Level B· Emerging clinical evidence with positive signalsClinical TrialPubMed

Human endothelial colony-forming cells serve as trophic mediators for mesenchymal stem cell engraftment via paracrine signaling.

Lin RZ., Moreno-Luna R., Li D., Jaminet SC., Greene AK., Melero-Martin JM.

Clinical Trial, published in Proc Natl Acad Sci U S A (2014) — summary generated from the PubMed abstract.

Open my reading list
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
Clinical Trial
Journal
Proc Natl Acad Sci U S A (2014)
Country
United States
Reported sample size
—
Source database
PubMed
PMID
24982174
PMCID
PMC4104912
DOI
10.1073/pnas.1405388111
Citations
127

Abstract (original English)

Endothelial colony-forming cells (ECFCs) are endothelial precursors that circulate in peripheral blood. Studies have demonstrated that human ECFCs have robust vasculogenic properties. However, whether ECFCs can exert trophic functions in support of specific stem cells in vivo remains largely unknown. Here, we sought to determine whether human ECFCs can function as paracrine mediators before the establishment of blood perfusion. We used two xenograft models of human mesenchymal stem cell (MSC) transplantation and studied how the presence of ECFCs modulates MSC engraftment and regenerative capacity in vivo. Human MSCs were isolated from white adipose tissue and bone marrow aspirates and were s.c. implanted into immunodeficient mice in the presence or absence of cord blood-derived ECFCs. MSC engraftment was regulated by ECFC-derived paracrine factors via platelet-derived growth factor BB (PDGF-BB)/platelet-derived growth factor receptor (PDGFR)-β signaling. Cotransplanting ECFCs significantly enhanced MSC engraftment by reducing early apoptosis and preserving stemness-related properties of PDGFR-β(+) MSCs, including the ability to repopulate secondary grafts. MSC engraftment was negligible in the absence of ECFCs and completely impaired in the presence of Tyrphostin AG1296, an inhibitor of PDGFR kinase. Additionally, transplanted MSCs displayed fate-restricted potential in vivo, w

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
AnimalsBecaplerminCells, CulturedCoculture TechniquesEndothelial CellsFemaleHeterograftsHumansMaleMesenchymal Stem Cell Transplantation

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.