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The bulk cell density as decisive parameter and simple method for mesendodermal patterning of human pluripotent stem cells

ABSTRACT: We showed that the relation of pluripotent stem cell count to culture volume influences cardiomyogenic differentiation by affecting the concentration of secreted proteins that function as paracrine factors

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Stem Cell

SUBMITTER: Falk Büttner

LAB HEAD: Rita Gerardy-Schahn

PROVIDER: PXD004874 | Pride | 2018-10-17

REPOSITORIES: Pride

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			Action	DRS
	HK01_1ml_06h_A.raw	Raw
	HK01_1ml_06h_C.raw	Raw
	HK01_1ml_06h_D.raw	Raw
	HK02_1ml_24h_A.raw	Raw
	HK02_1ml_24h_C.raw	Raw

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1 - 5 of 13

Publications

Bulk cell density and Wnt/TGFbeta signalling regulate mesendodermal patterning of human pluripotent stem cells.

Kempf Henning H Olmer Ruth R Haase Alexandra A Franke Annika A Bolesani Emiliano E Schwanke Kristin K Robles-Diaz Diana D Coffee Michelle M Göhring Gudrun G Dräger Gerald G Pötz Oliver O Joos Thomas T Martinez-Hackert Erik E Haverich Axel A Buettner Falk F R FFR Martin Ulrich U Zweigerdt Robert R

Nature communications 20161209

In vitro differentiation of human pluripotent stem cells (hPSCs) recapitulates early aspects of human embryogenesis, but the underlying processes are poorly understood and controlled. Here we show that modulating the bulk cell density (BCD: cell number per culture volume) deterministically alters anteroposterior patterning of primitive streak (PS)-like priming. The BCD in conjunction with the chemical WNT pathway activator CHIR99021 results in distinct paracrine microenvironments codifying hPSCs ...[more]

PMID: 27934856

Similar Datasets

Modulation of the bulk cell density as decisive parameter and simple method for mesendodermal patterning of human pluripotent stem cells

Project description:1 million human pluripotent cells cultured as suspension aggregates (hES3-NKX2.5 cell line) were treated with 0, 7.5 or 15µM CHIR99021 in 1 or 3 ml RPMI/B27 (w/o insulin) for 24h to induce the differentiation of human pluripotent stem cells (hPSCs). CHIR99021 is a potent GSK3 inhibitor that results in prominent WNT pathway activation and thereby induces mesendodermal differentiation.

2016-12-30 | E-MTAB-5051 | biostudies-arrayexpress

LINE-1 DNA methylation levels in DPPA3 KO overexpressing DPPA3 mutants

Project description:DPPA3 mutants were overexpressed using a doxycycline system to identify regions in DPPA3 necessary for DNA methylation maintenance suppression

2020-10-22 | E-MTAB-9653 | biostudies-arrayexpress

Amplicon bisulfite sequencing of LINE-1 elements in TET catalytic mutants and DPPA3 KO ESCs rescued by doxycylin induced overexpression

Project description:Tet1, Tet2 and Tet1/Tet2 catalytic mutants as well as DPPA3 KO ESCs harboring a doxycyclin inducible Dppa3 transgene were induced for several days to monitor LINE-1 methylation levels.

2020-10-23 | E-MTAB-9654 | biostudies-arrayexpress

Flutamide treated rat hepatocytes in microfluidic biochips

Project description:We investigated the effects of the flutamide (FLU) -induced liver injury in primary rat hepatocytes using our liver microfluidic biochips. Flutamide is used a non-steroidal anti-androgenic drug. Two flutamide concentrations, 10M-BM-5M and 100M-BM-5M, were used to expose the hepatocytes for 24h under perfusion. Primary rat hepatocytes were cultivated in microfluidic biochips and treated with 10 and 100M-BM-5M of flutamide for 24h

2013-12-01 | E-GEOD-44317 | biostudies-arrayexpress

Bulk mRNA Seq CAR.CCR7 vs. CAR

Project description:The study aimed to elucidate the transcriptional changes introduced by genetic engineering of CAR T cells to stably express the homeostatic chemokine receptor CCR7. In vitro killing assays hinted to a higher cytolytic capacity that could be tied to an altered cytoskeletal rearrangement. Human CAR and CAR.CCR7 T cells were generated by retroviral transduction and enriched by FACS at the end of the expansion phase (day 10), either without or with a previous over-night co-culture with target Jeko1 tumor cells that express the CAR target antigen CXCR5. Enriched cells were immediately processed for bulk mRNA Seq

2023-06-30 | E-MTAB-12778 | biostudies-arrayexpress

BIGenomics_Agilent_15k_templates

Project description:Hybridization of ligation probes to a zipcode (tag) microarray. The purpose of the experiment was to establish functionality and target specificity of the ligation probes by using pools of synthetic templates with all of the probes. The templates are 80-mer synthetic dsDNA molecules, each specific for a single probe. Each probe is a ssDNA molecule containing target recognition sequences, PCR primer binding sequences and a unique tag sequence. If a matching target sequence is present in the mixture, the probes is ligated into a circular molecule, which can be PCR amplified and hybrized on a microarray harbouring complementary tag sequences.

