Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA260059 | ENA |
REPOSITORIES: ENA
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Project description:EPC-derived VECs (EPCdECs) are categorized into two group according to their effects on the proliferation of vascular smooth muscle cells: type-I pro-proliferative VECs and type-II anti-proliferative VECs. Type-II EPCdECs were converted to type-I VECs by repetitive subcultures. Not only subculture-dependent cellular stresses but also donor differences greatly affect the phenotype determination of VECs. By comparing the gene expression profiles of type-II EPCdEC of the first donor (EPC1dEC) at early passage and those of type-II EPC1dEC at late passage and EPCdEC of the second donor at early passage, characteristic gene expression patterns that discriminate Type-I and type-II EPCdECs will be comprehended. Totally three samples of type-I EPC-derived VECs (EPC1dEC[P12], EPC2dEC[P7]) and type-II EPC-derived VEC (EPC1dEC[P7]) were subjected to the analyses.
2014-09-30 | E-GEOD-61000 | biostudies-arrayexpress
Project description:EPC-derived VECs (EPCdECs) are categorized into two group according to their effects on the proliferation of vascular smooth muscle cells: type-I pro-proliferative VECs and type-II anti-proliferative VECs. Type-II EPCdECs were converted to type-I VECs by repetitive subcultures. Not only subculture-dependent cellular stresses but also donor differences greatly affect the phenotype determination of VECs. By comparing the gene expression profiles of type-II EPCdEC of the first donor (EPC1dEC) at early passage and those of type-II EPC1dEC at late passage and EPCdEC of the second donor at early passage, characteristic gene expression patterns that discriminate Type-I and type-II EPCdECs will be comprehended.
2014-09-30 | GSE61000 | GEO
Project description:Human VECs are categorized into two groups regarding their effects on the proliferation of vascular smooth muscle cells (VSMCs):type-I, pro-proliferative VECs and type-II anti-proliferative VECs. The effects of VECs on VSMC proliferation were quantitatively assessed according to the following method: human aortic smooth muscle cells, which were stained by PKH-26 in advance, were cultured on the layer of CFSE-stained VECs, and VSMC proliferation were evaluated after four days by flow cytometry analyses using ModFit LTM-bM-^DM-" software (Verity Software House Inc., Topsham, ME). Commercially available primary human VECs including HUVEC, HAEC and HMVEC as well as the majority of endothelial progenitor cell (EPC)-derived VECs (EPCdECs), whether EPCs were obtained from adult or fetal tissues, enhanced VSMC proliferation, showing type-I phenotype. EPCdECs of minor donors including EPC1dEC suppressed VSMC proliferation, showing type-II phenotype. However, type-II VECs turned into type-I VECs after a few rounds of subcultures. Comparative analyses on gene expression profiles between type-I VECs and type-II VECs revealed that regulator of G-protein signaling 5 (RGS5) was the only gene that showed the discriminative expression pattern: high expressions in type-I VECs and low expressions in type-II VECs. Totally six samples of type-I VECs (HUVEC, HAEC, HMVEC, EPC1dEC[P12], UCEPC1dEC, EPC2dEC[P7]) and two samples of type-II VECs (EPC1dEC[P7] and EPC1dEC[P7] purchased at a different time point) were subjected to the analyses.
2014-09-30 | E-GEOD-60999 | biostudies-arrayexpress
Project description:Human VECs are categorized into two groups regarding their effects on the proliferation of vascular smooth muscle cells (VSMCs):type-I, pro-proliferative VECs and type-II anti-proliferative VECs. The effects of VECs on VSMC proliferation were quantitatively assessed according to the following method: human aortic smooth muscle cells, which were stained by PKH-26 in advance, were cultured on the layer of CFSE-stained VECs, and VSMC proliferation were evaluated after four days by flow cytometry analyses using ModFit LT™ software (Verity Software House Inc., Topsham, ME). Commercially available primary human VECs including HUVEC, HAEC and HMVEC as well as the majority of endothelial progenitor cell (EPC)-derived VECs (EPCdECs), whether EPCs were obtained from adult or fetal tissues, enhanced VSMC proliferation, showing type-I phenotype. EPCdECs of minor donors including EPC1dEC suppressed VSMC proliferation, showing type-II phenotype. However, type-II VECs turned into type-I VECs after a few rounds of subcultures. Comparative analyses on gene expression profiles between type-I VECs and type-II VECs revealed that regulator of G-protein signaling 5 (RGS5) was the only gene that showed the discriminative expression pattern: high expressions in type-I VECs and low expressions in type-II VECs.
