Key result
Endothelial production of PDGF-CC during white adipose tissue angiogenesis regulates WAT browning, and its blockade impairs the WAT-beige transition and thermogenesis.
Endothelial production of PDGF-CC during white adipose tissue angiogenesis regulates WAT browning via a paracrine mechanism, offering potential targets for obesity and metabolic diseases.
May inform adipose remodeling strategies; leaves open clinical translation of PDGF-CC targeting.
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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Seki et al. (2016) studied Obesity and metabolic diseases (preclinical models). PDGF-CC modulation (genetic deletion, pharmacological blockade, or adenoviral overexpression) vs. Vehicle or wild-type controls was evaluated on White adipose tissue browning (beige transition) and thermogenesis. Endothelial production of PDGF-CC during white adipose tissue angiogenesis regulates WAT browning, and its blockade impairs the WAT-beige transition and thermogenesis.
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