Role of transforming growth factor-activated kinase-1 on tumor necrosis factor-α actions in human adipose tissue-derived stromal cells.
Lee SY., Lee JH., Shin KK., Kim DS., Kim YS., Bae YC.
Laboratory Study, published in Stem Cells Dev (2014) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- Stem Cells Dev (2014)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 25350220
- DOI
- 10.1089/scd.2014.0272
Abstract (original English)
Tumor necrosis factor-α (TNF-α) has multiple effects on proliferation and differentiation of human mesenchymal stem cells. Transforming growth factor-activated kinase-1 (TAK1) mediates the activation of nuclear factor-kappa B (NF-κB), c-Jun N-terminal kinase (JNK), and p38 pathways in response to TNF-α. However, the role of TAK1 in TNF-α-induced effects in human adipose-derived stem cells (hADSCs) and its signaling pathway has not been clearly defined. Therefore, this study was designated to clarify the role of TAK1 in TNF-α-induced actions on proliferation and differentiation of hADSCs and its downstream signaling pathway. Inhibiting TAK1 expression inhibited the TNF-α-induced increase in osteogenic differentiation and basal osteogenic differentiation without affecting the TNF-α-induced effect on proliferation and adipogenic differentiation of hADSCs. A western blot analysis showed that TNF-α treatment induced degradation of IκB, but that TAK1 small interfering RNA (siRNA) transfection did not protect against TNF-α-induced IκB degradation. The transfection of TAK1 siRNA also did not affect TNF-α-induced IκB phosphorylation or ERK1/2 phosphorylation. However, downregulating TAK1 inhibited this TNF-α-induced S536 phosphorylation of the p65 subunit. TNF-α treatment induced p38 phosphorylation, which was inhibited by the transfection of TAK1 siRNA. Adding p38 inhibitor inhibited T
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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