imperfecta (OI) is commonly caused by mutations that compromise the biosynthesis or structure of type I collagen, the predominant organic structural component of bone. The two collagen I α-chain subunits, α1(I) and α2(I), which form the [α1(I)] 2 α2(I) collagen protein trimers are encoded by COL1A1 and COL1A2. Autosomal dominant mutations in these genes cause more than 85% of OI cases 1,2 and fall into two broad functional groups. Mutations that reduce collagen I

show abstract

The effect of carbamazepine on bone structure and strength in control and osteogenesis imperfecta (Col1a2^+/p.G610C) mice

Blank

McGregor

Rowley

et al. 2022

J Cellular Molecular Medi

Self Cite

View full text Add to dashboard Cite

show abstract

Preclinical Rodent Models for Human Bone Disease, Including a Focus on Cortical Bone

Koh,

Miszkiewicz,

Fac

et al. 2024

Endocrine Reviews

View full text Add to dashboard Cite

Preclinical models (typically the ovariectomized rat and genetically altered mice) have underpinned much of what we know about skeletal biology. They have been pivotal for developing therapies for osteoporosis and monogenic skeletal conditions, including osteogenesis imperfecta, achondroplasia, hypophosphatasia, and craniodysplasias. Further therapeutic advances, particularly to improve cortical strength, requires improved understanding and more rigorous use and reporting. We describe here how trabecular and cortical bone structure develop, are maintained, and degenerate with ageing in mice, rats, and humans, and how cortical bone structure is changed in preclinical models of endocrine conditions (e.g., postmenopausal osteoporosis, chronic kidney disease, hyperparathyroidism, diabetes). We provide examples of preclinical models used to identify and test current therapies for osteoporosis, and discuss common concerns raised when comparing rodent preclinical models to the human skeleton. We focus especially on cortical bone, because it differs between small and larger mammals in its organizational structure. We discuss mechanisms common to mouse and human controlling cortical bone strength and structure, including recent examples revealing genetic contributors to cortical porosity and osteocyte network configurations during growth, maturity, and ageing. We conclude with guidelines for clear reporting on mouse models with a goal for better consistency in the use and interpretation of these models.

show abstract

Transcriptome analysis reveals the pathogenesis of spontaneous tibial dyschondroplasia in broilers

Shi,

Wu,

Jiang

et al. 2024

Front. Genet.

View full text Add to dashboard Cite

Tibial dyschondroplasia (TD) is a severe bone disease that affects fast-growing broiler chickens and causes economic loss. Despite previous studies, the regulatory mechanism of TD remains unclear and is thought to be primarily based on thiram induction, which may differ from that of naturally occurring diseases. To better understand TD, a digital X-ray machine was used in the present study to determine its incidence in four hundred yellow-feathered broiler chickens. The results showed that the incidence of TD was 22% after 6 weeks and gradually decreased after 8 and 10 weeks. The body weight of broilers with TD decreased significantly compared to that of NTD broilers. In addition, the length and density of the tibia were reduced after eight and 10 weeks, and the density of the tibia was reduced after 6 weeks compared with the NTD chickens. This study also examined tibial quality parameters from TD (n = 12) and NTD broilers (n = 12) and found that bone mineral content, bone mineral density, bone ash content, calcium content, and phosphorus content were significantly reduced in TD broilers. Transcriptome analysis revealed 849 differentially expressed genes (DEGs) in the growth plate between TD (n = 6) and NTD groups (n = 6). These genes were enriched in ECM-receptor interaction, cytokine-cytokine receptor interaction, calcium signaling pathway, and TGF-β signaling. Genes encoding the alpha chain of type XII collagen, that is, COL1A1, COL5A1, and COL8A1) were identified as critical in the regulatory network of TD. Gene set enrichment analysis (GSEA) revealed that the pathways of cartilage development, circulatory system development, and nervous system development were changed in the growth plates of TD birds. In the blood transcriptome, 12 DEGs were found in TD (n = 4) and NTD chickens (n = 4), and GSEA revealed that the pathways from TD broilers’ blood related to the phagosome, linoleic acid metabolism, monoatomic ion homeostasis, and calcium ion transport were downregulated. This study provides a comprehensive understanding of TD, including its effects on tibial quality, tibial changes, and the circulatory system, along with identifying important genes that may lead to the development of TD.

show abstract

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

Contact Info

hi@scite.ai

10624 S. Eastern Ave., Ste. A-614

Henderson, NV 89052, USA

Blog Terms and Conditions API Terms Privacy Policy Contact Cookie Preferences Do Not Sell or Share My Personal Information

Made with 💙 for researchers

Part of the Research Solutions Family.

The effect of carbamazepine on bone structure and strength in control and osteogenesis imperfecta (Col1a2^+/p.G610C) mice

Cited by 5 publications

References 43 publications

The effect of carbamazepine on bone structure and strength in control and osteogenesis imperfecta (Col1a2^+/p.G610C) mice

The effect of carbamazepine on bone structure and strength in control and osteogenesis imperfecta (Col1a2^+/p.G610C) mice

Preclinical Rodent Models for Human Bone Disease, Including a Focus on Cortical Bone

Transcriptome analysis reveals the pathogenesis of spontaneous tibial dyschondroplasia in broilers

Contact Info

Product

Resources

About

The effect of carbamazepine on bone structure and strength in control and osteogenesis imperfecta (Col1a2+/p.G610C) mice

Cited by 5 publications

References 43 publications

The effect of carbamazepine on bone structure and strength in control and osteogenesis imperfecta (Col1a2+/p.G610C) mice

The effect of carbamazepine on bone structure and strength in control and osteogenesis imperfecta (Col1a2+/p.G610C) mice

Preclinical Rodent Models for Human Bone Disease, Including a Focus on Cortical Bone

Transcriptome analysis reveals the pathogenesis of spontaneous tibial dyschondroplasia in broilers

Contact Info

Product

Resources

About

The effect of carbamazepine on bone structure and strength in control and osteogenesis imperfecta (Col1a2^+/p.G610C) mice

The effect of carbamazepine on bone structure and strength in control and osteogenesis imperfecta (Col1a2^+/p.G610C) mice

The effect of carbamazepine on bone structure and strength in control and osteogenesis imperfecta (Col1a2^+/p.G610C) mice