ArticleStem cells (Dayton, Ohio)2009
A complex role for FGF-2 in self-renewal, survival, and adhesion of human embryonic stem cells.
Article in Stem cells (Dayton, Ohio), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 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
100 citing papers in PubMed, 211 citations in OpenAlex.
- Structure-function relationship in FGF signaling: rational design of highly stable FGF2 variants and their effect on cell growth, metabolism, and survival.Journal of biological engineering · 2026Article
- Transcriptional Bursting in Pluripotent Stem Cells.Biology · 2026Review
- Establishment and optimization of the two-step induction system for generating primordial germ cell-like cells from chicken embryonic stem cells.FEBS open bio · 2026Article
- A human epiblast model reveals dynamic TGFβ-mediated control of epithelial identity during mammalian epiblast development.Nature cell biology · 2026Article
- Yeast-derived low-purity FGF2 supports bovine ESC and MSC aggregates in suspension.Frontiers in nutrition · 2025Article
- Evaluating Strategies to Assess the Differentiation Potential of Human Pluripotent Stem Cells: A Review, Analysis and Call for Innovation.Stem cell reviews and reports · 2025Review
- FGF2 supports NANOG expression via pyruvate dehydrogenase-dependent histone acetylation under low oxygen conditions.Frontiers in cell and developmental biology · 2025Article
- Diversity of Microglia-Derived Molecules with Neurotrophic Properties That Support Neurons in the Central Nervous System and Other Tissues.Molecules (Basel, Switzerland) · 2024Review
- Embryonic stem cells overexpressing high molecular weight FGF2 isoform enhance recovery of pre-ganglionic spinal root lesion in combination with fibrin biopolymer mediated root repair.Stem cell research & therapy · 2024Article
- Endometrial cancer PDX-derived organoids (PDXOs) and PDXs with FGFR2c isoform expression are sensitive to FGFR inhibition.NPJ precision oncology · 2023Article
- Function of hepatocyte spheroids in bioactive microcapsules is enhanced by endogenous and exogenous hepatocyte growth factor.Bioactive materials · 2023Article
- Suspension culture improves iPSC expansion and pluripotency phenotype.Stem cell research & therapy · 2023Article
- Role of glycosphingolipid SSEA-3 and FGF2 in the stemness and lineage commitment of multilineage differentiating stress enduring (MUSE) cells.Cell proliferation · 2023Article
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- Interactions Networks for Primary Heart Sarcomas.Cancers · 2021Article
- Evaluation of Indonesian mangrove Xylocarpus granatum leaves ethyl acetate extract as potential anticancer drug.Scientific reports · 2021Article
- BCL2 enhances survival of porcine pluripotent stem cells through promoting FGFR2.Cell proliferation · 2021Article
- Unraveling the Spatiotemporal Human Pluripotency in Embryonic Development.Frontiers in cell and developmental biology · 2021Review
- Inhibition of FGF and TGF-β Pathways in hESCs Identify STOX2 as a Novel SMAD2/4 Cofactor.Biology · 2020Article
40 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription program that is responsible for the pluripotency of human ESCs (hESCs) is believed to be comaintained by exogenous fibroblast growth factor-2 (FGF-2), which activates FGF receptors (FGFRs) and stimulates the mitogen-activated protein kinase (MAPK) pathway. However, the same pathway is stimulated by insulin receptors, insulin-like growth factor 1 receptors, and epidermal growth factor receptors. This mechanism is further complicated by intracrine FGF signals. Thus, the molecular mechanisms by which FGF-2 promotes the undifferentiated growth of hESCs are unclear. Here we show that, in undifferentiated hESCs, exogenous FGF-2 stimulated the expression of stem cell genes while suppressing cell death and apoptosis genes. Inhibition of autocrine FGF signaling caused upregulation of differentiation-related genes and downregulation of stem cell genes. Thus, exogenous FGF-2 reinforced the pluripotency maintenance program of intracrine FGF-2 signaling. Consistent with this hypothesis, expression of endogenous FGF-2 decreased during hESC differentiation and FGF-2 knockdown-induced hESC differentiation. In addition, FGF-2 signaling via FGFR2 activated MAPK kinase/extracellular signal-regulated kinase and AKT kinases, protected hESC from stress-induced cell death, and increased hESC adhesion and cloning efficiency. This stimulation of self-renewal, cell survival, and adhesion by exogenous and endogenous FGF-2 may synergize to maintain the undifferentiated growth of hESCs.
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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.