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Hypoxia-independent angiogenesis in adipose tissues during cold acclimation.
Stockholms universitet, Naturvetenskapliga fakulteten, Wenner-Grens institut, Avdelningen för fysiologi.
Vise andre og tillknytning
2009 (engelsk)Inngår i: Cell Metabolism, ISSN 1550-4131, E-ISSN 1932-7420, Vol. 9, nr 1, s. 99-109Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

The molecular mechanisms of angiogenesis in relation to adipose tissue metabolism remain poorly understood. Here, we show that exposure of mice to cold led to activation of angiogenesis in both white and brown adipose tissues. In the inguinal depot, cold exposure resulted in elevated expression levels of brown-fat-associated proteins, including uncoupling protein-1 (UCP1) and PGC-1alpha. Proangiogenic factors such as VEGF were upregulated, and endogenous angiogenesis inhibitors, including thrombospondin, were downregulated. In wild-type mice, the adipose tissues became hypoxic during cold exposure; in UCP1(-/-) mice, hypoxia did not occur, but, remarkably, the augmented angiogenesis was unaltered and was thus hypoxia independent. Intriguingly, VEGFR2 blockage abolished the cold-induced angiogenesis and significantly impaired nonshivering thermogenesis capacity. Unexpectedly, VEGFR1 blockage resulted in the opposite effects: increased adipose vascularity and nonshivering thermogenesis capacity. Our findings have conceptual implications concerning application of angiogenesis modulators for treatment of obesity and metabolic disorders.

sted, utgiver, år, opplag, sider
2009. Vol. 9, nr 1, s. 99-109
HSV kategori
Forskningsprogram
cellbiologi
Identifikatorer
URN: urn:nbn:se:su:diva-32904DOI: 10.1016/j.cmet.2008.11.009ISI: 000262333000013PubMedID: 19117550OAI: oai:DiVA.org:su-32904DiVA, id: diva2:281915
Tilgjengelig fra: 2009-12-17 Laget: 2009-12-17 Sist oppdatert: 2022-02-25bibliografisk kontrollert

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Petrovic, NatasaNedergaard, JanCannon, Barbara

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