Autophagy Promoted Neural Differentiation of Human Placenta-derived Mesenchymal Stem Cells
Sotthibundhu A., Muangchan P., Phonchai R., Promjantuek W., Chaicharoenaudomrung N., Kunhorm P.
Prospective Study, published in In Vivo (2021) — summary generated from the PubMed abstract.
Early human evidence such as case series or small samples is exploring possible benefits.
- 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
- Prospective Study
- Journal
- In Vivo (2021)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 34410948
- PMCID
- PMC8408712
- DOI
- 10.21873/invivo.12543
- Citations
- 12
Abstract (original English)
Background/aim Human placenta-derived mesenchymal stem cells (hPMSCs) are multipotent and possess neurogenicity. Numerous studies have shown that Notch inhibition and DNA demethylation promote neural differentiation. Here, we investigated the modulation of autophagy during neural differentiation of hPMSCs, induced by DAPT and 5-Azacytidine. Materials and methods hPMSCs were treated with DAPT to induce neural differentiation, and the autophagy regulating molecules were used to assess the impact of autophagy on neural differentiation. Results The hPMSCs presented with typical mesenchymal stem cell phenotypes, in which the majority of cells expressed CD73, CD90 and CD105. hPMSCs were multipotent, capable of differentiating into mesodermal cells. After treatment with DAPT, hPMSCs upregulated the expression of neuronal genes including SOX2, Nestin, and βIII-tubulin, and the autophagy genes LC3I/II and Beclin. These genes were further increased when 5-Azacytidine was co-supplemented in the culture medium. The inhibition of autophagy by chloroquine impeded the neural differentiation of hPMSCs, marked by the downregulation of βIII-tubulin, while the activation of autophagy by valproic acid (VPA) instigated the emergence of βIII-tubulin-positive cells. Conclusion During the differentiation process, autophagy was modulated, implying that autophagy could play a significant role during the
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
Evidence level
Early human evidence such as case series or small samples is exploring possible benefits.
How we grade evidenceBrowse all related research
Filter the research library by this study's title keywords, author, or publication year.