Peroxiredoxin 2 deficiency reduces white adipogenesis due to the excessive ROS generation

Mi Hye Kim, Jae Yeop Kim, Jung Hak Kim, Hyun Shik Lee, Jae Won Huh, Dong Seok Lee

Research output: Contribution to journalArticlepeer-review

8 Scopus citations

Abstract

Reactive oxygen species (ROS) act as signaling molecules to regulate various cell functions. Numerous studies have demonstrated ROS to be essential for the differentiation of adipocytes. Peroxiredoxins (Prxs) are a ubiquitous family of antioxidant enzymes in mammalian cells. Prx2 is present in the cytoplasm and cell membranes and demonstrates ROS scavenging activity. We focused on Prx2 involvement in regulating adipogenesis and lipid accumulation and demonstrated that Prx2 expression was upregulated during adipocyte differentiation. In addition, the silencing of Prx2 (shPrx2) inhibited adipogenesis by modulating adipogenic gene expression, and cell death was enhanced via increased ROS production in shPrx2-3T3-L1 cells. These results demonstrate that shPrx2 triggers adipocyte cell death and weakens adipocyte function via ROS production. Taken together, our data suggest the participation of Prx2 in adipocyte function and differentiation. Our results also imply that the downregulation of Prx2 activity could help prevent obesity. Overall, findings support the development of ROS-based therapeutic solutions for the treatment of obesity and obesity-related metabolic disorders.

Original languageEnglish
Pages (from-to)2086-2093
Number of pages8
JournalCell Biology International
Volume44
Issue number10
DOIs
StatePublished - 1 Oct 2020

Keywords

  • adipose tissue/adipocytes
  • apoptosis
  • cell death
  • oxidative stress

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