A GLIS3-CD133-WNT-signaling axis regulates the self-renewal of adult murine pancreatic progenitor-like cells in colonies and organoids
Tremblay JR., Lopez K., Ku HT.
Animal Study, published in J Biol Chem (2019) — 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
- Animal Study
- Journal
- J Biol Chem (2019)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 31533988
- PMCID
- PMC6851293
- DOI
- 10.1074/jbc.ra118.002818
- Citations
- 6
Abstract (original English)
The existence and regenerative potential of resident stem and progenitor cells in the adult pancreas are controversial topics. A question that has been only minimally addressed is the capacity of a progenitor cell to self-renew, a key attribute that defines stem cells. Previously, our laboratory has identified putative stem and progenitor cells from the adult murine pancreas. Using an ex vivo colony/organoid culture system, we demonstrated that these stem/progenitor-like cells have self-renewal and multilineage differentiation potential. We have named these cells pancreatic colony-forming units (PCFUs) because they can give rise to three-dimensional colonies. However, the molecular mechanisms by which PCFUs self-renew have remained largely unknown. Here, we tested the hypothesis that PCFU self-renewal requires GLIS family zinc finger 3 (GLIS3), a zinc-finger transcription factor important in pancreas development. Pancreata from 2- to 4-month-old mice were dissociated, sorted for CD133 high CD71 low ductal cells, known to be enriched for PCFUs, and virally transduced with shRNAs to knock down GLIS3 and other proteins. We then plated these cells into our colony assays and analyzed the resulting colonies for protein and gene expression. Our results revealed a previously unknown GLIS3-to-CD133-to-WNT signaling axis in which GLIS3 and CD133 act as factors necessary for maintaining W
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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