The Emerging Role of Glucose Metabolism in Cartilage Development

Hollander, Judith M.; Zeng, Li

doi:10.1007/s11914-019-00506-0

Cited by 49 publications

(41 citation statements)

References 126 publications

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“…These results also showed a general increase in cytosolic (TPI1, GAPDH, ENO1), L-LDH, and mitochondrial (SUCLG1, HADHB and ECHS1, ATP synthase) enzymes, which are involved in energy production. These findings could be interpreted as an adaptative response to the reduction of nutrient supply, which occurs in OC fragments, where chondrocytes are far from the capillaries originated from the epiphyseal artery, the only source of glucose for growth plate cartilage [53].…”

Section: Discussionmentioning

confidence: 95%

Proteome Alterations in Equine Osteochondrotic Chondrocytes

Chiaradia

Pepe

Orvietani

et al. 2019

IJMS

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Osteochondrosis is a failure of the endochondral ossification that affects developing joints in humans and several animal species. It is a localized idiopathic joint disorder characterized by focal chondronecrosis and growing cartilage retention, which can lead to the formation of fissures, subchondral bone cysts, or intra-articular fragments. Osteochondrosis is a complex multifactorial disease associated with extracellular matrix alterations and failure in chondrocyte differentiation, mainly due to genetic, biochemical, and nutritional factors, as well as traumas. This study describes the main proteomic alterations occurring in chondrocytes isolated from osteochondrotic cartilage fragments. A comparative analysis performed on equine osteochondrotic and healthy chondrocytes showed 26 protein species as differentially represented. In particular, quantitative changes in the extracellular matrix, cytoskeletal and chaperone proteins, and in cell adhesion and signaling molecules were observed in osteochondrotic cells, compared to healthy controls. Functional group analysis annotated most of these proteins in “growth plate and cartilage development”, while others were included in “glycolysis and gluconeogenesis”, “positive regulation of protein import”, “cell–cell adhesion mediator activity”, and “mitochondrion nucleoid”. These results may help to clarify some chondrocyte functional alterations that may play a significant role in determining the onset and progression of equine osteochondrosis and, being related, of human juvenile osteochondrosis.

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Section: Discussionmentioning

confidence: 95%

Proteome Alterations in Equine Osteochondrotic Chondrocytes

Chiaradia

Pepe

Orvietani

et al. 2019

IJMS

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“…A clue might come from the P30 data where an increase in classical chondrocyte hypertrophy markers (IHH, COLX), as well as an upregulation of proteins involved in glycolysis, was observed. Hollander and Zeng (2019) demonstrated that hypertrophic chondrocytes express higher levels of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and lactate dehydrogenase (LDH), two proteins upregulated in P30 BMP7 ncko mice. It is possible that the cells surviving at P14 might be those that switched to glycolysis, and the cells with increased lipid metabolism are destined to die.…”

Section: Discussionmentioning

confidence: 99%

Nasal Septum Deviation as the Consequence of BMP-Controlled Changes to Cartilage Properties

Baddam

Young

Dunsmore

et al. 2021

Front. Cell Dev. Biol.

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The nasal septum cartilage is a specialized hyaline cartilage important for normal midfacial growth. Abnormal midfacial growth is associated with midfacial hypoplasia and nasal septum deviation (NSD). However, the underlying genetics and associated functional consequences of these two anomalies are poorly understood. We have previously shown that loss of Bone Morphogenetic Protein 7 (BMP7) from neural crest (BMP7ncko) leads to midfacial hypoplasia and subsequent septum deviation. In this study we elucidate the cellular and molecular abnormalities underlying NSD using comparative gene expression, quantitative proteomics, and immunofluorescence analysis. We show that reduced cartilage growth and septum deviation are associated with acquisition of elastic cartilage markers and share similarities with osteoarthritis (OA) of the knee. The genetic reduction of BMP2 in BMP7ncko mice was sufficient to rescue NSD and suppress elastic cartilage markers. To our knowledge this investigation provides the first genetic example of an in vivo cartilage fate switch showing that this is controlled by the relative balance of BMP2 and BMP7. Cellular and molecular changes similar between NSD and knee OA suggest a related etiology underlying these cartilage abnormalities.

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“…IGF-1 is secreted by the liver, an important organ that produces hormones that are essential for bone growth and development [ 20 ]. This growth factor induces chondrocyte proliferation and differentiation, via a mechanism involving the interaction of parathyroid hormone-related protein (PTHrP) with IHH.…”

Section: Dual Function Of Chondrocyte Hypertrophymentioning

confidence: 99%

Functional Duality of Chondrocyte Hypertrophy and Biomedical Application Trends in Osteoarthritis

et al. 2021

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Chondrocyte hypertrophy is one of the key indicators in the progression of osteoarthritis (OA). However, compared with other OA indications, such as cartilage collapse, sclerosis, inflammation, and protease activation, the mechanisms by which chondrocyte hypertrophy contributes to OA remain elusive. As the pathological processes in the OA cartilage microenvironment, such as the alterations in the extracellular matrix, are initiated and dictated by the physiological state of the chondrocytes, in-depth knowledge of chondrocyte hypertrophy is necessary to enhance our understanding of the disease pathology and develop therapeutic agents. Chondrocyte hypertrophy is a factor that induces OA progression; it is also a crucial factor in the endochondral ossification. This review elaborates on this dual functionality of chondrocyte hypertrophy in OA progression and endochondral ossification through a description of the characteristics of various genes and signaling, their mechanism, and their distinguishable physiological effects. Chondrocyte hypertrophy in OA progression leads to a decrease in chondrogenic genes and destruction of cartilage tissue. However, in endochondral ossification, it represents an intermediate stage at the process of differentiation of chondrocytes into osteogenic cells. In addition, this review describes the current therapeutic strategies and their mechanisms, involving genes, proteins, cytokines, small molecules, three-dimensional environments, or exosomes, against the OA induced by chondrocyte hypertrophy. Finally, this review proposes that the contrasting roles of chondrocyte hypertrophy are essential for both OA progression and endochondral ossification, and that this cellular process may be targeted to develop OA therapeutics.

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The Emerging Role of Glucose Metabolism in Cartilage Development

Cited by 49 publications

References 126 publications

Proteome Alterations in Equine Osteochondrotic Chondrocytes

Proteome Alterations in Equine Osteochondrotic Chondrocytes

Nasal Septum Deviation as the Consequence of BMP-Controlled Changes to Cartilage Properties

Functional Duality of Chondrocyte Hypertrophy and Biomedical Application Trends in Osteoarthritis

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