Whole-tissue 3D imaging reveals intra-adipose sympathetic plasticity regulated by NGF-TrkA signal in cold-induced beiging.
10.1007/s13238-018-0528-5
- Author:
Ying CAO
1
;
Huanhuan WANG
2
;
Wenwen ZENG
3
Author Information
1. Center for Life Sciences, Tsinghua University, Beijing, 100084, China.
2. School of Life Sciences, Peking University, Beijing, 100871, China.
3. Center for Life Sciences, Tsinghua University, Beijing, 100084, China. wenwenzeng@tsinghua.edu.cn.
- Publication Type:Journal Article
- Keywords:
NGF;
TrkA receptor;
cold-induced beiging;
sympathetic plasticity;
whole-tissue 3D imaging
- MeSH:
Adipose Tissue, Beige;
cytology;
diagnostic imaging;
innervation;
metabolism;
Animals;
Catecholamines;
metabolism;
Cold Temperature;
Imaging, Three-Dimensional;
Mice;
Nerve Growth Factor;
metabolism;
Neuronal Plasticity;
Receptor, trkA;
metabolism;
Signal Transduction;
Sympathetic Nervous System;
physiology
- From:
Protein & Cell
2018;9(6):527-539
- CountryChina
- Language:English
-
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 intra-adipose sympathetic plasticity, and moreover, the cold-induced 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.
