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Suppression of Nrf2 attenuates adipogenesis and decreases FGF21 expression through PPAR gamma in 3T3-L1 cells

Journal Article · · Biochemical and Biophysical Research Communications
;  [1];  [2];  [1]; ; ; ; ;
  1. Department of Internal Medicine, Seoul National University, College of Medicine, Seoul National University Bundang Hospital, Seongnam, South (Korea, Republic of)
  2. Department of Internal Medicine, Seoul National University, College of Medicine, Seoul, South (Korea, Republic of)
Highlights: • Suppression of Nrf2 in 3T3-L1 cells affects adipogenesis. • Master adipogenic genes are downregulated upon Nrf2 suppression. • FGF21 and MnSOD are downregulated in Nrf2-knockdown 3T3-L1 cells. Adipogenesis is the process of differentiation from preadipocytes to adipocytes and is orchestrated by various transcription factors, such as the peroxisome proliferator-activated receptor gamma (PPARγ) and the CCAAT-enhancer-binding protein alpha (C/EBPα). Oxidative stress is also a crucial factor in adipogenesis, and adipocyte differentiation is affected by the cellular redox status. The nuclear factor E2-related factor 2 (Nrf2), which is a basic leucine zipper (bZIP) transcription factor, acts as a regulator of cellular oxidative stress. Although several previous studies examined the function of Nrf2 in adipogenesis, their results were controversial. In this study, we investigated whether the suppression of Nrf2 in 3T3-L1 cells affected adipogenesis. We found that adipogenesis master regulator genes, such as PPARγ and C/EBPα, were downregulated during the differentiation stage in Nrf2-knockdown 3T3-L1 cells. Moreover, the fibroblast growth factor 21 (FGF21) and manganese superoxide dismutase (MnSOD) were markedly downregulated in Nrf2-knockdown 3T3-L1 cells. Taken together, the results of the present study suggest that the suppression of Nrf2 attenuates adipogenesis and decreases FGF21 expression through PPARγ in 3T3-L1 cells.
OSTI ID:
23137288
Journal Information:
Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 4 Vol. 497; ISSN 0006-291X; ISSN BBRCA9
Country of Publication:
United States
Language:
English

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