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Roth, L.* ; Johann, K.* ; Hönes, G.S.* ; Oelkrug, R.* ; Wagner, L.* ; Hoffmann, A. ; Krohn, K.* ; Moeller, L.C.* ; Weiner, J.* ; Heiker, J.T. ; Klöting, N. ; Tönjes, A.* ; Stumvoll, M. ; Blüher, M. ; Mittag, J.* ; Krause, K.*

Thyroid hormones regulate Zfp423 expression in regionally distinct adipose depots through direct and cell-autonomous action.

Cell Rep. 42:112088 (2023)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
The hypothalamic pituitary thyroid axis is a major regulator of many differentiation processes, including adipose tissue. However, it remains unclear whether and how thyroid hormone (TH) signaling contributes to preadipocyte commitment and differentiation into mature adipocytes. Here, we show a cell-autonomous effect of TH on the transcriptional regulation of zinc finger protein 423 (Zfp423), an early adipogenic determination factor, in murine adipose depots. Mechanistically, binding of the unliganded TH receptor to a negative TH responsive element within the Zfp423 promoter activates transcriptional activity that is reversed upon TH binding. Zfp423 upregulation is associated with increased GFP+ preadipocyte recruitment in stromal vascular fraction isolated from white fat of hypothyroid Zfp423GFP reporter mice. RNA sequencing identified Zfp423-driven gene programs that are modulated in response to TH during adipogenic differentiation. Collectively, we identified Zfp423 as a key molecule that integrates TH signaling into the regulation of adipose tissue plasticity.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Adipocyte Precursor ; Adipogenesis ; Adipose Tissue ; Cp: Metabolism ; Cp: Molecular Biology ; Hypothyroidism ; Preadipocyte ; Thyroid Hormone Receptors ; Thyroid Hormones ; Zfp423; Tissue; White; Thermogenesis; Preadipocytes; Receptors; Mice
ISSN (print) / ISBN 2211-1247
e-ISSN 2211-1247
Zeitschrift Cell Reports
Quellenangaben Band: 42, Heft: 2, Seiten: , Artikelnummer: 112088 Supplement: ,
Verlag Cell Press
Verlagsort 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)
Förderungen
Deutsche Forschungsgemeinschaft