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首页> 外文期刊>Journal of Cellular Physiology >In vitro regulation of proliferation and differentiation within a postnatal growth plate of the cranial base by parathyroid hormone-related peptide (PTHrP).
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In vitro regulation of proliferation and differentiation within a postnatal growth plate of the cranial base by parathyroid hormone-related peptide (PTHrP).

机译：体外增殖和监管产后生长板内分化甲状旁腺的颅基地与荷尔蒙相关的肽(PTHrP)。

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Parathyroid hormone-related peptide (PTHrP) is known to be an important regulator of chondrocyte differentiation in embryonic growth plates, but little is known of its role in postnatal growth plates. The present study explores the role of PTHrP in regulating postnatal chondrocyte differentiation using a novel in vitro organ culture model based on the ethmoidal growth plate of the cranial base taken from the postnatal day 10 mouse. In vitro the ethmoidal growth plate continued to mineralize and the chondrocytes progressed to hypertrophy, as observed in vivo, but the proliferative zone was not maintained. Treatment with PTHrP inhibited mineralization and reduced alkaline phosphatase (ALP) activity in the hypertrophic zone in the ethmoidal growth plates grown ex vivo, and also increased the proliferation of non-hypertrophic chondrocytes. In addition, exogenous PTHrP reduced the expression of genes associated with terminal differentiation: type X collagen, Runx2, and ALP, as well as the PTH/PTHrP receptor(PPR). Activation of the protein kinase A pathway using 8-Br-cAMP mimicked some of these pro-proliferative/anti-differentiative effects of PTHrP. PTHrP and PPR were found to be expressed within the ethmoidal growth plate using semi-quantitative PCR, and in other cranial growth plates such as the spheno-occipital and pre-sphenoidal synchondroses. These results provide the first functional evidence that PTHrP regulates proliferation and differentiation within the postnatal, cranial growth plate. J. Cell. Physiol. 219: 688-697, 2009. (c) 2009 Wiley-Liss, Inc.
机译：甲状旁腺与荷尔蒙相关的肽(PTHrP)软骨细胞的重要调节器分化的胚胎生长板,但是在产后增长所知甚少的作用盘子。PTHrP调节产后软骨细胞使用一种新的体外器官分化文化模型基于筛骨的生长板颅的基础来自于产后的一天10个鼠标。继续采集矿物和软骨细胞发展到肥大,观察到体内,但是增殖区没有维护。PTHrP抑制矿化和治疗减少碱性磷酸酶(ALP)活性肥厚性区域中筛骨的增长盘子体外生长,也增加了non-hypertrophic软骨细胞的增殖。此外,外源PTHrP减少了与终端相关的基因的表达分化:X型胶原蛋白、Runx2和高山,以及甲状旁腺素/ PTHrP受体(PPR)。激活的蛋白激酶通路使用8-Br-cAMP模仿其中的一些前导/ anti-differentiative的影响PTHrP。在筛骨的生长板使用半定量PCR和其他颅生长板如spheno-occipital和pre-sphenoidal synchondroses。提供PTHrP第一功能的证据调节细胞增殖和分化在产后、颅生长板。细胞。Wiley-Liss公司。

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