Level D· Scientific groundwork from lab and animal studiesAnimal StudyEurope PMCOpen access

Circulating healing (CH) cells expressing BST2 are functionally activated by the injury-regulated systemic factor HGFA

Lo Sicco C., Reverberi D., Villa F., Pfeffer U., Quarto R., Cancedda R.

Animal Study on Chronic Wound, published in Stem Cell Res Ther (2018) — summary generated from the PubMed abstract.

Open my reading list
Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

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
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
Animal Study
Journal
Stem Cell Res Ther (2018)
Reported sample size
—
Source database
Europe PMC
PMID
30409222
PMCID
PMC6225669
DOI
10.1186/s13287-018-1056-1
Citations
15

Abstract (original English)

Background Restoration of damaged tissues through the activation of endogenous progenitors is an attractive therapeutic option. A deep evaluation of the intrinsic stem/progenitor cell properties as well as the reciprocal interactions with injured environments is of critical importance. Methods Here, we show that bone marrow stromal cell antigen 2 (BST2) allows the isolation of a population of circulating progenitors, the circulating healing (CH) cells, characterized by a distinctive core signature. The bone marrow (BM) origin of BST2 pos CH cells has been strengthened by the co-expression of leptin receptor, the hallmark of a subpopulation of BM-skeletal stem cells. Results BST2 pos CH cells retained the capacity to (i) respond to injury signals generated by a bone fracture, (ii) modify the expression of cell motility genes following damage, and (iii) react to hepatocyte growth factor-activator (HGFA), an injury-related stimulus sufficient to induce their transition into G ALERT , a state in which cells are functionally activated and participate in tissue repair. Conclusions Taken together, these results could pave the way for the identification of new strategies to enhance and potentiate endogenous regenerative mechanisms for future therapies.

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 evidence
Bone Marrow CellsAnimalsMice, Inbred C57BLMice, TransgenicWounds and InjuriesSerine EndopeptidasesMembrane GlycoproteinsAntigens, CDGene Expression ProfilingWound Healing

Browse all related research

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

Related research