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研究揭示骨骼对急性应激反应的调节作用
作者:小柯机器人 发布时间:2019/9/13 12:47:42

美国哥伦比亚大学欧文医学中心Gerard Karsenty团队最新研究揭示了骨骼对急性应激反应的调节作用。 2019年9月12日,《细胞—代谢》在线发表了这项成果。

研究人员假设骨骼的进化是为了增强骨骼脊椎动物在野外逃避危险的能力。为了支持这一概念,研究者证实,骨源性信号是引起急性应激反应(ASR)所必需的。实际上,小鼠,大鼠(啮齿动物)和人类暴露于各种类型的应激物导致循环生物活性骨钙蛋白的快速和选择性激增,因为应激物有利于谷氨酸成骨细胞的摄取,其防止骨钙蛋白在其分泌之前失活。骨钙蛋白允许ASR的表现通过在突触后副交感神经元中发出信号来展开,以抑制它们的活性,从而使交感神经张力不受阻碍。

与野生型动物一样,肾上腺切除的啮齿动物和肾上腺不足的患者可以发展ASR,遗传研究表明这是由于它们的高循环骨钙素水平。研究人员因此提出了骨钙蛋白决定的ASR的骨 - 脊椎动物特异性内分泌调节网络。

附:英文原文

Title: Mediation of the Acute Stress Response by the Skeleton

Author: Julian Meyer Berger, Parminder Singh, Lori Khrimian, Donald A. Morgan, Subrata Chowdhury, Emilio Arteaga-Solis, Tamas L. Horvath, Ana I. Domingos, Anna L. Marsland, Vijay Kumal Yadav, Kamal Rahmouni, Xiao-Bing Gao, Gerard Karsenty

Issue&Volume: 12 September 2019

Summary: 

We hypothesized that bone evolved, in part, to enhance the ability of bony vertebrates to escape danger in the wild. In support of this notion, we show here that a bone-derived signal is necessary to develop an acute stress response (ASR). Indeed, exposure to various types of stressors in mice, rats (rodents), and humans leads to a rapid and selective surge of circulating bioactive osteocalcin because stressors favor the uptake by osteoblasts of glutamate, which prevents inactivation of osteocalcin prior to its secretion. Osteocalcin permits manifestations of the ASR to unfold by signaling in post-synaptic parasympathetic neurons to inhibit their activity, thereby leaving the sympathetic tone unopposed. Like wild-type animals, adrenalectomized rodents and adrenal-insufficient patients can develop an ASR, and genetic studies suggest that this is due to their high circulating osteocalcin levels. We propose that osteocalcin defines a bony-vertebrate-specific endocrine mediation of the ASR.

DOI: 10.1016/j.cmet.2019.08.012

Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(19)30441-3

期刊信息

Cell Metabolism:《细胞—代谢》,创刊于2005年。隶属于细胞出版社,最新IF:22.415
官方网址:https://www.cell.com/cell-metabolism/home
投稿链接:https://www.editorialmanager.com/cell-metabolism/default.aspx