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Ring finger protein 11 inhibits melanocortin 3 and 4 receptor signaling.
Front. Endocrin. 7:109 (2016)
Intact melanocortin signaling via the G protein-coupled receptors (GPCRs), melanocortin receptor 4 (MC4R), and melanocortin receptor 3 (MC3R) is crucial for body weight maintenance. So far, no connection between melanocortin signaling and hypothalamic inflammation has been reported. Using a bimolecular fluorescence complementation library screen, we identified a new interaction partner for these receptors, ring finger protein 11 (RNF11). RNF11 participates in the constitution of the A20 complex that is involved in reduction of tumor necrosis factor α (TNFα)-induced NFκB signaling, an important pathway in hypothalamic inflammation. Mice treated with high-fat diet (HFD) for 3 days demonstrated a trend toward an increase in hypothalamic Rnf11 expression, as shown for other inflammatory markers under HFD. Furthermore, Gs-mediated signaling of MC3/4R was demonstrated to be strongly reduced to 20-40% by co-expression of RNF11 despite unchanged total receptor expression. Cell surface expression was not affected for MC3R but resulted in a significant reduction of MC4R to 61% by co-expression with RNF11. Mechanisms linking HFD, inflammation, and metabolism remain partially understood. In this study, a new axis between signaling of specific body weight regulating GPCRs and factors involved in hypothalamic inflammation is suggested.
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
G Protein Coupled Receptor ; Inflammation ; Protein Complementation Assay ; Protein Network ; Weight Regulation; Necrosis-factor-alpha; High-fat Diet; Immortalized Hypothalamic Neurons; Nf-kappa-b; Insulin-resistance; Leptin Resistance; Human Obesity; Tnf-alpha; Rnf11; Inflammation
ISSN (print) / ISBN
1664-2392
e-ISSN
1664-2392
Zeitschrift
Frontiers in Endocrinology
Quellenangaben
Band: 7,
Artikelnummer: 109
Verlag
Frontiers
Verlagsort
Lausanne
Nichtpatentliteratur
Publikationen
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Diabetes and Obesity (IDO)