חיפוש מתקדם
Poultry Science
Praul, C.A., Department of Poultry Science, Pennsylvania State University, University Park, PA 16802-3501, United States
Ford, B.C., Department of Poultry Science, Pennsylvania State University, University Park, PA 16802-3501, United States
Gay, C.V., Department of Poultry Science, Pennsylvania State University, University Park, PA 16802-3501, United States, Dept. of Biochem. and Molec. Biology, Pennsylvania State University, University Park, PA 16802-3501, United States
Pines, M., Agricultural Research Organization, Volcani Center, Institute of Animal Science, PO Box 6, Bet-Dagan 50250, Israel
Leach, R.M., Department of Poultry Science, Pennsylvania State University, University Park, PA 16802-3501, United States, Department of Poultry Science, 213 William L. Henning Bldg., Pennsylvania State University, University Park, PA 16802-3501, United States
Tibial dyschondroplasia (TD) is a skeletal deformity associated with rapid growth in a number of avian species. The disease is the result of a disruption in the cascade of events that occur in the epiphyseal growth plate. Whereas the incidence of TD is susceptible to genetic selection, no specific genetic defect has been identified. Although there are extensive data describing the morphological and biochemical characteristics of the lesion, the mechanism of lesion formation is unknown. However, naturally occurring or induced genetic mutations in other species can provide important clues to possible mechanisms responsible for lesion development. Disruption of normal chondrocyte differentiation by constitutive activation of the parathyroid hormone/parathyroid hormone-related peptide (PTH/PTHrP) receptor, inactivation of the fibroblast growth factor receptor-3 (FGFR-3) receptor, and blocking vascular endothelial growth factor (VEGF) signaling all result in lesions that resemble TD. Impairment of vascular penetration due to the ablation of matrix metalloproteinase-9 (MMP-9) or tartrate-resistant acid phosphatase (TRAP) activity also results in similar cartilage abnormalities. We have integrated these observations with our current knowledge of TD to describe a hypothesis for the sequence of events responsible for the development of tibial dyschondroplastic lesions.
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תנאי שימוש
Gene expression and tibial dyschondroplasia
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Praul, C.A., Department of Poultry Science, Pennsylvania State University, University Park, PA 16802-3501, United States
Ford, B.C., Department of Poultry Science, Pennsylvania State University, University Park, PA 16802-3501, United States
Gay, C.V., Department of Poultry Science, Pennsylvania State University, University Park, PA 16802-3501, United States, Dept. of Biochem. and Molec. Biology, Pennsylvania State University, University Park, PA 16802-3501, United States
Pines, M., Agricultural Research Organization, Volcani Center, Institute of Animal Science, PO Box 6, Bet-Dagan 50250, Israel
Leach, R.M., Department of Poultry Science, Pennsylvania State University, University Park, PA 16802-3501, United States, Department of Poultry Science, 213 William L. Henning Bldg., Pennsylvania State University, University Park, PA 16802-3501, United States
Gene expression and tibial dyschondroplasia
Tibial dyschondroplasia (TD) is a skeletal deformity associated with rapid growth in a number of avian species. The disease is the result of a disruption in the cascade of events that occur in the epiphyseal growth plate. Whereas the incidence of TD is susceptible to genetic selection, no specific genetic defect has been identified. Although there are extensive data describing the morphological and biochemical characteristics of the lesion, the mechanism of lesion formation is unknown. However, naturally occurring or induced genetic mutations in other species can provide important clues to possible mechanisms responsible for lesion development. Disruption of normal chondrocyte differentiation by constitutive activation of the parathyroid hormone/parathyroid hormone-related peptide (PTH/PTHrP) receptor, inactivation of the fibroblast growth factor receptor-3 (FGFR-3) receptor, and blocking vascular endothelial growth factor (VEGF) signaling all result in lesions that resemble TD. Impairment of vascular penetration due to the ablation of matrix metalloproteinase-9 (MMP-9) or tartrate-resistant acid phosphatase (TRAP) activity also results in similar cartilage abnormalities. We have integrated these observations with our current knowledge of TD to describe a hypothesis for the sequence of events responsible for the development of tibial dyschondroplastic lesions.
Scientific Publication
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