Journal
CELLULAR & MOLECULAR BIOLOGY LETTERS
Volume 27, Issue 1, Pages -Publisher
BMC
DOI: 10.1186/s11658-022-00314-y
Keywords
Obesity; Adipogenic differentiation; Slc25a5; ERK; Transcriptome; Metabolome
Categories
Funding
- National Natural Science Foundation of China [31771539 [YQC], 82000808[SLZ]]
- Innovation and Application Project of Medical and Public Health Technology of Wuxi Science and Technology [N20202005]
- Major Special Fund for Translational Medicine [2020ZHZD03, 2021ZHZD01, 2021ZHZD03]
- Fundamental Research Funds for the Central Universities [JUSRP12048]
- Key Research and Development Program of Jiangsu Province [BE2018624]
- Fund of Wuxi Healthcare Commission [M202004]
Ask authors/readers for more resources
This study identified the role of Slc25a5 in adipogenesis and further confirmed that adipogenic differentiation may be mediated by ERK1/2 phosphorylation. These findings provide a potential new therapeutic target for the treatment of obesity.
Background A comprehensive understanding of the molecular mechanisms of adipogenesis is a critically important strategy for identifying new targets for obesity intervention. Methods Transcriptomic and lipidomic approaches were used to explore the functional genes regulating adipogenic differentiation and their potential mechanism of action in OP9 cells and adipose-derived stem cells. Oil Red O staining was used to detect oil droplets in adipocytes. Results RNA sequencing (RNA-seq) showed that Slc25a5 expression was significantly upregulated in adipogenic differentiation. Depletion of Slc25a5 led to the suppressed expression of adipogenesis-related genes, reduced the accumulation of triglycerides, and inhibited PPAR gamma protein expression. Moreover, the knockdown of Slc25a5 resulted in significant reduction of oxidative phosphorylation (OXPHOS) protein expression (ATP5A1, CQCRC2, and MTCO1) and ATP production. The RNA-seq and real-time quantitative polymerase chain reaction (RT-qPCR) results suggested that adipogenic differentiation is possibly mediated by ERK1/2 phosphorylation, and this hypothesis was confirmed by intervention with PD98059 (an ERK 1/2 inhibitor). Conclusions This study indicates that Slc25a5 inhibits adipogenesis and might be a new therapeutic target for the treatment of obesity.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available