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

Seki, T (author)
Karolinska Institutet
Hosaka, K (author)
Karolinska Institutet
Lim, S (author)
Karolinska Institutet
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Fischer, C (author)
Karolinska Institutet
Honek, J (author)
Yang, YL (author)
Andersson, P (author)
Karolinska Institutet
Nakamura, M (author)
Naslund, E (author)
Karolinska Institutet
Yla-Herttuala, S (author)
Sun, ML (author)
Iwamoto, H (author)
Li, XR (author)
Liu, YZ (author)
Samani, NJ (author)
Cao, YH (author)
Karolinska Institutet
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 (creator_code:org_t)
2016-08-05
2016
English.
In: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 7, s. 12152-
  • Journal article (peer-reviewed)
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  • 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.

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