PPAR γ/Nnat/NF-κ B Axis Involved in Promoting Effects of Adiponectin on Preadipocyte Differentiation
Open accessAbstract
A previous study has demonstrated that adiponectin (APN) could promote preadipocyte differentiation, and the present study further explored its mechanism. 3T3-L1 cells were infected with adenovirus holding human adiponectin gene apM1 and mouse neuronatin (Nnat) shRNA and initiated differentiation while coculturing with mature adipocytes stimulated with LPS. After 8 days, preadipocyte differentiation was observed by Oil Red O staining. Real-time quantitative PCR was used to evaluate mRNA expression levels of monocyte chemoattractant protein-1 (MCP-1), interleukin- (IL-) 6, IL-8, and tumor necrosis factor α (TNF-α). The levels of reactive oxygen species (ROS), total antioxidant capacity (T-AOC), malondialdehyde (MDA), and superoxide dismutase (SOD) in 3T3-L1 cells were detected. Western blotting was done to quantify the protein expression levels of Nnat, peroxisome proliferator-activated receptor (PPAR) γ, p65, and inhibitor of nuclear factor κB (IκB) α. Results demonstrated that APN overexpression markedly increased preadipocyte differentiation; inhibited gene expression of MCP-1, IL-6, IL-8, and TNF-α; reduced ROS and MDA release; increased T-AOC and SOD levels; upregulated Nnat, PPAR γ, and IκB α protein expressions; and downregulated p65 protein expression under LPS stimulation. However, the effects of APN were markedly attenuated when Nnat expression was knocked down. Taken together, the present study provided evidences that the effects of APN on promoting preadipocyte differentiation under inflammatory conditions via anti-inflammation and antioxidative stress may be regulated by the PPAR γ/Nnat/NF-κB signaling pathway.
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PPAR-γ is implicated in attenuation of inflammation and oxidative stress determined by adiponectin in LPS-induced inhibition of pre-adipocyte differentiation.
“The PPAR-γ has been implicated in the attenuation of inflammation and oxidative stress determined by adiponectin in LPS-induced inhibition of pre-adipocyte differentiation [162].”
From Dysregulated epicardial adipose tissue as a risk factor and potential therapeutic target of heart failure with preserved ejection fraction in diabetes (2022) · cites this paper as [162]
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- Authors
- Yang, W., Yuan, W., Peng, X., Wang, M., Xiao, J., Wu, C., & Luo, L.
- Affiliations
- Guangdong Medical College (CN)
- Ganzhou People's Hospital (CN)
- Corresponding author
- Yang, Wenkai
- Venue
- Mediators of Inflammation
- Publisher
- Wiley
- Published
- 2019-11-21
- Volume
- 2019
- Pages
- 1-9
- ISSN
- 0962-9351 (ISSN-L)
- 1466-1861
- PMC
- PMC6906841
- OpenAlex
- W2990637760
- Cited by
- 35
- References
- 38
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 8 · 2023: 7 · 2022: 10 · 2021: 6 · 2020: 2
- FWCI
- 3.42
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Mediators of Inflammation (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- adiponectin, preadipocyte differentiation, neuronatin, PPARγ, NF-κB signaling, inflammation, oxidative stress, 3T3-L1 cells, MCP-1, TNF-α, interleukin-6, interleukin-8, lipopolysaccharide stimulation, adipogenesis
- MeSH terms
- Animals, Cell Differentiation, Humans, Membrane Proteins, Nerve Tissue Proteins, Signal Transduction, Interleukin-6, Interleukin-8, NF-kappa B, Adipocytes, Chemokine CCL2, 3T3-L1 Cells, PPAR gamma, Mice, Adiponectin
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