Cell‐cycle control and the cartilage growth plate

Beier, Frank

doi:10.1002/jcp.20111

Cited by 85 publications

(65 citation statements)

References 112 publications

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“…The epiphyseal plate is made up by two zones that have different morphofunctional characteristics (19)(20)(21), and is affected by several hormones, growth factors, and genes (22)(23)(24)(25)(26)(27). However, in spite of the years of research on bone formation and growth, the mechanisms by which specific transcription factors affect the development of the epiphyseal plate and formation of trabecular bones are still unclear, and the role of hypertrophic chondrocytes in the morphogenesis of the trabecular bone is still controversial.…”

Section: Discussionmentioning

confidence: 99%

Effects of excess maternal thyroxin on the bones of rat offspring from birth to the post-weaning period

Maia

Santos

Batista

et al. 2016

Arch. Endocrinol. Metab.

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Objective: To evaluate, in rat offspring, bone changes induced by excess maternal thyroxin during pregnancy and lactation, and to assess the reversibility of these changes after weaning. Material and methods: Twenty Wistar rats were distributed in two groups, hyperthyroid and control, that were treated daily with L-thyroxin (50 mcg/animal) and placebo, respectively. The treatment was initiated seven days before mating and continued throughout pregnancy and lactation. From every female of each of the two groups, two offspring were euthanized after birth, two at 21 days of age (weaning), and two at 42 days of age (21 days after weaning). In newborns, the length of pelvic and thoracic limbs were measured, and in the other animals, the length and width of the femur and humerus were measured. Bones were dissected, decalcified, embedded in paraffin, and analyzed histomorphometrically. Results: Excess maternal thyroxin significantly reduced the length of the pelvic limb in neonates. In 21-day-old individuals, excess maternal thyroxine reduced the length and the width of the femur and the humerus. It also increased thickness of the epiphyseal plate and the percentage of trabecular bone tissue. In 42-day-old individuals, there were no significant differences between groups in relation to the parameters evaluated in the previous periods. Conclusion: Excess maternal thyroxine reduced growth in suckling rats both at birth and at weaning, and it also increased the percentage of trabecular bone tissue in 21-day-old animals. These changes, however, were reversible at 42 days, i.e., 21 days after weaning. Arch Endocrinol Metab. 2016;60(2):130-7

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Section: Discussionmentioning

confidence: 99%

Effects of excess maternal thyroxin on the bones of rat offspring from birth to the post-weaning period

Maia

Santos

Batista

et al. 2016

Arch. Endocrinol. Metab.

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“…The cell cycle plays an important role in the influence on division and duplication of chondrocyte, which can be divided into four phases: G 1 (gap 1), S (synthesis), during which DNA is replicated, G 2 and M (mitosis), in which cell division occurs (19,20). The DNA content of cells is a constant parameter that varies over the progression of the cell cycle.…”

Section: Discussionmentioning

confidence: 99%

Millimeter wave treatment promotes chondrocyte proliferation via G1/S cell cycle transition

