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Bromodomain inhibitor PFI-3 induces cellular plasticity and enhances iPSC reprogramming efficiency by targeting extracellular matrix

ABSTRACT: Bromodomain inhibitor PFI-3 induces cellular plasticity and enhances iPSC reprogramming efficiency by targeting extracellular matrix

PROVIDER: PRJNA1008157 | ENA |

REPOSITORIES: ENA

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Bromodomain inhibitor PFI-3 induces cellular plasticity and enhances iPSC reprogramming efficiency by targeting extracellular matrix

Project description:The study assessed fibroblast reprogramming into induced pluripotent stem cells (iPS), and the effects on efficiency of iPS reprogramming by treatment with 10-uM PFI-3. Samples were collected across multiple time points during reprogramming: day 0, 3, 5, 7, 14, and day 21, each in the presence or absence of PFI-3 treatment, with n=3 biological replicates.

2024-08-08 | GSE241435 | GEO

Trophoblast stem cells (TSC) global transcriptome in stemness and differentiation conditions after treatment with PF1-3

Project description:Here we report a potent, acetyl-lysine competitive and cell active inhibitor, PFI-3, that tightly binds to the bromodomain present in BRG1/BRM and the fifth bromodomain in Polybromo (BAF180). The high specificity of PFI-3 was achieved based on a novel binding mode of a salicylic acid head group that led to the replacement of water molecules typically maintained in bromodomain inhibitor complexes. Embryonic stem cells exposure to PFI-3 led to deprivation of stemness and deregulated lineage specification. Furthermore, differentiation of trophoblast stem cells in the presence of PFI-3 was dramatically enhanced. TSC were treated with PF1-3 or control compound in stemness or differentiation conditions, 2 replicates were used for treatment in stemness and differentiation conditions together with 2 control replicates in stemness and one during differentiation; DFKZ genomics and proteomics

2015-12-16 | E-GEOD-65358 | biostudies-arrayexpress

Trophoblast stem cells (TSC) global transcriptome in stemness and differentiation conditions after treatment with PF1-3

2015-12-16 | GSE65358 | GEO

Gene expression changes in MV4-11 cells upon SMARCA4 knock-down and PFI-3 treatment

Project description:Pharmacological inhibition of the SMARCA4 bromodomain inhibited human leukemic cell proliferation, phenocopying SMARCA4 knockdown in these cells. We performed microarray analysis of global gene expression changes in MV4-11 cells after 6 days of PFI-3 treatment and after SMARCA4 knock-down. With this analysis we identified several genes whose expression was similarly up- or down-regulated upon inhibitor treatment and SMARCA4 depletion. Human acute monocytic leukemia cells (MV4-11, ACC 102) were lentivirally transduced with shRNA taregting SMARCA4 (KD) or with a negative control shRNA (Scr). In a parallel experiment MV4-11 cells were treated for 6 days with 10 uM PFI-3, which is SMARCA4, SMARCA2 and PBRM1 bromodomain inhibitor, or DMSO as a negative control. All sample types were prepared in triplicates.

2015-07-12 | E-GEOD-67920 | biostudies-arrayexpress

The Bromodomains of the mammalian SWI/SNF (mSWI/SNF) ATPases Brahma (BRM) and Brahma Related Gene 1 (BRG1) promote chromatin interaction and are critical for skeletal muscle differentiation

Project description:We performed RNA-seq analysis for C2C12 myoblasts as a function of differentiation. Cells were treated with either DMSO or family VIII bromodomain-specific inhibitor PFI-3 at a concentration of 50uM. We find that PFI-3 treatment affects proper differentiation of myoblasts as compared to DMSO-treated C2C12 cells. We conclude that function of mammalian SWI/SNF bromodomains is important for regulation of myoblast differentiation.

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BET bromodomain inhibition

Project description:BET bromodomain inhibition

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Extracellular Matrix Formation Enhances the Ability of Streptococcus pneumoniae to Cause Invasive Disease

Project description:Background. During infection, pneumococci exist mainly in sessile biofilms rather than in planktonic form, except during sepsis. However, relatively little is known about how biofilms contribute to pneumococcal pathogenesis. Methods. We performed a biofilm assay and mouse infection experiments on opaque and transparent variants of a clinical serotype 19F strain. Results. After 4 days incubation, scanning electron microscopy revealed that opaque biofilm bacteria produced an extracellular matrix, whereas the transparent variant did not. The opaque biofilm-derived bacteria translocated from the nasopharynx to the lungs and brain of mice, and showed 100-fold greater in vitro adherence to A549 cells. Microarray analysis of planktonic and sessile bacteria from transparent and opaque variants showed differential gene expression in two operons: the lic operon, involved in choline uptake, and in the two-component system, ciaRH. Mutants of these genes did not form an extracellular matrix, could not translocate from the nasopharynx to the lungs or the brain, and adhered poorly to A549 cells. Conclusions. We conclude that only the opaque phenotype is able to form extracellular matrix, and that the lic operon and ciaRH contribute to this process. We propose that during infection, extracellular matrix formation enhances the ability of pneumococci to cause invasive disease. Data is also available from http://bugs.sgul.ac.uk/E-BUGS-117

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Gestational diabetes mellitus alters placental structure, efficiency, and plasticity

Project description:The hemochorial placenta provides a critical barrier at the maternal-fetal interface to modulate maternal immune tolerance and enable gas and nutrient exchange between mother and conceptus. Pregnancy outcomes are adversely affected by gestational diabetes mellitus (GDM); however, the effects of GDM on placental formation, and subsequently fetal development, are not fully understood. In this report, streptozotocin was used to induce hyperglycemia in pregnant rats for the purpose of investigating the impact of GDM on placental formation and fetal development. GDM caused placentomegaly and placenta malformation, decreasing placental efficiency and fetal size. Elevated glucose disrupted rat trophoblast stem (TS) cell differentiation in vitro. Evidence of altered trophoblast differentiation was also observed in vivo, as hyperglycemia affected the junctional zone transcriptome and interfered with intrauterine trophoblast invasion and uterine spiral artery remodeling. When exposed to hypoxia, rats with GDM showed decreased proliferation and ectoplacental cone development on gestation day (gd) 9.5 and complete pregnancy loss by gd 13.5. Furthermore, elevated glucose concentrations inhibited TS cell responses to hypoxia in vitro. Overall, these results indicate that alterations in placental development, efficiency, and plasticity could contribute to the suboptimal fetal outcomes in offspring from pregnancies complicated by GDM.

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Gestational diabetes mellitus alters placental structure, efficiency, and plasticity

Project description:Gestational diabetes mellitus alters placental structure, efficiency, and plasticity

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Microglial remodeling of the extracellular matrix promotes synapse plasticity

Project description:Microglial remodeling of the extracellular matrix promotes synapse plasticity

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