ArticleJournal of cellular biochemistry2016
Fibroblast Growth Factor 2 Regulates High Mobility Group A2 Expression in Human Bone Marrow-Derived Mesenchymal Stem Cells.
Article in Journal of cellular biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Digit regeneration in mice is stimulated by sequential treatment with FGF2 and BMP2.Nature communications · 2026Article
- Investigating the Associations Between Hmga2 Overexpression, R-Loop Reduction, and Bone Loss in Aging Mice.Medicina (Kaunas, Lithuania) · 2025Article
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Article
- The role of miRNAs in the diagnosis of stable atherosclerosis of different arterial territories: A critical review.Frontiers in cardiovascular medicine · 2022Review
- Review
- MicroRNA-497-5p stimulates osteoblast differentiation through HMGA2-mediated JNK signaling pathway.Journal of orthopaedic surgery and research · 2020Article
- HMGA2-mediated tumorigenesis through angiogenesis in leiomyoma.Fertility and sterility · 2020Article
- High Mannose N-Glycans Promote Migration of Bone-Marrow-Derived Mesenchymal Stromal Cells.International journal of molecular sciences · 2020Article
- Hypoxia induces an endometrial cancer stem-like cell phenotype via HIF-dependent demethylation of SOX2 mRNA.Oncogenesis · 2020Article
- The Mammalian High Mobility Group Protein AT-Hook 2 (HMGA2): Biochemical and Biophysical Properties, and Its Association with Adipogenesis.International journal of molecular sciences · 2020Review
- Molecular and Lifestyle Factors Modulating Obesity Disease.Biomedicines · 2020Review
- HMGA Genes and Proteins in Development and Evolution.International journal of molecular sciences · 2020Review
- MicroRNA-98-5p prevents bone regeneration by targeting high mobility group AT-Hook 2.Experimental and therapeutic medicine · 2019Article
- Determinants of stem cell lineage differentiation toward chondrogenesis versus adipogenesis.Cellular and molecular life sciences : CMLS · 2019Review
- Knockdown of high mobility group box 3 impairs cell viability and colony formation but increases apoptosis in A549 human non-small cell lung cancer cells.Oncology letters · 2019Article
- Mechanisms supporting potential use of bone marrow-derived mesenchymal stem cells in psychocardiology.American journal of translational research · 2019Review
- Bone remodeling induced by mechanical forces is regulated by miRNAs.Bioscience reports · 2018Review
- FGF2 Induces Migration of Human Bone Marrow Stromal Cells by Increasing Core Fucosylations on N-Glycans of Integrins.Stem cell reports · 2018Article
- MicroRNA Let-7f-5p Promotes Bone Marrow Mesenchymal Stem Cells Survival by Targeting Caspase-3 in Alzheimer Disease Model.Frontiers in neuroscience · 2018Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Mesenchymal stem cells (MSCs) are an excellent source for numerous cellular therapies due to their simple isolation, low immunogenicity, multipotent differentiation potential and regenerative secretion profile. However, over-expanded MSCs show decreased therapeutic efficacy. This shortcoming may be circumvented by identifying methods that promote self-renewal of MSCs in culture. HMGA2 is a DNA-binding protein that regulates self-renewal in multiple types of stem cells through chromatin remodeling, but its impact on human bone marrow-derived MSCs is not known. Using an isolation method to obtain pure MSCs within 9 days in culture, we show that expression of HMGA2 quickly decreases during early expansion of MSCs, while let-7 microRNAs (which repress HMGA2) are simultaneously increased. Remarkably, we demonstrate that FGF-2, a growth factor commonly used to promote self-renewal in MSCs, rapidly induces HMGA2 expression in a time- and concentration-dependent manner. The signaling pathway involves FGF-2 receptor 1 (FGFR1) and ERK1/2, but acts independent from let-7. By silencing HMGA2 using shRNAs, we demonstrate that HMGA2 is necessary for MSC proliferation. However, we also show that over-expression of HMGA2 does not increase cell proliferation, but rather abrogates the mitogenic effect of FGF-2, possibly through inhibition of FGFR1. In addition, using different methods to assess in vitro differentiation, we show that modulation of HMGA2 inhibits adipogenesis, but does not affect osteogenesis of MSCs. Altogether, our results show that HMGA2 expression is associated with highly proliferating MSCs, is tightly regulated by FGF-2, and is involved in both proliferation and adipogenesis of MSCs. J. Cell. Biochem. 117: 2128-2137, 2016. © 2016 Wiley Periodicals, Inc.
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