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Chung, K.-J. ; Chatzigeorgiou, A.* ; Economopoulou, M.* ; Garcia-Martin, R.* ; Alexaki, V.I.* ; Mitroulis, I.* ; Nati, M.* ; Gebler, J.* ; Ziemssen, T.* ; Goelz, S.E.* ; Phieler, J.* ; Lim, J.H.* ; Karalis, K.P.* ; Papayannopoulou, T.* ; Blueher, M.* ; Hajishengallis, G.* ; Chavakis, T.

A self-sustained loop of inflammation-driven inhibition of beige adipogenesis in obesity.

Nat. Immunol. 18, 654-664 (2017)
Postprint DOI PMC
Open Access Green
In obesity, inflammation of white adipose tissue (AT) is associated with diminished generation of beige adipocytes ('beige adipogenesis'), a thermogenic and energy-dissipating function mediated by beige adipocytes that express the uncoupling protein UCP1. Here we delineated an inflammation-driven inhibitory mechanism of beige adipogenesis in obesity that required direct adhesive interactions between macrophages and adipocytes mediated by the integrin alpha(4) and its counter-receptor VCAM-1, respectively; expression of the latter was upregulated in obesity. This adhesive interaction reciprocally and concomitantly modulated inflammatory activation of macrophages and downregulation of UCP1 expression dependent on the kinase Erk in adipocytes. Genetic or pharmacological inactivation of the integrin alpha(4) in mice resulted in elevated expression of UCP1 and beige adipogenesis of subcutaneous AT in obesity. Our findings, established in both mouse systems and human systems, reveal a self-sustained cycle of inflammation-driven impairment of beige adipogenesis in obesity.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Adipose-tissue Inflammation; Diet-induced Obesity; Insulin-resistance; Brown Fat; Macrophage Polarization; Cell Recruitment; White Adipocytes; Precursor Cells; Protein-kinase; Adult Humans
Sprache englisch
Veröffentlichungsjahr 2017
HGF-Berichtsjahr 2017
ISSN (print) / ISBN 1529-2908
e-ISSN 1529-2916
Zeitschrift Nature Immunology
Quellenangaben Band: 18, Heft: 6, Seiten: 654-664 Artikelnummer: , Supplement: ,
Verlag Nature Publishing Group
Verlagsort New York
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Pancreatic Islet Research (IPI)
POF Topic(s) 90000 - German Center for Diabetes Research
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-502600-008
DOI 10.1038/ni.3728
WOS ID WOS:000401520900010
Scopus ID 85017514320
PubMed ID 28414311
Erfassungsdatum 2017-06-23
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