Korean mistletoe lectin regulates self-renewal of placenta-derived mesenchymal stem cells via autophagic mechanisms
Choi JH., Lyu SY., Lee HJ., Jung J., Park WB., Kim GJ.
Laboratory Study, published in Cell Prolif (2012) — 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
- Cell Prolif (2012)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 22925501
- PMCID
- PMC6496602
- DOI
- 10.1111/j.1365-2184.2012.00839.x
- Citations
- 22
Abstract (original English)
Objectives The balance between survival and death is a key point for regulation of physiology of stem cells. Recently, applications of natural products to enhance efficiencies in culturing and differentiation of stem cells are increasing. Korean mistletoe lectin (Viscum album L. var. coloratum agglutinin, VCA) has been known to be toxic to some cancer cells, but it is still unclear whether VCA has a cytotoxic or indeed a proliferative effect on mesenchymal stem cells (MSCs). Here, we have compared effects of VCA in naïve placenta-derived stem cells (PDSCs), immortalized PDSCs and cancer cells (HepG2), and analysed their mechanisms. Materials and methods MTT assay was performed to analyse effects of VCA on naïve PDSCs, immortalized PDSCs and HepG2. FACS, ROS, caspase-3 assay, western blotting and immunofluorescence were performed to detect signalling events involved in self-renewal of the above cell types. Results VCA had cancer cell-specific toxicity to HepG2 cells even with low concentrations of VCA (1-5 pg/ml), toxicity was observed to immortalized PDSCs and HepG2s, while proliferation of naïve PDSCs was significantly increased (P Conclusions VCA can promote MSC proliferation through an activated autophagic mechanism.
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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