Endochondral Ossification
Mostrando 13-24 de 47 artigos, teses e dissertações.
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13. Dysregulation of Chondrogenesis in Human Cleidocranial Dysplasia
Cleidocranial dysplasia (CCD) is an autosomal dominant skeletal dysplasia caused by heterozygosity of mutations in human RUNX2. The disorder is characterized by delayed closure of the fontanel and hypoplastic clavicles that result from defective intramembranous ossification. However, additional features, such as short stature and cone epiphyses, also suggest
The American Society of Human Genetics.
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14. Vascular endothelial growth factor stimulates bone repair by promoting angiogenesis and bone turnover
Several growth factors are expressed in distinct temporal and spatial patterns during fracture repair. Of these, vascular endothelial growth factor, VEGF, is of particular interest because of its ability to induce neovascularization (angiogenesis). To determine whether VEGF is required for bone repair, we inhibited VEGF activity during secondary bone healing
The National Academy of Sciences.
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15. Consequences of avascular necrosis of the femoral head in aluminium-related renal osteodystrophy and the role of endochondral ossification in the repair process.
A patient with chronic renal failure, a dialysis encephalopathy syndrome and renal osteodystrophy associated with aluminium intoxication developed an avascular necrosis of the left femoral head. Histological examination of the excised head confirmed the zone of avascular necrosis and demonstrated an exuberant formation of cartilage around this zone. Calcific
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16. Atf4 regulates chondrocyte proliferation and differentiation during endochondral ossification by activating Ihh transcription
Activating transcription factor 4 (Atf4) is a leucine-zipper-containing protein of the cAMP response element-binding protein (CREB) family. Ablation of Atf4 (Atf4−/−) in mice leads to severe skeletal defects, including delayed ossification and low bone mass, short stature and short limbs. Atf4 is expressed in proliferative and prehypertrophic growth plat
Company of Biologists.
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17. Localization of tartrate-resistant acid phosphatase (TRAP), membrane type-1 matrix metalloproteinases (MT1-MMP) and macrophages during early endochondral bone formation
Endochondral bone formation, the process by which most parts of our skeleton evolve, leads to the establishment of the diaphyseal primary (POC) and epiphyseal secondary ossification centre (SOC) in long bones. An essential event for the development of the SOC is the early generation of vascularized cartilage canals that requires the proteolytic cleavage of t
Blackwell Science Inc.
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18. Continuous expression of Cbfa1 in nonhypertrophic chondrocytes uncovers its ability to induce hypertrophic chondrocyte differentiation and partially rescues Cbfa1-deficient mice
Chondrocyte hypertrophy is a mandatory step during endochondral ossification. Cbfa1-deficient mice lack hypertrophic chondrocytes in some skeletal elements, indicating that Cbfa1 may control hypertrophic chondrocyte differentiation. To address this question we generated transgenic mice expressing Cbfa1 in nonhypertrophic chondrocytes (α1(II) Cbfa1). This co
Cold Spring Harbor Laboratory Press.
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19. Simulation of the initial stage of endochondral ossification: in vitro sequential culture of growth cartilage cells and bone marrow cells.
Growth cartilage cells were isolated from the ribs of young rats and cultured at high cell density in Ham's F-12 medium supplemented with 10% fetal calf serum. During 7 days, glycosaminoglycans and proteoglycans were actively synthesized and secreted, forming a metachromatic matrix. When cultured together with growth cartilage cells precultured and biosynthe
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20. Three new allelic mouse mutations that cause skeletal overgrowth involve the natriuretic peptide receptor C gene (Npr3)
In 1979, a BALB/cJ mouse was identified with an exceptionally long body. This phenotype was found to be caused by a recessive mutation, designated longjohn (lgj), that mapped to the proximal region of chromosome 15. Several years later, a mouse with a similarly elongated body was identified in an outbred stock after chemical mutagenesis with ethylnitrosourea
The National Academy of Sciences.
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21. Impaired endochondral ossification and angiogenesis in mice deficient in membrane-type matrix metalloproteinase I
Membrane-type matrix metalloproteinase I (MT1-MMP)-deficient mice were found to have severe defects in skeletal development and angiogenesis. The craniofacial, axial, and appendicular skeletons were severely affected, leading to a short and domed skull, marked deceleration of postnatal growth, and death by 3 wk of age. Shortening of bones is a consequence of
The National Academy of Sciences.
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22. Development of the mandibular condylar cartilage in human specimens of 10–15 weeks’ gestation
This study analyses some morphological and histological aspects that could have a role in the development of the condylar cartilage (CC). The specimens used were serial sections from 49 human fetuses aged 10–15 weeks. In addition, 3D reconstructions of the mandibular ramus and the CC were made from four specimens. During weeks 10–11 of development, the v
Blackwell Science Inc.
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23. Gly369Cys mutation in mouse FGFR3 causes achondroplasia by affecting both chondrogenesis and osteogenesis
Missense mutations in fibroblast growth factor receptor 3 (FGFR3) result in several human skeletal dysplasias, including the most common form of dwarfism, achondroplasia. Here we show that a glycine-to-cysteine substitution at position 375 (Gly375Cys) in human FGFR3 causes ligand-independent dimerization and phosphorylation of FGFR3 and that the equivalent s
American Society for Clinical Investigation.
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24. Coordination of chondrogenesis and osteogenesis by fibroblast growth factor 18
Gain of function mutations in fibroblast growth factor (FGF) receptors cause chondrodysplasia and craniosynostosis syndromes. The ligands interacting with FGF receptors (FGFRs) in developing bone have remained elusive, and the mechanisms by which FGF signaling regulates endochondral, periosteal, and intramembranous bone growth are not known. Here we show tha
Cold Spring Harbor Laboratory Press.