Ultraviolet a regulates adipogenic differentiation of human adipose tissue-derived mesenchymal stem cells via up-regulation of Kruppel-like factor 2
Open accessAbstract
Adipocyte dysfunction is strongly associated with the development of obesity, which is a major risk factor for many disorders, including diabetes, hypertension, and heart disease. This study shows that ultraviolet A (UVA) inhibits adipogenic differentiation of human adipose tissue-derived mesenchymal stem cells and its action mechanisms. The mRNA levels of peroxidase proliferator-activated receptor (PPAR) γ and CCAAT/enhancer-binding protein α (C/EBPα), but not CCAAT/enhancer-binding protein ((C/EBP) β and δ, were reduced by UVA. Moreover, the mRNA levels of PPAR γ target genes (lipoprotein lipase (LPL), CD36, adipocyte protein (aP2), and liver X receptor α (LXR)) were down-regulated by UVA. Additionally, attempts to elucidate a possible mechanism underlying the UVA-mediated effects revealed that UVA induced migration inhibitory factor (MIF) gene expression, and this was mediated through activation of AP-1 (especially JNK and p42/44 MAPK) and nuclear factor-κB. In addition, reduced adipogenesis by UVA was recovered upon the treatment with anti-MIF antibodies. AMP-activated protein kinase phosphorylation and up-regulation of Kruppel-like factor 2 (KLF2) were induced by UVA. Taken together, these findings suggest that the inhibition of adipogenic differentiation of human adipose tissue-derived mesenchymal stem cells by UVA occurs primarily through the reduced expression of PPAR γ, which is mediated by up-regulation of KLF2 via the activation of MIF-AMP-activated protein kinase signaling.
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Chronic UV radiation inhibits preadipocyte differentiation and PPARγ expression, reducing triglyceride accumulation in mature adipocytes.
“Chronic UV radiation dramatically inhibits the differentiation of preadipocytes and the expression of peroxisome proliferator activated receptor γ, reducing the accumulation of triglycerides in mature adipocytes [51].”
From Boosting the Photoaged Skin: The Potential Role of Dietary Components (2021) · cites this paper as [51]
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References 35 · Cited by 38
- Authors
- Lee, J., Lee, J., Jung, E., Kim, Y.-S., Roh, K., Jung, K.-H., & Park, D.
- Corresponding author
- Park, Deokhoon
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2010-10
- Volume
- 285
- Issue
- 42
- Pages
- 32647-32656
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC2952267
- OpenAlex
- W2031937394
- Cited by
- 38
- References
- 35
- Citations by year
- 2026: 3 · 2023: 1 · 2021: 3 · 2020: 2 · 2019: 5 · 2018: 2 · 2017: 2 · 2016: 4 · 2015: 3 · 2014: 1 · 2013: 2 · 2012: 8
- FWCI
- 1.56
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Genetics › Mesenchymal stem cell research
- Keywords
- UVA, adipogenesis, adipose-derived stem cells, KLF2, PPARγ, C/EBPα, macrophage migration inhibitory factor, AMPK, JNK, mitogen-activated protein kinase, NF-κB, AP-1, obesity, adipocyte dysfunction, adipogenesis inhibition
- MeSH terms
- Adipose Tissue, Animals, Cell Differentiation, Humans, Transcription Factors, Ultraviolet Rays, Up-Regulation, Cytokines, RNA, Small Interfering, 3T3-L1 Cells, PPAR gamma, Adipogenesis, Mice, Kruppel-Like Transcription Factors, AMP-Activated Protein Kinases, Mesenchymal Stem Cells
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