한빛사 논문
한국기초과학지원연구원
Hyuek Jong Lee1,5, Jueun Lee2,5, Myung Jin Yang1,3,5, Young-Chan Kim1,3,5, Seon Pyo Hong1, Jung Mo Kim1, Geum-Sook Hwang2,4 & Gou Young Koh1,3
1Center for Vascular Research, Institute for Basic Science (IBS), Daejeon 34141, Republic of Korea.
2Integrated Metabolomics Research Group, Western Seoul Center, Korea Basic Science Institute, Seoul 03760, Republic of Korea.
3Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 34141, Republic of Korea.
4Colleage of Pharmacy, Chung-Ang University, Seoul 06974, Republic of Korea.
5These authors contributed equally: Hyuek Jong Lee, Jueun Lee, Myung Jin Yang, Young-Chan Kim.
Corresponding authors : Correspondence to Hyuek Jong Lee, Geum-Sook Hwang or Gou Young Koh.
Abstract
Active thermogenesis in the brown adipose tissue (BAT) facilitating the utilization of lipids and glucose is critical for maintaining body temperature and reducing metabolic diseases, whereas inactive BAT accumulates lipids in brown adipocytes (BAs), leading to BAT whitening. Although cellular crosstalk between endothelial cells (ECs) and adipocytes is essential for the transport and utilization of fatty acid in BAs, the angiocrine roles of ECs mediating this crosstalk remain poorly understood. Using single-nucleus RNA sequencing and knock-out male mice, we demonstrate that stem cell factor (SCF) derived from ECs upregulates gene expressions and protein levels of the enzymes for de novo lipogenesis, and promotes lipid accumulation by activating c-Kit in BAs. In the early phase of lipid accumulation induced by denervation or thermoneutrality, transiently expressed c-Kit on BAs increases the protein levels of the lipogenic enzymes via PI3K and AKT signaling. EC-specific SCF deletion and BA-specific c-Kit deletion attenuate the induction of the lipogenic enzymes and suppress the enlargement of lipid droplets in BAs after denervation or thermoneutrality in male mice. These data provide insight into SCF/c-Kit signaling as a regulator that promotes lipid accumulation through the increase of lipogenic enzymes in BAT when thermogenesis is inhibited.
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