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Innervation of thermogenic adipose tissue via a calsyntenin 3β-S100b axis

机译：通过Calsyntenin3β-S100b轴对产热脂肪组织的神经支配

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摘要

The sympathetic nervous system drives brown and beige adipocyte thermogenesis through the release of noradrenaline from local axons. However, the molecular basis of higher levels of sympathetic innervation of thermogenic fat, compared to white fat, has remained unknown. Here we show that thermogenic adipocytes express a previously unknown, mammal-specific protein of the endoplasmic reticuhim that we term calsyntenin 3 beta. Genetic loss or gain of expression of calsyntenin 3 beta in adipocytes reduces or enhances functional sympathetic innervation, respectively, in adipose tissue. Ablation of calsyntenin 3 beta predisposes mice on a high-fat diet to obesity. Mechanistically, calsyntenin 3 beta promotes endoplasmic-reticulum localization and secretion of S100b-a protein that lacks a signal peptide-from brown adipocytes. S100b stimulates neurite outgrowth from sympathetic neurons in vitro. A deficiency of S100b phenocopies deficiency of calsyntenin 3 beta, and forced expression of S100b in brown adipocytes rescues the defective sympathetic innervation that is caused by ablation of calsyntenin 3 beta. Our data reveal a mammal-specific mechanism of communication between thermogenic adipocytes and sympathetic neurons.
机译：交感神经系统通过从局部轴突释放去甲肾上腺素来驱动棕色和米色的脂肪细胞生热。然而，与白色脂肪相比，产热脂肪更高水平的交感神经支配的分子基础仍然未知。在这里，我们显示产热脂肪细胞表达内质网的一种先前未知的，哺乳动物特异性的蛋白，我们称其为Calsyntenin 3 beta。脂肪细胞中Calsyntenin 3 beta基因的遗传损失或表达的获得分别减少或增强了脂肪组织中的功能交感神经。消融Calsyntenin 3β会使高脂饮食的小鼠容易肥胖。从机理上讲，Calsyntenin 3β促进棕色脂肪细胞内质网定位和S100b-一种缺乏信号肽的蛋白质的分泌。 S100b体外刺激交感神经元的神经突生长。 S100b的表型不足或Calsyntenin 3 beta的表型不足，以及棕色脂肪细胞中S100b的强制表达可挽救因Calsyntenin 3 beta的消融而引起的有缺陷的交感神经。我们的数据揭示了产热脂肪细胞和交感神经元之间的哺乳动物特定的通信机制。

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  • 来源
    《Nature》 |2019年第7755期|229-235|共7页
  • 作者

    Zeng Xing; Ye Mengchen; Resch Jon M.; Jedrychowski Mark P.; Hu Bo; Lowell Bradford B.; Ginty David D.; Spiegelman Bruce M.;

  • 作者单位

    Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA|Harvard Med Sch, Dept Cell Biol, Boston, MA 02115 USA;

    Harvard Med Sch, Dept Neurobiol, Howard Hughes Med Inst, Boston, MA 02115 USA;

    Harvard Med Sch, Div Endocrinol Diabet & Metab, Dept Med, Beth Israel Deaconess Med Ctr, Boston, MA 02115 USA;

    Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA|Harvard Med Sch, Dept Cell Biol, Boston, MA 02115 USA;

    Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA|Harvard Med Sch, Dept Cell Biol, Boston, MA 02115 USA;

    Harvard Med Sch, Div Endocrinol Diabet & Metab, Dept Med, Beth Israel Deaconess Med Ctr, Boston, MA 02115 USA|Harvard Med Sch, Program Neurosci, Boston, MA 02115 USA;

    Harvard Med Sch, Dept Neurobiol, Howard Hughes Med Inst, Boston, MA 02115 USA;

    Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA|Harvard Med Sch, Dept Cell Biol, Boston, MA 02115 USA;

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