ArticleCurrent stem cell research & therapy2016
BMI1 Regulation of Self-Renewal and Multipotency in Human Mesenchymal Stem Cells.
Article in Current stem cell research & therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Understanding the molecular basis of mesenchymal stem cell stemness: implications for clinical applications.Cell death & disease · 2025Review
- A Systems Biology Approach for Prioritizing ASD Genes in Large or Noisy Datasets.International journal of molecular sciences · 2025Article
- LRRC15 expression indicates high level of stemness regulated by TWIST1 in mesenchymal stem cells.iScience · 2023Article
- Immortalized cell lines derived from dental/odontogenic tissue.Cell and tissue research · 2023Review
- Epigenetics in Prader-Willi Syndrome.Frontiers in genetics · 2021Review
- Isolation and Characterization of Human Suture Mesenchymal Stem CellsInternational journal of stem cells · 2020Article
- Ribosomes: An Exciting Avenue in Stem Cell Research.Stem cells international · 2020Review
- Epigenetic-Based Mechanisms of Osteoblast Suppression in Multiple Myeloma Bone Disease.JBMR plus · 2019Review
- Potential Research Tool of Stem Cells from Human Exfoliated Deciduous Teeth: Lentiviral Bmi-1 Immortalization with EGFP Marker.Stem cells international · 2019Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
We have previously described generation of mesenchymal stem cells (MSCs) from human embryonic and induced pluripotent stem cells. One of the central questions in stem cell biology is to understand how stem cells regulate the decision to self-renew vs. differentiate, at the molecular level. In the current studies we used loss-of-function and gain-of-function analyses in primary human MSCs to demonstrate that BMI1 is a critical regulator for self-renewal and multipotency in this interesting cell type. Knockdown of BMI1 in MSCs reduced self-renewal by upregulation of p16(INK4A) and increased apoptosis. Knockdown of p16(INK4A) partially rescued the self-renewal defect in MSCs with loss of BMI1. Overexpressed BMI1 reduced apoptosis and increased cell proliferation by repressing p16(INK4A). Loss of BMI1 resulted in deregulation of PPARγ, an adipogenic factor, and imprinted gene network (IGN), which blocks osteogenesis. Knockdown of PPARγ or IGN in BMI1 defect models restored osteogenesis. Overexpression of BMI1 repressed transcripts of RUNX2 and PPARγ, in osteogenesis and adipogenesis, respectively, which lead to decreased lineage specification potential in MSCs. These data show that BMI1 regulates cell proliferation, apoptosis, and differentiation of human MSCs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.