Downregulation of SUV39H1 and CITED2 Exerts Additive Effect on Promoting Adipogenic Commitment of Human Mesenchymal Stem Cells.
Tan L., Tran L., Ferreyra S., Moran JA., Skovgaard Z., Trujillo A.
Laboratory Study, published in Stem Cells Dev (2021) — 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 (2021)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 33691475
- DOI
- 10.1089/scd.2020.0190
Abstract (original English)
Human adipogenesis is the process through which uncommitted human mesenchymal stem cells (hMSCs) differentiate into adipocytes. Through a siRNA -based high-throughput screen that identifies adipogenic regulators whose expression knockdown leads to enhanced adipogenic differentiation of hMSCs, two new regulators, SUV39H1, a histone methyltransferase that catalyzes H3K9Me3, and CITED2, a CBP/p300-interacting transactivator with Glu/Asp-rich carboxy-terminal domain 2 were uncovered. Both SUV39H1 and CITED2 are normally downregulated during adipogenic differentiation of hMSCs. Further expression knockdown induced by siSUV39H1 or siCITED2 at the adipogenic initiation stage significantly enhanced adipogenic differentiation of hMSCs as compared with siControl treatment, with siSUV39H1 acting by both accelerating fat accumulation in individual adipocytes and increasing the total number of committed adipocytes, whereas siCITED2 acting predominantly by increasing the total number of committed adipocytes. In addition, both siSUV39H1 and siCITED2 were able to redirect hMSCs to undergo adipogenic differentiation in the presence of osteogenic inducing media, which normally only induces osteogenic differentiation of hMSCs in the absence of siSUV39H1 or siCITED2 . Interestingly, simultaneous knockdown of both SUV39H1 and CITED2 resulted in even greater levels of adipogenic differentiation of h
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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