Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/38443
Title: Endothelial PDGF-CC regulates angiogenesis-dependent thermogenesis in beige fat.
Authors: Seki, T.
Hosaka, K.
Lim, S.
Fischer, C.
Honek, J.
Yang, Y.
Andersson, P.
Nakamura, M.
Näslund, E.
Ylä-Herttuala, S.
Sun, M.
Iwamoto, H.
Li, X.
Liu, Y.
Samani, Nilesh J.
Cao, Yihai
First Published: 5-Aug-2016
Publisher: Nature Publishing Group
Citation: Nature Communications, 2016, 7:12152
Abstract: Cold- and β3-adrenoceptor agonist-induced sympathetic activation leads to angiogenesis and UCP1-dependent thermogenesis in mouse brown and white adipose tissues. Here we show that endothelial production of PDGF-CC during white adipose tissue (WAT) angiogenesis regulates WAT browning. We find that genetic deletion of endothelial VEGFR2, knockout of the Pdgf-c gene or pharmacological blockade of PDGFR-α impair the WAT-beige transition. We further show that PDGF-CC stimulation upregulates UCP1 expression and acquisition of a beige phenotype in differentiated mouse WAT-PDGFR-α(+) progenitor cells, as well as in human WAT-PDGFR-α(+) adipocytes, supporting the physiological relevance of our findings. Our data reveal a paracrine mechanism by which angiogenic endothelial cells modulate adipocyte metabolism, which may provide new targets for the treatment of obesity and related metabolic diseases.
DOI Link: 10.1038/ncomms12152
eISSN: 2041-1723
Links: http://www.nature.com/articles/ncomms12152
http://hdl.handle.net/2381/38443
Version: Publisher Version
Status: Peer-reviewed
Type: Journal Article
Rights: Copyright The Author(s) 2016 This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
Description: Supplementary Information accompanies this paper at http://www.nature.com/naturecommunications
Appears in Collections:Published Articles, Dept. of Cardiovascular Sciences

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