Autologous decellularized extracellular matrix promotes adipogenic differentiation of adipose derived stem cells in low serum culture system by regulating the ERK1/2-PPARγ pathway.
Qian Y., Chen H., Pan T., Li T., Zhang Z., Lv X.
Laboratory Study, published in Adipocyte (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
- Adipocyte (2021)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 33825675
- PMCID
- PMC8032248
- DOI
- 10.1080/21623945.2021.1906509
- Citations
- 12
Abstract (original English)
High viability and further adipogenic differentiation of adipose-derived stem cells (ADSCs) are fundamental for engraftment and growth of the transplanted adipose tissue. It has been demonstrated that extracellular matrix (ECM) regulates cell proliferation and differentiation by interacting with ERK1/2 signalling pathway. In this study, we prepared autologous decellularized extracellular matrix (d-ECM) and explored its effect on the proliferation and adipogenic ability of ADSCs in low serum culture. We found that 2% foetal bovine serum (FBS) in growth medium inhibited cell viability and DNA replication, and decreased mRNA and protein levels of PPARγ and C/EPBα compared with 10% FBS. Correspondingly, after 14-days adipogenic induction, cells cultured in 2% FBS possessed lower efficiency of adipogenesis and expressed less adipocyte differentiation markers ADIPOQ and aP2. On the contrary, the d-ECM-coated substrate continuously promoted the expression of PPARγ, and regulated the phosphorylation of ERK1/2 in different manners during differentiation. Pretreatment with ERK1/2 inhibitor PD98059 neutralized the effects of d-ECM, which suggested d-ECM might regulate the adipogenesis of ADSCs through ERK1/2-PPARγ pathway. In addition, d-ECM was revealed to regulate the transcription and expression of stemness-associated genes, such as OCT4, NANOG and SOX2, in the undifferentiated ADSCs,
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.
How we grade evidenceBrowse all related research
Filter the research library by this study's title keywords, author, or publication year.