Increased c-myc and mi R-33 Expression in Expanded Hematopoietic Stem Cells Cultured on Adipose Stem Cells Feeder Layer.
Foroutan T.
Laboratory Study, published in Int J Organ Transplant Med (2017) — 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
- Int J Organ Transplant Med (2017)
- Country
- Iran
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 29321834
- PMCID
- PMC5756900
- Citations
- 4
Abstract (original English)
Background Umbilical cord blood has been used for transplantation in regenerative medicine of hematological disorders. MicroRNAs are important regulators of gene expression that control both physiological and pathological processes such as development and cancer. Some studies have shown that miR-33, p53 and c-myc have critical roles in control of self-renewal cells. Objective To understand the effect of adipose-derived mesenchymal stem cells (ADSCs), as a feeder layer, on expansion of HSCs, the expression of p53 and miR-33a were evaluated. Methods Isolated human ADSCs in passage 3 were cultured as a feeder layer. Ex vivo cultures of cord blood CD34+ cells were performed in three culture conditions for 7 days: cytokines with ADSCs feeder layer, cytokines without ADSCs feeder layer, and co-culture with ADSCs without cytokine. Expression of genes p53, c-myc and miR-33 were analyzed by real-time PCR. Results The expression of p53 was significantly down-regulated in HSCs directly cultured on ADSCs feeder layer compared to that cultured without feeder layer. The expression of miR-33a was significantly up-regulated in HSCs directly cultured on feeder layer compare to that cultured without feeder layer. Conclusion Defining the role of ADSCs in controlling the HSC self-renewal through miR-33 , p53 and c-myc may lead to the treatment and prevention of hematopoietic disorders.
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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