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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Conversion of human fibroblasts into vascular cells (methylation)

ABSTRACT: We report a novel technique to reprogram human fibroblasts into endothelial and smooth muscle cells using partial iPSC reprogramming and chemically defined media. Using appropriate media conditions for differentiation of human pluripotent cells to CD34+ vascular progenitor cells, we show that temporary expression of pluripotent transcription factors and treatment with chemically-defined media, will induce differentiation of human fibroblasts to CD34+ vascular progenitor cells. Sorted CD34+ cells can then be directed to differentiate into vascular endothelial cells expressing a variety of smooth muscle markers. We have assessed the global DNA methylation (Illumina Infinium HD 450K DNA methylationBeadChips) and transcriptional (Illumina HT12v4 Gene Expression Bead Array) profiles of transdifferentiated endothelial cells and smooth muscle, human embryonic stem cell (hESC) and human induced pluripotent stem cell (hiPSC) differentiated CD34+ angioblasts, hESCs, hiPSC, primary smooth muscle and primary human umbilical vein endothelial cells using microarrays.

ORGANISM(S): Homo sapiens

SUBMITTER: Rathi Thiagarajan

PROVIDER: E-GEOD-40909 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Conversion of human fibroblasts into vascular cells (gene expression)

Project description:We report a novel technique to reprogram human fibroblasts into endothelial and smooth muscle cells using partial iPSC reprogramming and chemically defined media. Using appropriate media conditions for differentiation of human pluripotent cells to CD34+ vascular progenitor cells, we show that temporary expression of pluripotent transcription factors and treatment with chemically-defined media, will induce differentiation of human fibroblasts to CD34+ vascular progenitor cells. Sorted CD34+ cells can then be directed to differentiate into vascular endothelial cells expressing a variety of smooth muscle markers. We have assessed the global DNA methylation (Illumina Infinium HD 450K DNA methylationBeadChips) and transcriptional (Illumina HT12v3 and HT12v4 Gene Expression Bead Array) profiles of transdifferentiated endothelial cells and smooth muscle, human embryonic stem cell (hESC) and human induced pluripotent stem cell (hiPSC) differentiated CD34+ angioblasts, hESCs, hiPSC, primary smooth muscle and primary human umbilical vein endothelial cells using microarrays.

2012-09-18 | E-GEOD-40793 | biostudies-arrayexpress

Conversion of human fibroblasts into vascular cells (methylation)

2012-09-18 | GSE40909 | GEO

Conversion of human fibroblasts into vascular cells (gene expression)

2012-09-18 | GSE40793 | GEO

Differential gene expressions of human pluripotent stem cells derived cells in different culture system

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2018-01-26 | GSE109683 | GEO

Exosomes secreted by the CCND2OECMs promote proliferation and hypoxia tolerance in cultured CMs

Project description:CCND2OEExos (exosomes from CCND2-overexpressing hiPSC-derived cardiomyocytes (CCND2OECMs)) were found to be able to promote proliferation of not only cardiomyocytes, but also human umbilical vein endothelial cells (HUVEC) and human vascular smooth muscle cells (HVSMC) in vitro, as indicated by the large number of ki67+ and PH3+ HUVECs and SMCs in the CCND2OEExos-treated group, relative to those in the vehicle only- or CCND2WTExos-treated groups. A comparative bulk sequence analysis of miRNAs from CCND2WTExos and CCND2OEExos (exosomes from wild type hiPSC-derived cardiomyocytes) was performed to identify some underlying mechanisms about proliferation induction.

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Expression profiling in primary and stem-cell derived Human Endothelial and Vascular Smooth Muscle Cells

Project description:Whole transcriptome gene expression profiling of Normal Human Endothelial and Vascular Smooth Muscle Cells

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Project description:While therapeutic angiogenesis holds promise for vascular diseases, progress has been limited due to discrepancies in defining adult endothelial progenitors. We have identified and characterized a population of pluripotent derived NRP1+CD34+ nascent endothelial cells, immediately diverged from NRP1+CD34- mesodermal cells. We contrasted the transcriptional profile of NRP1+ CD34+ nascent endothelial cells against undifferentiated human pluripotent stem cells and human umbilical vein endothelial cells (HUVECs) to gain insights into the pathways that are uniquely activated in formation of new endothelium. We found significant upregulation of IL-6 related growth factor receptors, including ciliary neurotrophic factor receptor (CNTFR), and their downstream JAK/STAT signaling components in NRP1+CD34+ endothelial cells. When exposed to CNTF, angiogenic sprouting of NRP1+CD34+ was induced in Matrigel, which was abolished with JAK2 inhibition. Furthermore, we found evidence of JAK2 dependent cytokine signaling in more mature endothelium, highlighting the significance of the IL6R/JAK2 pathway, well known in hematopoiesis, in vascular biology. The findings identify a novel group of growth factor receptors and downstream signaling components that may be targeted to modulate angiogenesis and vasculogenesis. 7 samples analyzed, 2 replicates for NRP1+CD34+, 3 replicates for NRP1+CD34-

2013-12-14 | E-GEOD-44328 | biostudies-arrayexpress

Multi-Lineage Heart-Chip Models Drug Cardiotoxicity and Enhances Maturation of Human Stem Cell-Derived Cardiovascular Cells

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2023-09-01 | GSE241223 | GEO

Gene expression of differentiated human induced pluripotent stem cells

Project description:Gene expression of Human DiPS 1016 SeVA iPSCs and hiPSCs-differentiated into endothelial, vascular smooth muscle or white adipose tissue cells.

2022-12-08 | GSE188240 | GEO

Endothelial DNA methalytion signature in pulmonary arterial hypertension

Project description:Pulmonary arterial hypertension (PAH) is a severe and incurable pulmonary vascular disease. One of the primary origins of PAH is pulmonary endothelial dysfunction leading to vasoconstriction, aberrant angiogenesis and smooth muscle cell proliferation, endothelial-to-mesenchymal transition, thrombosis and inflammation. Our objective was to study the epigenetic variations in pulmonary endothelial cells (PEC) through a specific pattern of DNA methylation. DNA was extracted from cultured PEC from patients with idiopathic PAH (n=11), heritable PAH (n=10) and controls (n=18). ). DNA methylation was assessed using the Illumina HumanMethylation450 Assay. After normalization, samples and probes were clustered according to their methylation profile. Differential clusters were functionally analysed using bioinformatics tools.

2016-07-15 | E-GEOD-84395 | biostudies-arrayexpress

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