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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Estrogen receptor-α expression in neuronal cells affects bone mass
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Estrogen receptor-α expression in neuronal cells affects bone mass

机译：神经细胞中雌激素受体-α的表达影响骨量

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摘要

It has generally been assumed that bone mass is controlled by endocrine mechanisms and the local bone environment. Recent findings demonstrate that central pathways are involved in the regulation of bone mass. Estrogen is involved in the regulation of bone homeostasis and the CNS is also a target for estrogen actions. The aim of this study was to investigate in vivo the role of central estrogen receptor-α (ERα) expression for bone mass. flestin-Cre mice were crossed with ERα~(flox) mice to generate mice lacking ERa expression specifically in nervous tissue (nestin-ERα~(-/-)). Bone mineral density was increased in both the trabecular and cortical bone compartments in nestin-ERα~(-/-) mice compared with controls. Femoral bone strength was increased in nestin-ERα~(-/-) mice, as demonstrated by increased stiffness and maximal load of failure. The high bone mass phenptype in nestin-ERα~(-/-) mice was mainly caused by increased bone formation. Serum leptin levels were elevated as a result of increased leptin expression in white adipose tissue (WAT) and slightly increased amount of WAT in nestin-ERα~(-/-) mice. Leptin receptor mRNA levels were reduced in the hypothalamus but not in bone. In conclusion, inactivation of central ERa signaling results in increased bone mass, demonstrating that the balance between peripheral stimulatory and central inhibitory ERa actions is important for the regulation of bone mass. We propose that the increased bone mass in nestin-ERα~(-/-) mice is mediated via decreased central leptin sensitivity and thereby increased secretion of leptin from WAT, which, in turn, results in increased peripheral leptin-induced bone formation.
机译：通常认为骨量是由内分泌机制和局部骨环境控制的。最近的发现表明，中枢通路参与骨量的调节。雌激素参与骨稳态的调节，CNS也是雌激素作用的靶标。这项研究的目的是研究体内雌激素受体α（ERα）表达对骨量的作用。 flestin-Cre小鼠与ERα〜（flox）小鼠杂交产生了在神经组织中特异性缺乏ERa表达的小鼠（nestin-ERα〜（-/-））。与对照组相比，巢蛋白-ERα〜（-/-）小鼠的小梁和皮质骨腔中骨矿物质密度均增加。 Nestin-ERα〜（-/-）小鼠的股骨骨强度增加，表现为刚度增加和最大衰竭负荷。 nestin-ERα〜（-/-）小鼠的高骨量表型主要是由增加的骨形成引起的。血清瘦素水平升高是由于白色脂肪组织（WAT）中瘦素表达增加，而Nestin-ERα〜（-/-）小鼠中WAT量略有增加。瘦素受体mRNA水平在下丘脑中降低，但在骨中没有降低。总之，中枢ERa信号的失活导致骨量增加，表明外周刺激和中枢抑制性ERa作用之间的平衡对于调节骨量很重要。我们建议在Nestin-ERα〜（-/-）小鼠中增加的骨量是通过降低中央瘦素敏感性来介导的，从而增加了WAT中瘦素的分泌，从而导致外周瘦素诱导的骨形成增加。

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    Claes Ohlsson; Cecilia Engdahl; Anna E. Boerjesson; Sara H. Windahl; Erik Studer; Lars Westberg; Elias Eriksson; Antti Koskela; Juha Tuukkanen; Andree Krust; Pierre Chambon; Hans Carlsten; Marie K. Lagerquist;

  • 作者单位

    Centre for Bone and Arthritis Research, Institute of Medicine, and University of Gothenburg, Gothenburg 413 45, Sweden;

    Centre for Bone and Arthritis Research, Institute of Medicine, and University of Gothenburg, Gothenburg 413 45, Sweden;

    Centre for Bone and Arthritis Research, Institute of Medicine, and University of Gothenburg, Gothenburg 413 45, Sweden;

    Centre for Bone and Arthritis Research, Institute of Medicine, and University of Gothenburg, Gothenburg 413 45, Sweden;

    Department of Pharmacology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg 413 45, Sweden;

    Department of Pharmacology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg 413 45, Sweden;

    Department of Pharmacology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg 413 45, Sweden;

    Department of Anatomy and Cell Biology, Institute of Biomedicine, University of Oulu,Oulu 90014, Finland;

    Department of Anatomy and Cell Biology, Institute of Biomedicine, University of Oulu,Oulu 90014, Finland;

    lnstitut de Genetique et de Biologie Moleculaire et Cellulaire, Centre National de la Recherche Scientifique, Institut National de la Sante et de la Recherche Medicale, Universite de Strasbourg, College de France, Illkirch, Strasbourg 67404, France;

    lnstitut de Genetique et de Biologie Moleculaire et Cellulaire, Centre National de la Recherche Scientifique, Institut National de la Sante et de la Recherche Medicale, Universite de Strasbourg, College de France, Illkirch, Strasbourg 67404, France;

    Centre for Bone and Arthritis Research, Institute of Medicine, and University of Gothenburg, Gothenburg 413 45, Sweden;

    Centre for Bone and Arthritis Research, Institute of Medicine, and University of Gothenburg, Gothenburg 413 45, Sweden;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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