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Nature Immunology:巨噬细胞缺陷在脂肪组织中妨碍交感神经分布及脂肪代谢

2017-05-22 MedSci MedSci原创

这一报告揭示了缺陷的脂肪组织中的巨噬细胞能够妨碍脂肪组织中交感神经的分布,以及激素的分泌,从而中断脂肪细胞消耗脂肪产生能量和热量的过程,并且导致肥胖。

组织中的巨噬细胞一方面提供了机体免疫防御外来病原的侵袭,另一方面同时参与建立和维持机体组织代谢的平衡。机体各个组织中的巨噬细胞如果发生了缺陷,除了影响对于细菌病毒的免疫力以外,同时也会产生各种各样的代谢疾病。在最新一期的Nature Immunology杂志中,Yochi Wolf及其同事发现,如果在巨噬细胞中特定引起核转录调节因子Mecp2蛋白的缺失突变,会引起自发性的肥胖。

核转录调节因子Mecp2蛋白的缺失突变在之前的报道中,已知能够引起Rett综合症(Rett Syndrome)。Rett综合症是由于Mecp2蛋白突变引起的神经功能发育停滞和消退为特征的神经发育障碍综合症。在之前的报导中,研究人员怀疑Mecp2蛋白在巨噬细胞中的突变,是造成这一神经发育缺陷的主要因素。因此研究人员,通过基因调节手段,在巨噬细胞中特定降低了Mecp2蛋白的表达量。出人意料的是,这一调节并没有导致实验小鼠产生Rett综合征相关的神经发育障碍的迹象,但是显示出自发性肥胖的症状。表现为,其负责燃烧和消耗脂肪的棕色(或米色)脂肪组织(Beige adipose tissue)的功能受损。具体来说,在棕色脂肪组织中驻留的带有Cx3Cr1+标志的巨噬细胞亚群收到了损害,从而抑制了棕色脂肪细胞燃烧脂肪产生热量和能量的过程。

在分子机理上,发生这一巨噬细胞突变的实验小鼠在肥胖发生之前,交感神经的神经分布(sympathetic innervation)减少和去甲肾上腺素(norepinephrine)的局部含量及滴度的下降,导致脂肪细胞中的重要生热因子UCP1蛋白的表达降低。这一现象可能是因为,Mecp2蛋白突变后巨噬细胞过度表达和分泌配体PlexinA4,从而排斥表达跨膜信号蛋白Sema6A的交感神经轴突细胞。

总的来说,这一报告揭示了缺陷的脂肪组织中的巨噬细胞能够妨碍脂肪组织中交感神经的分布,以及激素的分泌,从而中断脂肪细胞消耗脂肪产生能量和热量的过程,并且导致肥胖。

原始出处:
Yochai Wolf et al. Brown-adipose-tissue macrophages control tissue innervation and homeostatic energy expenditure. Nature Immunology 18, 665–674 (2017) doi:10.1038/ni.3746

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    2018-03-03 liye789132251
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    2017-06-28 周周人

    学习。

    0

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    2017-05-23 135****7952平儿

    学习了。。。。。。

    0

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    2017-05-23 flysky120

    学习一下知识

    0

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    2017-05-22 天涯183

    非常好的文章,学习了,很受益

    0

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    2017-05-22 惠映实验室

    药代药效的研究

    0

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    2017-05-22 dhzzm

    好,继续深入研究

    0

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