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CD157+ vascular endothelial cells derived from human induced pluripotent stem cells have high angiogenic potential

ABSTRACT: CD157+ vascular endothelial cells derived from human induced pluripotent stem cells have high angiogenic potential

PROVIDER: PRJNA1211030 | ENA |

REPOSITORIES: ENA

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	SRR32007556.fastq.gz	Fastqsanger.gz
	SRR32007557.fastq.gz	Fastqsanger.gz
	SRR32007560.fastq.gz	Fastqsanger.gz

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CD157+ vascular endothelial cells derived from human induced pluripotent stem cells have high angiogenic potential

Project description:We previously reported that a vascular endothelial stem cell population resides in pre-existing blood vessels in mice and may contribute to vascular endothelial cells in liver injury or hind limb ischemia models in the long-term. However, whether such stem cells exist in humans and can differentiate specifically into vascular endothelial cells have not been determined. We hypothesized that CD157+ vascular endothelial cells in humans may also possess high angiogenic potential. First, human-derived induced pluripotent stem cells were differentiated into vascular endothelial cells, and the expression of CD157 was monitored during the differentiation process. We found that CD157 emerged 11 days after the induction of differentiation, peaked at 14 days, and then declined by 24 days. WNext, we also evaluated blood vessel formation by 14- and 24-day-old vascular endothelial cells.It was found that 14-day-old cells, when CD157 expression was at its peak, formed more blood vessels than 24-day-old cells.These results suggest that vascular endothelial cells expressing CD157 have high angiogenic potential and may exist as vascular endothelial stem cells.

2025-06-01 | GSE287034 | GEO

MeRIP sequencing reveals angiogenic properties of vascular endothelial cells

Project description:MeRIP sequencing reveals angiogenic properties of vascular endothelial cells

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Induced-pluripotent stem-derived vascular endothelial cells in Down syndrome

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Angiogenic and Immunologic Proteins Identified by Deep Proteomic Profiling of Human Choroidal and Retinal Vascular Endothelial Cells

Project description:PURPOSE Diseases that involve choroidal or retinal endothelial vascular cells are leading causes of vision loss: age-related macular degeneration, retinal ischemic vasculopathies and non-infectious posterior uveitis. Proteins differentially expressed by these endothelial cell populations are potential drug targets. We used deep proteomics to define the molecular phenotype of human choroidal and retinal endothelial cells at the protein level. METHODS Choroidal and retinal endothelial cells were separately isolated from 5 human eye pairs by selection on CD31. Total protein was extracted and digested, and peptide fractions were analysed by reverse-phase liquid chromatography tandem mass spectrometry. Peptide sequences were assigned to fragment ion spectra and proteins were inferred using public protein databases. Protein abundance was determined by spectral counting. Protein expression in choroidal versus retinal endothelial cells was compared using edgeR package in R, and annotation enrichment analysis was performed. RESULTS Human choroidal or retinal endothelial cells expressed 5042 non-redundant proteins. Setting the false discovery rate at 5%, 498 proteins (14.4%) of 3454 quantifiable proteins with minimum mean spectral counts of 2.5 were differentially expressed between cell populations. Choroidal and retinal endothelial cells were enriched in angiogenic proteins, and retinal endothelial cells were also enriched in immunologic proteins. CONCLUSIONS This work demonstrates the protein heterogeneity of human choroidal and retinal vascular endothelial cells and provides multiple candidates for further study as novel treatments or drug targets for posterior eye diseases.

