Endothelial PDGF-CC regulates angiogenesis-dependent thermogenesis in beige fat

Takahiro Seki, Kayoko Hosaka, Sharon Lim, Carina Fischer, Jennifer Honek, Yunlong Yang, Patrik Andersson, Masaki Nakamura, Erik Näslund, Seppo Ylä-Herttuala, Meili Sun, Hideki Iwamoto, Xuri Li, Yizhi Liu, Nilesh J. Samani and Yihai Cao ()
Additional contact information
Takahiro Seki: Tumor and Cell Biology, Karolinska Institute
Kayoko Hosaka: Tumor and Cell Biology, Karolinska Institute
Sharon Lim: Tumor and Cell Biology, Karolinska Institute
Carina Fischer: Tumor and Cell Biology, Karolinska Institute
Jennifer Honek: Tumor and Cell Biology, Karolinska Institute
Yunlong Yang: Tumor and Cell Biology, Karolinska Institute
Patrik Andersson: Tumor and Cell Biology, Karolinska Institute
Masaki Nakamura: Tumor and Cell Biology, Karolinska Institute
Erik Näslund: Danderyd Hospital, Karolinska Institute
Seppo Ylä-Herttuala: A.I. Virtanen Institute, Molecular Sciences University of Eastern Finland
Meili Sun: Tumor and Cell Biology, Karolinska Institute
Hideki Iwamoto: Tumor and Cell Biology, Karolinska Institute
Xuri Li: State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University
Yizhi Liu: State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University
Nilesh J. Samani: University of Leicester and NIHR Leicester Cardiovascular Biomedical Research Unit, Glenfield Hospital
Yihai Cao: Tumor and Cell Biology, Karolinska Institute

Nature Communications, 2016, vol. 7, issue 1, 1-16

Abstract: 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.

Date: 2016
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DOI: 10.1038/ncomms12152

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