Level B· Emerging clinical evidence with positive signalsRandomized Controlled TrialPubMed

Platelet-rich plasma greatly potentiates insulin-induced adipogenic differentiation of human adipose-derived stem cells through a serine/threonine kinase Akt-dependent mechanism and promotes clinical fat graft maintenanc

Cervelli V., Scioli MG., Gentile P., Doldo E., Bonanno E., Spagnoli LG.

Randomized Controlled Trial, published in Stem Cells Transl Med (2012) — summary generated from the PubMed abstract.

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Level B· Emerging clinical evidence with positive signalsEvidence level of this study

Several human studies show positive signals, while research methods and sample sizes continue to develop.

  • 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
Read the A–D evidence level guide

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
Randomized Controlled Trial
Journal
Stem Cells Transl Med (2012)
Country
England
Reported sample size
—
Source database
PubMed
PMID
23197780
PMCID
PMC3659852
DOI
10.5966/sctm.2011-0052
Citations
125

Abstract (original English)

The potential plasticity and therapeutic utility in tissue regeneration of human adipose-derived stem cells (ASCs) isolated from adult adipose tissue have recently been highlighted. The use of autologous platelet-rich plasma (PRP) represents an alternative strategy in regenerative medicine for the local release of multiple endogenous growth factors. Here we investigated the signaling pathways and effects of PRP and human recombinant insulin on proliferation and adipogenic differentiation of ASCs in vitro. PRP stimulated proliferation (EC(50) = 15.3 ± 1.3% vol/vol), whereas insulin's effect was the opposite (IC(50) = 3.0 ± 0.5 μM). Although PRP alone did not increase adipogenesis, in association with insulin it prevented ASC proliferative arrest, greatly enhanced intracytoplasmic lipid accumulation, strongly increased serine/threonine kinase Akt phosphorylation and mouse monoclonal anti-sterol regulatory element binding protein-1 accumulation, and downregulated Erk-1 activity; adipogenic effects were markedly prevented by the Akt inhibitor wortmannin. PRP with insulin synergistically upregulated fibroblast growth factor receptor (FGFR) and downregulated epidermal growth factor receptor (ErbB) expression; moreover, PRP in association prevented insulin-induced insulin-like growth factor-1 receptor and insulin receptor downregulation. The inhibition of FGFR-1, epidermal growth fact

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.

Evidence level

Several human studies show positive signals, while research methods and sample sizes continue to develop.

How we grade evidence
AdipogenesisAdipose TissueAdolescentAdultAgedApoptosisBlotting, WesternCell DifferentiationCell ProliferationFemale

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