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BRCA1 haploinsufficient Mesenchyme Derived from human peripheral blood Induced Pluripotent Stem Cell

ABSTRACT: BRCA1 haploinsufficient Mesenchyme Derived from human peripheral blood Induced Pluripotent Stem Cell

PROVIDER: PRJNA413524 | ENA |

REPOSITORIES: ENA

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BRCA1 haploinsufficient Mesenchyme Derived from human peripheral blood Induced Pluripotent Stem Cell

Project description:BRCA1 molecule, known to be implicated in DNA repair and its alterations were associated to familial breast cancer prediposition. Genome of the patients with familial breast cancer predispostion harbor some germinal alterations in BRCA1 locus. Cells from peripheral blood of human with haplodeficiency BRCA1 locus and also from comparative sample (BRCA1 unaffected) were collected to produce induced pluripotent stem cell by classical protocol (Yamanaka OKSM) and Sendai Stem cell reprogammation which was validated by expression assessment of pluripotent stem cell markers and induction of teratoma after xenotransplantation mice model. Induced pluripotent stem cell (IPSC) were differentiated in mesenchymal lineage in order to see influence of BRCA1 effects during developmental steps of the stroma: effectively microenvironment of breast tumor is infiltrate of mesenchymal stromal cell. Total RNA of the mesenchyme derived IPS from control and BRCA1 haploinsufficient were respectively collected to screen whole expression analysis by transcriptome microarray.

2019-01-31 | GSE104693 | GEO

BRCA1 Mutations Attenuate Super-Enhancer Function and Chromatin Looping in Haploinsufficient Human Breast Epithelial Cells

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BRCA1 Mutations Attenuate Super-Enhancer Function and Chromatin Looping in Haploinsufficient Human Breast Epithelial Cells

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Single cell RNA sequencing of mouse indced pluripotent stem cell (iPSC)-derived and mouse primary embryonic lung mesenchyme

Project description:The lung mesenchyme plays important roles in lung development and is affected in many respiratory diseases, yet relatively little is known about the biology of lung mesenchymal progenitors. We sought to establish an induced pluripotent stem cell (iPSC)-based model to study lung mesenchyme development and epithelial-mesenchymal interactions. We generated a mouse iPSC line carrying a lung mesenchyme-specific reporter/tracer to establish a protocol for differentiation into lung mesenchymal progenitors. We derived lung mesenchyme from iPSCs both by directed differentiation via a lateral plate mesodermal progenitor state (induced lung mesenchyme, iLM), and by co-development during lung epithelial differentiation (co-developed lung mesenchyme, cLM). We found that directed differentiation via a lateral plate mesoderm progenitor was not only more efficient, but also yielded engineered lung mesenchymal cells that were more similar to primary lung mesenchyme from day 12.5 mouse embryos, as determined by single cell RNAseq. Our iPSC-derived population will provide an inexhaustible source of cells for studying lung development, modeling diseases, and developing therapeutics.

2023-05-12 | GSE203245 | GEO

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Human iPSC-Derived Fallopian Tube Organoids with BRCA1 Mutation Recapitulate Early Stage Carcinogenesis

Project description:We generate induced pluripotent stem cells (iPSCs) from healthy individuals and young ovarian cancer patients with germline pathogenic BRCA1 mutations. We then differentiate them into a human iPSC-derived fallopian tube organoid model. We recapitulated BRCA1 mutant ovarian carcinogenesis in vitro and showed tumors in vivo. Using the IPSC derived fallopian tube organoid model, we identify a unique transcriptional profile associated with BRCA1 mutation similar to the ovarian cancer profile.

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small pluripotent stem cell proteome

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Effect of Network-Correcting Molecules on NOTCH1 (N1)-Haploinsufficient Human Induced Pluripotent Stem Cell (iPSC)-Derived Endothelial Cells (ECs)

Project description:Discovery of small molecules that correct gene networks dysregulated in human disease may allow identification of therapies that treat disease at its fundamental basis by leveraging mechanism-based data. Here, we report the first broad gene network-based drug screen, which led to discovery of a drug candidate that effectively treats aortic valve disease in an animal model. We previously reported haploinsufficiency of NOTCH1 (N1) as a genetic cause of human aortic valve thickening and calcification, the third most common form of heart disease, and described the resulting gene network dysregulation in human induced pluripotent stem cell (iPSC)-derived endothelial cells (ECs). We exposed isogenic N1+/+ or N1+/– iPSC-derived ECs to each of 1595 small molecules or control and developed a machine learning approach that accurately distinguished WT or N1-haploinsufficient cells based on expression of 119 genes assayed by targeted RNA-sequencing. 9 small molecules corrected the gene network of N1+/– ECs sufficiently to be classified as WT. Among hits tested in vivo, the estrogen receptor-related alpha inverse agonist XCT790 significantly reduced aortic valve thickening, calcification, and stenosis in N1-haploinsufficient mice with shortened telomeres, which model the range of age-dependent cardiac disease observed in humans. This strategy, made feasible by human iPSC technology, next generation sequencing approaches, and machine learning, may represent a more effective path for drug discovery compared to conventional screening approaches.

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