2012-02-24 | E-MEXP-3538 | biostudies-arrayexpress

Pre-patterning of differentiation-driven nuclear lamin A/C-associated chromatin domains by GlcNAcylated histone H2B

Project description:Dynamic interactions of nuclear lamins with chromatin through so-called lamin-associated domains (LADs) contribute to spatial arrangements of the genome. Here, we provide evidence for pre-patterning of differentiation-driven formation of lamin A/C LADs by domains of histone H2B modified by the nutrient sensor O-linked N-acetylglucosamine (H2BGlcNAc), which we term GADs. We demonstrate a two-step process of lamin A/C LAD formation during in vitro adipogenesis, involving (i) a spreading of lamin A/C-chromatin interactions during the transition from progenitor cell proliferation to cell cycle arrest, and (ii) a genome-scale redistribution these interactions through a process of LAD ‘exchange’ within hours of adipogenic induction. Chromatin state modeling reveals that lamin A/C LADs can be found both in active and repressive chromatin contexts which can be influenced by cell differentiation status. De novo formation of adipogenic lamin A/C LADs occurs non-randomly on GADs, consisting of megabase-size intergenic and repressive chromatin domains. Accordingly, while pre-differentiation lamin A/C LADs are gene-rich, post-differentiation LADs harbor repressive features reminiscent of lamin B1 LADs. Moreover, release of lamin A/C from genes directly involved in glycolysis concurs with their transcriptional upregulation after adipogenic induction, and with concordant downstream elevations in H2BGlcNAc levels and O-GlcNAc cycling. Our results unveil an epigenetic pre-patterning of adipogenic LADs by GADs, suggesting a coupling of developmentally regulated lamin A/C-genome interactions to a metabolically sensitive chromatin modification. Examination of LMNA and H2BGlcNAc binding in ASCs across differentiation

2015-09-04 | E-GEOD-63346 | biostudies-arrayexpress

Bulk cell density and Wnt/TGFbeta signalling regulate mesendodermal patterning of human pluripotent stem cells.

Project description:In vitro differentiation of human pluripotent stem cells (hPSCs) recapitulates early aspects of human embryogenesis, but the underlying processes are poorly understood and controlled. Here we show that modulating the bulk cell density (BCD: cell number per culture volume) deterministically alters anteroposterior patterning of primitive streak (PS)-like priming. The BCD in conjunction with the chemical WNT pathway activator CHIR99021 results in distinct paracrine microenvironments codifying hPSCs towards definitive endoderm, precardiac or presomitic mesoderm within the first 24?h of differentiation, respectively. Global gene expression and secretome analysis reveals that TGFß superfamily members, antagonist of Nodal signalling LEFTY1 and CER1, are paracrine determinants restricting PS progression. These data result in a tangible model disclosing how hPSC-released factors deflect CHIR99021-induced lineage commitment over time. By demonstrating a decisive, functional role of the BCD, we show its utility as a method to control lineage-specific differentiation. Furthermore, these findings have profound consequences for inter-experimental comparability, reproducibility, bioprocess optimization and scale-up.

| S-EPMC5155150 | biostudies-literature

Multiscale Anisotropic Tissue Biofabrication via Bulk Acoustic Patterning of Cells and Functional Additives in Hybrid Bioinks.

Project description:Recapitulation of the microstructural organization of cellular and extracellular components found in natural tissues is an important but challenging feat for tissue engineering, which demands innovation across both process and material fronts. In this work, a highly versatile ultrasound-assisted biofabrication (UAB) approach is demonstrated that utilizes radiation forces generated by superimposing ultrasonic bulk acoustic waves to rapidly organize arrays of cells and other biomaterial additives within single and multilayered hydrogel constructs. UAB is used in conjunction with a novel hybrid bioink system, comprising of cartilage-forming cells (human adipose-derived stem cells or chondrocytes) and additives to promote cell adhesion (collagen microaggregates or polycaprolactone microfibers) encapsulated within gelatin methacryloyl (GelMA) hydrogels, to fabricate cartilaginous tissue constructs featuring bulk anisotropy. The hybrid matrices fabricated under the appropriate synergistic thermo-reversible and photocrosslinking conditions demonstrate enhanced mechanical stiffness, stretchability, strength, construct shape fidelity and aligned encapsulated cell morphology and collagen II secretion in long-term culture. Hybridization of UAB is also shown with extrusion and stereolithography printing to fabricate constructs featuring 3D perfusable channels for vasculature combined with a crisscross or circumferential organization of cells and adhesive bioadditives, which is relevant for further translation of UAB toward complex physiological-scale biomimetic tissue fabrication.

| S-EPMC9117510 | biostudies-literature

Bulk RNA-seq of the human malaria parasite Plasmodium falciparum 3D7 cultured under different iron conditions

Project description:Background: Host iron deficiency is protective against severe malaria as the human malaria parasite Plasmodium falciparum depends on free iron from its host to proliferate. Due to the absence of transferrin, ferritin, ferroportin, and a functional heme oxygenase, the parasite’s essential pathways of iron acquisition, storage, export, and detoxification differ from those in humans and may thus be excellent targets for therapeutic development. However, the proteins involved in these processes in P. falciparum remain largely unknown. Experimental design: To identify iron-regulated mechanisms and putative iron transporters in the human malaria parasite Plasmodium falciparum 3D7, we carried out whole-transcriptome profiling using bulk RNA-sequencing. The parasites were cultured either using erythrocytes from a donors with high, medium (healthy) or low iron status (experiment 1); or with red blood cells from another healthy donor in the presence or absence of 0.7 µM hepcidin, a specific ferroportin inhibitor and iron-regulatory hormone (experiment 2). This concentration of hepcidin was reported to reduce binding of ferrous iron to ferroportin by 50% in vitro (39). Samples from three biological replicates each were harvested at the ring and trophozoite stage (6 – 9 and 26 – 29 hours post invasion, hpi) during the second intra-erythrocytic developmental cycle under the conditions specified.

2024-04-08 | E-MTAB-13411 | biostudies-arrayexpress

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