Dataset related to the article "Prenylcysteine Oxidase 1 Is a Key Regulator of Adipogenesis"
Authors/Creators
- 1. Centro Cardiologico Monzino IRCCS
- 2. Dipartimento di Biologia e Biotecnologie "Lazzaro Spallanzani", Università di Pavia; Centro Cardiologico Monzino IRCCS
- 3. Science for Life Laboratory, KTH—Royal Institute of Technology, Tomtebodavägen, Solna
Description
This record contains raw data related to the article “Prenylcysteine Oxidase 1 Is a Key Regulator of Adipogenesis"
Abstract: The process of adipogenesis involves the differentiation of preadipocytes into mature
adipocytes. Excessive adipogenesis promotes obesity, a condition that increasingly threatens global
health and contributes to the rapid rise of obesity-related diseases. We have recently shown that
prenylcysteine oxidase 1 (PCYOX1) is a regulator of atherosclerosis-disease mechanisms, which
acts through mechanisms not exclusively related to its pro-oxidant activity. To address the role
of PCYOX1 in the adipogenic process, we extended our previous observations confirming that
Pcyox1//Apoe/ mice fed a high-fat diet for 8 or 12 weeks showed significantly lower body
weight, when compared to Pcyox1+/+/Apoe/ mice, due to an evident reduction in visceral adipose
content. We herein assessed the role of PCYOX1 in adipogenesis. Here, we found that PCYOX1 is
expressed in adipose tissue, and, independently from its pro-oxidant enzymatic activity, is critical for
adipogenesis. Pcyox1 gene silencing completely prevented the differentiation of 3T3-L1 preadipocytes,
by acting as an upstream regulator of several key players, such as FABP4, PPAR , C/EBP. Proteomic
analysis, performed by quantitative label-free mass spectrometry, further strengthened the role of
PCYOX1 in adipogenesis by expanding the list of its downstream targets. Finally, the absence of
Pcyox1 reduces the inflammatory markers in adipose tissue. These findings render PCYOX1 a novel
adipogenic factor with possible pathophysiological or therapeutic potential.
Notes
Files
Additional details
Related works
- Is supplement to
- Journal article: 10.3390/antiox12030542 (DOI)
Funding
- Ministry of Health
- Ricerca Corrente to Centro Cardiologico Monzino IRCCS RC