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Whole-tissue 3D imaging reveals intra-adipose sympathetic plasticity regulated by NGF-TrkA signal in

本站小编 Free考研考试/2022-01-02

Ying Cao1,4,
Huanhuan Wang5,
Wenwen Zeng1,2,3,
1 Center for Life Sciences, Tsinghua University, Beijing 100084, China;
2 Institute for Immunology and School of Medicine, Tsinghua University, Beijing 100084, China;
3 Beijing Key Laboratory for Immunological Research on Chronic Diseases, Beijing 100084, China;
4 Academy for Advanced Interdisciplinary Studies, Peking University, Beijing 100871, China;
5 School of Life Sciences, Peking University, Beijing 100871, China
Funds: We thank members of the Zeng laboratory for helps and discussions. This work was supported by National Natural Science Foundation of China (Grant Nos. 31770936 and 91742106) to Wenwen Zeng, Beijing Natural Science Foundation (5172016) to Wenwen Zeng, Thousand-Talent Young Investigator Program to Wenwen Zeng, and National Key R&D Program of China (2017YFA0505800). The Zeng laboratory was also supported by Center for Life Sciences, Institute for Immunology, and School of Medicine at Tsinghua University.

Received Date: 2018-03-03
Rev Recd Date:2018-03-12




Abstract
Sympathetic arborizations act as the essential efferent signals in regulating the metabolism of peripheral organs including white adipose tissues (WAT). However, whether these local neural structures would be of plastic nature, and how such plasticity might participate in specific metabolic events of WAT, remains largely uncharacterized. In this study, we exploit the new volume fluorescence-imaging technique to observe the significant, and also reversible, plasticity of intra-adipose sympathetic arborizations in mouse inguinal WAT in response to cold challenge. We demonstrate that this sympathetic plasticity depends on the cold-elicited signal of nerve growth factor (NGF) and TrkA receptor. Blockage of NGF or TrkA signaling suppresses intraadipose sympathetic plasticity, and moreover, the coldinduced beiging process of WAT. Furthermore, we show that NGF expression in WAT depends on the catecholamine signal in cold challenge. We therefore reveal the key physiological relevance, together with the regulatory mechanism, of intra-adipose sympathetic plasticity in the WAT metabolism.
Keywords: sympathetic plasticity,
NGF,
TrkA receptor,
cold-induced beiging,
whole-tissue 3D imaging



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