2018-03-26 | PXD005972 | Pride

Pro-angiogenic transcriptome of zebrafish endothelial cells

Project description:Pro-angiogenic transcriptome of zebrafish endothelial cells

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Pro-angiogenic transcriptome of zebrafish endothelial cells

Project description:To identify previously unknown determinants of endothelial cell sprouting, we defined and exploited a pharmacological strategy for the manipulation of angiogenic cell behavior in vivo. Whereas high vascular endothelial growth factor receptor (Vegfr) signaling is known to promote tip cell (TC) specification, activation of the Notch receptor via its ligand Delta-like 4 (Dll4) represses the TC phenotype to promote stalk cell (SC) fate. Conversely, suppression of Notch activity upon antagonistic interaction with its ligand Jagged1 pro- motes TC formation. Hence, specification of TCs involves tight spatiotemporal control of Vegfr/Notch signaling. Consequently, we hypothesized that the pharmacological manipulation of Vegfr/Notch signaling selectively during zebrafish intersegmental vessel (ISV) angiogenesis would enable the precise control of angiogenic EC behavior and sprouting- associated gene expression in vivo. For more information, see Herbert et al., 2012, PMID 22921365.

2019-05-09 | GSE130889 | GEO

NOS3 regulates angiogenic potential of human induced pluripotent stem cell-derived endothelial cells.

Project description:Incorporation of blood capillaries in engineered tissues and their functional connection to host blood vessels is essential for success in engineering vascularized tissues, a process which involves spatial patterning of endothelial cells (ECs) to form functional and integrated vascular networks. Different types of ECs have been employed for vascular network formation and each source offers advantages and disadvantages. While ECs derived from induced pluripotent stem cells (iPSC-ECs) offer advantages over primary ECs in that they can be generated in large quantities for autologous applications, their suitability for disease modelling and cell replacement therapies is not well-explored. The present study compares the angiogenic capacity of iPSC-ECs and primary ECs (cardiac microvascular ECs and lymphatic microvascular ECs) using an in vitro tubulogenesis assay, revealing comparable performance in forming a pseudo-capillary network on Matrigel. Analysis of genes encoding angiogenic factors (VEGFA, VEGFC, VEGFD and ANG), endothelial cell markers (PECAM1, PCDH12 and NOS3) and proliferation markers (AURKB and MKI67) indicates a significant positive correlation between NOS3 mRNA expression levels and various tubulogenic parameters. Further experimentation using a CRISPR activation system demonstrates a positive impact of NOS3 on tubulogenic activity of ECs, suggesting that iPSC-ECs can be enhanced with endogenous NOS3 activation. Collectively, these findings highlight the potential of iPSC-ECs in generating vascularized tissues and advancing therapeutic vascularization.

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Pro-angiogenic Ginsenoside F1 and Rh1 Inhibit Vascular Leakage by Modulating NR4A1

Project description:Angiogenesis is an essential process in human physiology and disease pathology. Particularly, in ischemic disease condition, the proper induction of angiogenesis without vascular leakage will be crucial for its effective therapy. Ginsenosides, triterpenoid saponins from a well-known medicinal plant ginseng, have been considered as a strong candidate for modulating angiogenesis. However, the biologic activity of individual gensenoside compounds and their target pathway have not been elucidated systematically. To find the candidates of vascular-related therapeutic agents, we evaluated in vitro angiogenic efficacy of 10 ginsenosides using tube formation assay with human umbilical vein endothelial cells (HUVECs). Among them, F1 and Rh1 showed strong in vitro angiogenic properties including EC tube formation, proliferation, and migration similar to vascular endothelial growth factor (VEGF). However, RNA transcriptome analysis showed that F1 and Rh1 differentially regulate gene expressions in HUVECs compared to VEGF. Not only that, F1 and Rh1 significantly inhibited vascular endothelial growth factor (VEGF)-induced vascular leakage both in vitro and in vivo. From RNA transcriptome analysis, we identified that nuclear receptor subfamily 4 group A member 1 (NR4A1) is regulated by F1 and Rh1 for suppression of VEGF-induced vascular leakage. By suppressing the expression and transcriptional activity of NR4A1, F1 and Rh1 could stabilize the expression and localization of junctional vascular endothelial (VE)-cadherin. These findings demonstrate that F1 and Rh1 could be potential compounds in the development of vascular pharmaceuticals.

2019-03-20 | GSE116121 | GEO

Vascular organoids differentiation from human induced pluripotent stem cells (iPSC)

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Vascular niche induction of hematopoietic progenitors from pluripotent stem cells

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