The Receptor-Dependent Actions of 1,25-Dihydroxyvitamin D Are Required for Normal Growth Plate Maturation in NPt2a Knockout Mice
作者： Susanne U. Miedlich , Eric D. Zhu , Yves Sabbagh , Marie B. Demay
DOI: 10.1210/EN.2010-0354
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摘要: Rickets is a growth plate abnormality observed in growing animals and humans. Rachitic expansion of the hypertrophic chondrocyte layer plate, setting hypophosphatemia, due to impaired apoptosis these cells. humans mice with X-linked hypophosphatemia that associated renal phosphate wasting secondary elevated levels fibroblast factor-23. also seen settings vitamin D action, PTH increase excretion. However, ablation sodium-dependent transport protein 2a (Npt2a), have not been reported develop rickets. Because activation mitochondrial apoptotic pathway by required for vivo, investigations were undertaken address this paradox. Analyses Npt2a null demonstrate at 2 wk age, resolution 5 age. This temporally an circulating 1,25-dihydroxyvitamin D. To whether receptor-dependent actions steroid hormone are normalization phenotype, mated lacking receptor or rendered deficient. These studies maintenance normal phenotype mice.
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