期刊
CELL
卷 175, 期 3, 页码 695-+出版社
CELL PRESS
DOI: 10.1016/j.cell.2018.09.005
关键词
-
资金
- U.S. NIH grants [R01-DK55758, P01-DK088761, R01-DK099110, P01-AG051459]
- Novo Nordisk Research Foundation
- NIH grant [F32-DK113704]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL069229, R01HL114806] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK099110, P01DK088761, F32DK113704, R01DK055758] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [P01AG051459] Funding Source: NIH RePORTER
- OFFICE OF THE DIRECTOR, NATIONAL INSTITUTES OF HEALTH [S10OD021684] Funding Source: NIH RePORTER
We have uncovered the existence of extracellular vesicle (EV)-mediated signaling between cell types within the adipose tissue (AT) proper. This phenomenon became evident in our attempts at generating an adipocyte-specific knockout of caveolin 1 (cav1) protein. Although we effectively ablated the CAV1 gene in adipocytes, cav1 protein remained abundant. With the use of newly generated mouse models, we show that neighboring endothelial cells (ECs) transfer cav1-containing EVs to adipocytes in vivo, which reciprocate by releasing EVs to ECs. AT-derived EVs contain proteins and lipids capable of modulating cellular signaling pathways. Furthermore, this mechanism facilitates transfer of plasma constituents from ECs to the adipocyte. The transfer event is physiologically regulated by fasting/refeeding and obesity, suggesting EVs participate in the tissue response to changes in the systemic nutrient state. This work offers new insights into the complex signaling mechanisms that exist among adipocytes, stromal vascular cells, and, potentially, distal organs.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据