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瘦素在颈椎后纵韧带骨化症成骨刺激中的作用和机制。

Roles and mechanisms of leptin in osteogenic stimulation in cervical ossification of the posterior longitudinal ligament.

机构信息

Department of Orthopedics Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100730, China.

出版信息

J Orthop Surg Res. 2018 Jul 3;13(1):165. doi: 10.1186/s13018-018-0864-4.

DOI:10.1186/s13018-018-0864-4
PMID:29970120
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6029428/
Abstract

BACKGROUND

Hyperleptinemia is a common feature of obese people, and leptin, an adipocyte-derived cytokine, is believed to be an important factor in the pathogenesis of cervical ossification of the posterior longitudinal ligament(C-OPLL). So this research was to identify the relation between the serum leptin and bone metabolic markers and how the leptin induced osteogenic effect in C-OPLL.

METHODS

Sixty-four samples were selected to determine the concentration of leptin, insulin, and alkaline phosphatase. And the association of leptin with these factors was also examined. We also evaluate the effect of leptin on the development of C-OPLL and further explored the possible underlying mechanism in vitro.

RESULTS

We found that serum leptin concentrations were higher in females than in males. Serum leptin and ALP concentrations were increased significantly in C-OPLL females compared to non-OPLL females. In OPLL subjects, the serum leptin concentration corrected for body mass index correlated negatively with the ALP concentrations. In C-OPLL cells, leptin treatment led to a significant increase in mRNA expressions of ALP and OCN and formation of mineralized nodule. Our experiments reported here that osteogenic effect of leptin in C-OPLL cells could be mediated via ERK1/2, p38 MAPK, and/or JNK signaling pathways.

CONCLUSIONS

From this research, we got that leptin treatment led to a significant increase in mRNA expressions of ALP and OCN and formation of mineralized nodule. And the osteogenic effect of leptin in C-OPLL cells could be mediated via ERK1/2, p38 MAPK, and/or JNK signaling pathways.

摘要

背景

高瘦素血症是肥胖人群的常见特征,而瘦素作为一种脂肪细胞衍生的细胞因子,被认为是颈椎后纵韧带骨化症(C-OPLL)发病机制中的重要因素。因此,本研究旨在确定血清瘦素与骨代谢标志物之间的关系,以及瘦素在 C-OPLL 中的成骨作用。

方法

选择 64 例样本,测定瘦素、胰岛素和碱性磷酸酶的浓度,并检验瘦素与这些因素的相关性。我们还评估了瘦素对 C-OPLL 发展的影响,并在体外进一步探讨了其可能的潜在机制。

结果

我们发现,女性血清瘦素浓度高于男性。与非 C-OPLL 女性相比,C-OPLL 女性的血清瘦素和 ALP 浓度显著升高。在 OPLL 患者中,校正体重指数的血清瘦素浓度与 ALP 浓度呈负相关。在 C-OPLL 细胞中,瘦素处理导致 ALP 和 OCN 的 mRNA 表达显著增加,并形成矿化结节。我们的实验报告表明,瘦素在 C-OPLL 细胞中的成骨作用可以通过 ERK1/2、p38 MAPK 和/或 JNK 信号通路介导。

结论

从本研究中我们得出结论,瘦素处理导致 ALP 和 OCN 的 mRNA 表达显著增加,并形成矿化结节。瘦素在 C-OPLL 细胞中的成骨作用可以通过 ERK1/2、p38 MAPK 和/或 JNK 信号通路介导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30c1/6029428/f5581f7da737/13018_2018_864_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30c1/6029428/a5c3c6cfc2a2/13018_2018_864_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30c1/6029428/5c37af78d007/13018_2018_864_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30c1/6029428/947a86d3fc7d/13018_2018_864_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30c1/6029428/dd03bdd483ab/13018_2018_864_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30c1/6029428/f5581f7da737/13018_2018_864_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30c1/6029428/a5c3c6cfc2a2/13018_2018_864_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30c1/6029428/5c37af78d007/13018_2018_864_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30c1/6029428/947a86d3fc7d/13018_2018_864_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30c1/6029428/dd03bdd483ab/13018_2018_864_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30c1/6029428/f5581f7da737/13018_2018_864_Fig5_HTML.jpg

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Leptin Overexpression in Bone Marrow Stromal Cells Promotes Periodontal Regeneration in a Rat Model of Osteoporosis.骨髓基质细胞中瘦素的过表达促进骨质疏松症大鼠牙周再生。
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