Ontology highlight
ABSTRACT:
PROVIDER: PRJNA175380 | ENA |
REPOSITORIES: ENA
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Project description:This SuperSeries is composed of the following subset Series: GSE40793: Conversion of human fibroblasts into vascular cells (gene expression) GSE40909: Conversion of human fibroblasts into vascular cells (methylation) Refer to individual Series
2012-09-18 | E-GEOD-40927 | biostudies-arrayexpress
Project description:Conversion of human fibroblasts into vascular cells (methylation)
| PRJNA175382 | ENA
Project description:Conversion of human fibroblasts into vascular cells (gene expression)
| PRJNA175381 | ENA
Project description:Chemical conversion of human fibroblasts into functional Schwann cells
| PRJNA254474 | ENA
Project description:Direct conversion from fibroblasts to neurons is a potential cell replacement therapy for neurological disorders, and a variety of combinations of transcription factors have been tried. We notice that the efficiency of conversion from aging fibroblasts was much lower than in early stage cells, which is consistent with the notion that cellular senescence impairs conversion of fibroblasts to neurons. Here, we found that the transient knockdown of the p16Ink4a/p19Arf locus was sufficient to convert human fibroblasts to neurons. Futhermore, expression of hTERT alone, another mechanism behind immortalization, also induced neuron conversion. Our results show that the acquisition of immortality is a crucial step for the conversion of human fibroblasts into induced neurons.
2012-12-28 | GSE43175 | GEO
Project description:Direct Conversion of Adult Human Fibroblasts into Authentic Endothelial Cells
| PRJEB33632 | ENA
Project description:Direct conversion from fibroblasts to neurons is a potential cell replacement therapy for neurological disorders, and a variety of combinations of transcription factors have been tried. We notice that the efficiency of conversion from aging fibroblasts was much lower than in early stage cells, which is consistent with the notion that cellular senescence impairs conversion of fibroblasts to neurons. Here, we found that the transient knockdown of the p16Ink4a/p19Arf locus was sufficient to convert human fibroblasts to neurons. Futhermore, expression of hTERT alone, another mechanism behind immortalization, also induced neuron conversion. Our results show that the acquisition of immortality is a crucial step for the conversion of human fibroblasts into induced neurons. Transient knockdown of p16/p19 or p53 expression or exogenous overexpression of hTERT can induce primary fibroblasts to immortality. In the following, treated cells were cultured in neuron-induction medium. We can observe the morphology change and detect the neuronal markers. Also, some of the induced neurons could generate action potentials and neurotransmitter-induced currents in optimal conditions.
2012-12-28 | E-GEOD-43175 | biostudies-arrayexpress
Project description:In order to find the difference between human lung tissue-derived fibroblasts and human vascular adventitial fibroblasts for enhancing tumor formation ablity of human lung adenocarcinoma cell line A549, we found that human vascular adventitial fibroblasts enhance A549 tumor formation in vivo compared to human lung tissue-derived fibroblasts. To find the responsible genes for this phenomena, we used microarray analysis to find the expression difference between lung tissue-derived fibroblasts and vascular adventitial fibroblas Cultured human lung tissue-derived fibroblasts and human vascular adventitial fibroblasts were analyzed in replicates.
2010-12-18 | E-GEOD-26146 | biostudies-arrayexpress
Project description:<p>BACKGROUND: Myocardial infarction (MI), one of the leading causes of mortality worldwide, remains a clinical challenge due to limitations in current therapeutic strategies. The cardiac vascular network, as the fundamental architecture sustaining myocardial function, delivers oxygen and nutrients with high precision to the heart tissue. However, the dynamic regulatory mechanisms governing this network post-MI remain incompletely elucidated. Notably, the pivotal role of cardiac endothelial cells in the pathophysiological progression of MI calls for further comprehensive investigation.</p><p>METHODS: We examined alterations in Signal Peptide, CUB Domain And EGF Like Domain Containing 3 (SCUBE3) protein expression in the myocardium of MI-afflicted mice and human MI heart tissues. Utilizing genetically engineered mouse models in combination with diverse cellular and molecular biology techniques, we systematically dissected the functional role of SCUBE3 in MI and its underlying mechanisms in cardiac endothelial cell metabolism.</p><p>RESULTS: Proteomic profiling of serum samples from MI patients demonstrated a significant elevation in SCUBE3 protein levels. Immunohistochemical assessment revealed markedly increased SCUBE3 expression localized predominantly within fibroblasts in the infarct zone of cardiac tissues from MI patients. Consistently, in a murine MI model, SCUBE3 expression was also upregulated and primarily distributed in fibroblasts within the infarcted myocardial regions. Employing inducible, fibroblast-specific SCUBE3 overexpression and knockout mouse models, we observed that SCUBE3 overexpression robustly enhanced post-MI angiogenesis, improved microcirculatory network integrity, and attenuated myocardial injury. In contrast, SCUBE3 ablation exacerbated infarct-induced cardiac damage. Subsequent protein tracking and mass spectrometry analyses demonstrated that SCUBE3 selectively binds to and activates vascular endothelial growth factor receptor 1 (VEGFR1) on endothelial cells, thereby mediating downstream biological effects. Transcriptomic sequencing revealed that SCUBE3 significantly upregulates fatty acid metabolism–related pathways. Live-cell dynamic analysis further confirmed that SCUBE3 promotes fatty acid uptake and enhances the metabolic activity of endothelial cells. Metabolomic profiling indicated that SCUBE3 facilitates the conversion of unsaturated fatty acids into phosphosugars and nucleotides, supplying essential substrates and energy to support endothelial cell proliferation. In SCUBE3-overexpressing mice, endothelial cell–specific inducible VEGFR1 knockout completely abrogated SCUBE3-driven fatty acid metabolism and its associated cardioprotective effects. Moreover, beyond its role in angiogenesis SCUBE3 also markedly enhances cardiomyocyte regenerative capacity, highlighting its potential as a novel therapeutic target for myocardial repair. Conclusions: Our findings establish that fibroblast-derived SCUBE3 interacts with VEGFR1 on endothelial cells to promote fatty acid metabolism, thereby providing energy substrates necessary for endothelial proliferation. This study elucidates the critical function of the SCUBE3–VEGFR1 signaling axis in post-MI vascular regeneration through metabolic regulation, presenting a promising avenue for therapeutic intervention in cardiac repair.</p>
2025-09-18 | MTBLS13004 | MetaboLights
Project description:Direct cell conversion is now expected to apply to therapeutic purposes. Although that has been succeeded in several cell types, the mechanism or general way to identify the key transcription factors are still unclear. In addition, most of the cases are not completely identical with the target cells. In previous work, we suggested that cell status is maintained by a homeostatic network of limited number of TFs and no single transcription factor is both necessary and sufficient to drive the differentiation process. Here, identifying the key TFs of human monocyte by combining comparative gene expression analysis and literature based text-mining, we mimicked the monocytic regulatory network in human dermal fibroblasts to induce direct cell conversion of the fibroblasts to monocytes. We suggested that although it is a primary master TF, single TF is not sufficient to induce the direct cell conversion and orchestrated TF regulation is necessary to complete the cell conversion. Total RNA obtained from human dermal fibroblasts(FIB), human CD14+ monocytes(MON), mock lentivirus vector transduced fibroblasts (FIB-mock), SPI1 transduced fibroblasts (FIB-SPI1), and SPI1, CEBPA, MNDA, IRF8 transduced fibroblasts(FIB-4Fs). The fold change was computed compared with fibroblasts or FIB-mock.
2011-02-15 | E-GEOD-27304 | biostudies-arrayexpress