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首页> 外文期刊>Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research >Measurement of plasma, serum, and platelet serotonin in individuals with high bone mass and mutations in LRP5
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Measurement of plasma, serum, and platelet serotonin in individuals with high bone mass and mutations in LRP5

机译：测量具有高骨量和LRP5突变的个体的血浆，血清和血小板血清素

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It has recently been suggested that the low-density lipoprotein receptor-related protein 5 (LRP5) regulates bone mass by suppressing secretion of serotonin from duodenal enterochromaffin cells. In mice with targeted expression of a high bone mass-causing (HBM-causing) LRP5 mutation and in humans with HBM LRP5 mutations, circulating serotonin levels have been reported to be lower than in controls whereas individuals with loss-of-function mutations in LRP5 have high blood serotonin. In contrast, others have reported that conditionally activating a knock-in allele of an HBM-causing LRP5 mutation in several tissues, or genetic deletion of LRP5 in mice has no effect on serum serotonin levels. To further explore the possible association between HBM-causing LRP5 mutations and circulating serotonin, levels of the hormone were measured in the platelet poor plasma (PPP), serum, and platelet pellet (PP) of 16 affected individuals from 2 kindreds with HBM-causing LRP5 mutations (G171V and N198S) and 16 age-matched controls. When analyzed by HPLC, there were no differences in levels of serotonin in PPP and PP between affected individuals and age-matched controls. Similarly, when analyzed by ELISA, there were no differences in PPP or PP between these two groups. By ELISA, serum levels of serotonin were higher in the affected individuals when compared to age-matched controls. A subgroup analysis of only the G171V subjects (n = 14) demonstrated that there were no differences in PPP and PP serotonin between affected individuals and controls when analyzed by HPLC. PP serotonin was lower in the affected individuals when measured by ELISA but serum serotonin levels were not different. We conclude that there is no change in PPP serotonin in individuals with HBM-causing mutations in LRP5.
机译：最近已经提出，低密度脂蛋白受体相关蛋白5（LRP5）通过抑制十二指肠肠嗜铬细胞的血清素分泌来调节骨量。在具有高骨量引起（HBM）LRP5突变的靶向表达的小鼠和具有HBM LRP5突变的人中，据报道循环血清素水平低于对照组，而具有LRP5失功能突变的个体血液中的血清素含量高。相反，其他人则报告说，有条件地激活几种组织中导致HBM的LRP5突变的敲入等位基因，或小鼠中LRP5的基因缺失对血清5-羟色胺水平没有影响。为了进一步探讨造成HBM的LRP5突变与循环血清素之间的可能关系，在来自2个HBM致病家庭的16名受影响个体的血小板不足血浆（PPP），血清和血小板沉淀（PP）中测量了激素水平LRP5突变（G171V和N198S）和16个年龄匹配的对照。通过HPLC分析时，受影响个体与年龄匹配的对照组之间PPP和PP中5-羟色胺的含量没有差异。同样，通过ELISA分析时，两组之间的PPP或PP也没有差异。通过ELISA，与年龄匹配的对照组相比，患病个体的血清素水平更高。仅对G171V受试者（n = 14）进行的亚组分析表明，通过HPLC分析时，受影响的个体与对照组之间的PPP和PP 5-羟色胺没有差异。通过ELISA测定时，PP5-羟色胺在受影响的个体中较低，但血清5-羟色胺水平没有差异。我们得出的结论是，具有LBM5导致HBM突变的个体的PPP血清素没有变化。

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