et al. 2012

Int J Mol Med

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Abstract. Millimeter waves, high-frequency electromagnetic waves, can effectively alleviate the clinical symptoms in osteoarthritis patients, as a non-pharmaceutical and non-invasive physical therapy regimen. However, the molecular mechanisms of the therapeutic effects of millimeter wave treatment are not well understood. In the present study, the effect of millimeter waves on the G 1 /S cell cycle progression in chondrocytes and the underlying mecha nism was investigated. Chondrocytes isolated from the knee of SD rats were cultured and identified using toluidine blue staining. The second generation chondrocytes were collected and stimulated with or without millimeter waves for 48 h. Chondrocyte viability was analyzed using the MTT assay. The cell cycle distribution of chondrocytes was analyzed by flow cytometry. mRNA and protein expression levels of cyclin D1, cyclin-dependent kinases 4 and 6 (CDK4 and CDK6) and p21 were detected using real-time PCR and western blotting, respectively. Millimeter wave stimulation was found to significantly enhance chondrocyte viability. Moreover, the percentage of chondrocytes in the G 0 /G 1 phase was significantly decreased, whereas that in the S phase was significantly increased. In addition, following millimeter wave treatment, cyclin D1, CDK4 and CDK6 expression was significantly upregulated, whereas p21 expression was significantly downregulated. The results indicate that millimeter wave treatment promotes chondrocyte proliferation via cell cycle progression. IntroductionOsteoarthritis (OA), the most frequent arthropathy, is characterized by progressive degradation of hyaline articular cartilage and is associated with aging (1). A complex interplay of mechanical, and functional changes of chondrocytes could precipitate the imbalance between matrix anabolic and catabolic processes in articular cartilage and thus the pathogenesis of OA (2,3). Chondroctyes can rapidly respond to changes in the articular microenvironment and regulate the dynamic equilibrium between the anabolism and catabolism of the extracellular matrix (ECM), which plays a crucial role in the maintenance of the cartilage function (4). Therefore, enhancing chondrocyte function might be an efficient treatment to cure or even delay the progression of OA by promoting chondrocyte proliferation.The cell cycle plays an important role in the influence on chondrocyte function, which takes place in chondrocytes leading to its division and duplication. Cell cycle control is a highly regulated process that involves a complex cascade of events, in which regulation can be realized through a complicated network by cyclins, cyclin-dependent kinases (CDKs) and cyclin dependent kinase inhibitors (CDKI). G 1 /S transition, one of the two main checkpoints, is a rate-limiting step in the cell cycle and regulates cell proliferation (5,6). Cyclin D1 is a key cell cycle regulatory protein, which binds to CDK4 or CDK6 to control cell cycle progression from the G 1 to the S phase (7). Meanwhile, p21 competes with cyclin D1 for bindin...

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“…These chondrocytes do not differentiate further or mineralize their ECM (Trippel et al, 1980). Chondrocytes that continue to differentiate to the hypertrophic state contribute to the formation of the growth plate (Beier, 2005).…”

Section: Chondrogenesismentioning

confidence: 99%

Regulation of chondrocyte differentiation by the actin cytoskeleton and adhesive interactions

Woods¹,

Wang²,

Beier³

2007

Journal Cellular Physiology

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230

176

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Chondrocyte differentiation is a multi-step process characterized by successive changes in cell morphology and gene expression. In addition to tight regulation by numerous soluble factors, these processes are controlled by adhesive events. During the early phase of the chondrocyte life cycle, cell-cell adhesion through molecules such as N-cadherin and neural cell adhesion molecule (N-CAM) is required for differentiation of mesenchymal precursor cells to chondrocytes. At later stages, for example in growth plate chondrocytes, adhesion signaling from extracellular matrix (ECM) proteins through integrins and other ECM receptors such as the discoidin domain receptor (DDR) 2 (a collagen receptor) and Annexin V is necessary for normal chondrocyte proliferation and hypertrophy. Cell-matrix interactions are also important for chondrogenesis, for example through the activity of CD44, a receptor for Hyaluronan and collagens. The roles of several signaling molecules involved in adhesive signaling, such as integrin-linked kinase (ILK) and Rho GTPases, during chondrocyte differentiation are beginning to be understood, and the actin cytoskeleton has been identified as a common target of these adhesive pathways. Complete elucidation of the pathways connecting adhesion receptors to downstream effectors and the mechanisms integrating adhesion signaling with growth factor-and hormone-induced pathways is required for a better understanding of physiological and pathological skeletal development.

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Cell‐cycle control and the cartilage growth plate

Cited by 85 publications

References 112 publications

Effects of excess maternal thyroxin on the bones of rat offspring from birth to the post-weaning period

Effects of excess maternal thyroxin on the bones of rat offspring from birth to the post-weaning period

Millimeter wave treatment promotes chondrocyte proliferation via G1/S cell cycle transition

Regulation of chondrocyte differentiation by the actin cytoskeleton and adhesive interactions

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