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Expression file from FGF-10 experiment

ABSTRACT: Differentiating embryonic stem cells into cardiomyocytes is inefficient, and we discover that FGF-10 can induce embryonic stem cells differentiation into cardiomyocytes. We use microarray to gain insight into the global gene expression and elucidate the machenism that FGF-10 induces embryonic stem cells differentiation into cardiomyocytes.

ORGANISM(S): Mus musculus

PROVIDER: GSE22637 | GEO | 2010/07/01

SECONDARY ACCESSION(S): PRJNA128105

REPOSITORIES: GEO

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Expression file from FGF-10 experiment

Project description:Differentiating embryonic stem cells into cardiomyocytes is inefficient, and we discover that FGF-10 can induce embryonic stem cells differentiation into cardiomyocytes. We use microarray to gain insight into the global gene expression and elucidate the machenism that FGF-10 induces embryonic stem cells differentiation into cardiomyocytes. Two-day embryoid bodies were treated with or without 100 ng/ml FGF10 and RNA was obtained 24 hours later and hybridized by Affymetrix microarray

2010-07-30 | E-GEOD-22637 | biostudies-arrayexpress

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FGF inhibition directs BMP4-mediated differentiation of Human Embryonic Stem Cells to syncytiotrophoblast

Project description:Bone morphogenetic protein (BMP) signaling is known to support differentiation of human embryonic stem cells (hESCs) into mesoderm and extraembryonic lineages, whereas other signaling pathways can largely influence this lineage specification. Here, we set out to reinvestigate the influence of ACTIVIN/NODAL and fibroblast growth factor (FGF) pathways on the lineage choices made by hESCs during BMP4-driven differentiation. We show that BMP activation, coupled with inhibition of both ACTIVIN/NODAL and FGF signaling, induces differentiation of hESCs, specifically to M-NM-2hCG hormone-secreting multinucleated syncytiotrophoblast and does not support induction of embryonic and extraembryonic lineages, extravillous trophoblast, and primitive endoderm. It has been previously reported that FGF2 can switch BMP4-induced hESC differentiation outcome to mesendoderm. Here, we show that FGF inhibition alone, or in combination with either ACTIVIN/NODAL inhibition or BMP activation, supports hESC differentiation to hCG-secreting syncytiotrophoblast. We show that the inhibition of the FGF pathway acts as a key in directing BMP4-mediated hESC differentiation to syncytiotrophoblast. Human embryonic Stem Cells (hESCs) were treated under defined conditions (N2B27) with BMP4 (B), SB431542 (SB) (ACTIVIN/NODAL inhibitor), SU5402 (SU) (FGFR1 inhibitor), FGF2 (F) either alone or in various combinations as mentioned, followed by isolation of total RNA.

2012-10-17 | E-GEOD-30125 | biostudies-arrayexpress

The Fgf/Erf/NCoR1/2 repressive axis controls trophoblast cell fate

Project description:Here, we demonstrate that upon inhibition of the Fgf/Erk pathway in mouse trophoblast stem cells (TSCs), the Ets2 repressor factor (Erf) interacts with components of the Nuclear Receptor Corepressor Complex 1 and 2 (NCoR1 and NCoR2). Upon attenuation of Fgf signalling, unphosphorylated, nuclear Erf recruits the NCoR1/2 complex to key trophoblast genes, brings about their transcriptional silencing and facilitates differentiation and placental development.

2023-04-26 | PXD037892 | Pride

FGF inhibition directs BMP4-mediated differentiation of Human Embryonic Stem Cells to syncytiotrophoblast

Project description:Bone morphogenetic protein (BMP) signaling is known to support differentiation of human embryonic stem cells (hESCs) into mesoderm and extraembryonic lineages, whereas other signaling pathways can largely influence this lineage specification. Here, we set out to reinvestigate the influence of ACTIVIN/NODAL and fibroblast growth factor (FGF) pathways on the lineage choices made by hESCs during BMP4-driven differentiation. We show that BMP activation, coupled with inhibition of both ACTIVIN/NODAL and FGF signaling, induces differentiation of hESCs, specifically to βhCG hormone-secreting multinucleated syncytiotrophoblast and does not support induction of embryonic and extraembryonic lineages, extravillous trophoblast, and primitive endoderm. It has been previously reported that FGF2 can switch BMP4-induced hESC differentiation outcome to mesendoderm. Here, we show that FGF inhibition alone, or in combination with either ACTIVIN/NODAL inhibition or BMP activation, supports hESC differentiation to hCG-secreting syncytiotrophoblast. We show that the inhibition of the FGF pathway acts as a key in directing BMP4-mediated hESC differentiation to syncytiotrophoblast.

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Cardiac differentiation time-courses of human ES cells using distinct initial induction conditions

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2024-04-01 | GSE230854 | GEO

Transcription profiling of neural stem cells treated with FGF-2, PDGF-AA or in the absence of growth factor (differentiation)

Project description:We compared the gene expression profiles of neural stem cells treated with FGF-2, PDGF-AA or in the absence of growth factor (differentiation). Cells grown in the presence of FGF-2 were used as a reference.

2006-03-15 | E-TABM-39 | biostudies-arrayexpress

Systematic in vitro and in vivo characterization of Leukemia-inhibiting factor (LIF)- and Fibroblast growth factor (FGF) -derived porcine induced pluripotent stem cells (piPSC) vs. embryonic stages

Project description:Systematic in vitro and in vivo characterization of Leukemia-inhibiting factor (LIF)- and Fibroblast growth factor (FGF) -derived porcine induced pluripotent stem cells (Cell reprogramming -basic developmental studies in the pig) vs Porcine embryonic stages (Plurisys) Global gene expression analyses and comparisons of LIF piPSC, FGF piPSC, Parental fibroblast line day 7-8 porcine embryo, day 10-11 porcine embryo, day 12-13 porcine embryo. Gene network analyses of piPSC lines, pNF and ICM from day 7-8 porcine embryos.

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Profiling of Y1 cells treated with FGF-2 reveals parallels with oncogene-induced senescence

Project description:Paradoxically, oncogenes that drive cell cycle progression may also trigger pathways leading to senescence, thereby inhibiting the growth of tumorigenic cells. Along these lines, Y1 cells, which carry an amplification of Ras, become senescent after treatment with the mitogen FGF-2. To understand how FGF-2 promotes senescence, we profiled the epigenome, transcriptome, proteome, and phospho-proteome of Y1 cells stimulated with FGF-2. FGF-2 caused delayed acetylation of histone H4 and higher levels of H3K27me3. Sequencing analysis revealed decreased expression of cell cycle-related genes with concomitant loss of H3K27ac. In contrast, FGF-2 promoted the expression of p21, various cytokines, and MAPK-related genes. Nuclear envelope proteins, particularly lamin B1, displayed increased phosphorylation in response to FGF-2. Proteome analysis suggested alterations in cellular metabolism, as evident by modulated expression of enzymes involved in purine biosynthesis, tRNA aminoacylation, and the TCA cycle. Altogether, the response of Y1 cells to FGF-2 is consistent with oncogene-induced senescence. We propose that Y1 cells enter senescence due to deficient cyclin expression and high levels of p21, which may stem from DNA damage or TGFb signaling.

2021-06-16 | PXD020688 | Pride

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