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首页> 外文期刊>Cytokine >RANKL/OPG system regulation by endogenous PTH and PTH1R/ATF4 axis in bone: Implications for bone accrual and strength in growing rats with mild uremia
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RANKL/OPG system regulation by endogenous PTH and PTH1R/ATF4 axis in bone: Implications for bone accrual and strength in growing rats with mild uremia

机译：骨内源性PTH和PTH1R / ATF4轴的RANKL / OPG系统调节：对患有轻度尿毒质的生长大鼠的骨归因和强度的影响

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摘要

Osteoprotegerin (OPG), receptor activator of NF-kappa 13 ligand (RANKL), and parathyroid hormone (PTH) play a central role in the regulation of bone turnover in chronic kidney disease (CKD), but their influence on bone mineral density (BMD) and strength remains unclear, particularly in children. We studied the clinical significance of OPG and RANKL in relation to PTH, femur weight, BMD, and bone biomechanical properties in growing rats after one month (CKD-1) and three months (CKD-3) of surgically-induced mild CKD. Gene expression of parathyroid hormone 1 receptor (PTH1R) and activating transcription factor 4 (ATF4), major regulators of anabolic PTH response in bone, was also determined. Serum PTH and bone PTH1R/ATF4 expression was elevated in CKD-3 compared with other groups, and it positively correlated with femur weight, BMD, and the biomechanical properties of the femoral diaphysis reflecting cortical bone strength. In contrast, bone RANKL/OPG ratios were decreased in CKD-3 rats compared with other groups, and they were inversely correlated with PTH and the other abovementioned bone parameters. However, the PTH-PTH1R-ATF4 axis exerted an unfavorable effect on the biomechanical properties of the femoral neck. In conclusion, this study showed for the first time an inverse association between serum PTH and the bone RANKL/OPG system in growing rats with mild CKD. A decrease in the RANKL/OPG ratio, associated with PTH-dependent activation of the anabolic PTH1R/ ATF4 pathway, seems to be responsible for the unexpected, beneficial effect of PTH on cortical bone accrual and strength. Simultaneously, impaired biomechanical properties of the femoral neck were observed, making this bone site more susceptible to fractures.
机译：骨蛋白酶（OPG），NF-Kappa 13配体（RANKL）的受体活化剂，和甲状旁腺激素（PTH）在慢性肾疾病（CKD）中的骨周转调节中起着核心作用，但它们对骨矿物密度的影响（BMD ）和力量仍然尚不清楚，特别是在儿童中。我们研究了OPG和RANKL在一个月（CKD-1）和三个月（CKD-3）后生长大鼠的PTH，股骨重量，BMD和骨生物力学性能相关的临床意义。还确定了甲状旁腺激素1受体（PTH1R）和活化转录因子4（ATF4）的基因表达，骨骼中代谢PTH反应的主要调节剂。与其他基团相比，血清PTH和骨PTH1R / ATF4表达在CKD-3中升高，与股骨重量，BMD和反射皮质骨强度的股骨骨体的生物力学性能呈正相关。相比之下，与其他基团相比，CKD-3大鼠中的骨RankL / OPG比率降低，它们与PTH和其他上述骨参数相反。然而，PTH-PTH1R-ATF4轴对股骨颈部的生物力学性质产生了不利影响。总之，该研究表明，血清PTH与骨rancall / OPG系统之间的逆关联，在生长的大鼠中具有轻度CKD。 rankL / OPG比率的降低，与合成依赖于合成的合成型PTH1R / ATF4途径的活化，似乎负责PTH对皮质骨归因和强度的意外，有益的影响。同时，观察到股骨颈的生物力学性质受损，使这种骨头位点更容易受到裂缝的影响。

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