2014-09-30 | GSE60999 | GEO
Project description:ETS transcription factors ETV2, FLI1 and ERG1 specify pluripotent stem cells into endothelial cells (PSC-ECs). However, these PSC-ECs are unstable and often drift towards non-vascular cell fates. We show that human mid-gestation c-Kit- lineage-committed amniotic cells (ACs) can be reprogrammed into induced vascular endothelial cells (rAC-VECs). Transient ETV2 expression in ACs generated immature iVECs, while co-expression with FLI1/ERG1 endowed rAC-VECs with a vascular repertoire and morphology matching mature ECs. Brief TGFb-inhibition functionalizes VEGFR2 signaling, augmenting specification of ACs into rAC-VECs. Genome-wide transcriptional analyses showed that rAC-VECs are similar to adult ECs in which vascular-specific genes are expressed and non-vascular genes are silenced. Functionally, rAC-VECs form stable vasculature in Matrigel plugs and regenerating livers. Thus, short-term ETV2 expression and TGFb-inhibition along with constitutive ERG1/FLI1 co-expression reprogram mature ACs into generic rAC-VECs with clinical-scale expansion potential. Public banking of HLA-typed rAC-VECs would establish a vascular inventory for treatment of genetically diverse disorders. Transcriptome sequencing of clonal and non-clonal rAC-VECs, HUVECs, LSECs, CD34+/Lin-, BMS
2012-10-30 | E-GEOD-40291 | biostudies-arrayexpress
Project description:Comparison between type-I vascular endothelial cells (VECs) and type-II VECs
| PRJNA260060 | ENA
Project description:ETS transcription factors ETV2, FLI1 and ERG1 specify pluripotent stem cells into endothelial cells (PSC-ECs). However, these PSC-ECs are unstable and often drift towards non-vascular cell fates. We show that human mid-gestation c-Kit- lineage-committed amniotic cells (ACs) can be reprogrammed into induced vascular endothelial cells (rAC-VECs). Transient ETV2 expression in ACs generated immature iVECs, while co-expression with FLI1/ERG1 endowed rAC-VECs with a vascular repertoire and morphology matching mature ECs. Brief TGFb-inhibition functionalizes VEGFR2 signaling, augmenting specification of ACs into rAC-VECs. Genome-wide transcriptional analyses showed that rAC-VECs are similar to adult ECs in which vascular-specific genes are expressed and non-vascular genes are silenced. Functionally, rAC-VECs form stable vasculature in Matrigel plugs and regenerating livers. Thus, short-term ETV2 expression and TGFb-inhibition along with constitutive ERG1/FLI1 co-expression reprogram mature ACs into generic rAC-VECs with clinical-scale expansion potential. Public banking of HLA-typed rAC-VECs would establish a vascular inventory for treatment of genetically diverse disorders.
2012-10-30 | GSE40291 | GEO
Project description:The gene expression in vascular endothelial cells (VECs) and circulating fibrocytes (CFs) was tested either culturing alone or co-cultured. Our previous study showed that CFs inhibit both proliferation and apoptosis of VECs. In this present study, we co-cultured CFs and VECs in Transwell and tested the gene expression in CFs and VECs in order to delight the mechanism under which CFs affect the proliferation and apoptosis of VECs.
2017-12-30 | GSE108626 | GEO
Project description:The decline of endothelial autophagy is closely related to vascular senescence and disease, although the molecular mechanisms connecting these outcomes in vascular endothelial cells (VECs) remain unclear. Here, we identify a crucial role for CD44, a multifunctional adhesion molecule, in controlling autophagy and aging in VECs. The CD44 intercellular domain (CD44ICD) negatively regulates autophagy by reducing PIK3R4 and PIK3C3 levels and disrupting STAT3-dependent PtdIns3K complexes. CD44 and its homologue clec-31 are increased in aging vascular endothelium and Caenorhabditis elegans, respectively, suggesting that an age-dependent increase in CD44 induces autophagy decline and aging phenotypes. Accordingly, CD44 knockdown ameliorates age-associated phenotypes in VECs. The endothelium-specific CD44ICD knock-in mouse is shorter-lived, with VECs exhibiting obvious premature aging characteristics associated with decreased basal autophagy. Autophagy activation suppresses the premature aging of human and mouse VECs overexpressing CD44ICD, function conserved in the CD44 homologue clec-31 in C. elegans. Our work describes a mechanism coordinated by CD44 function bridging autophagy decline and aging.
2023-08-30 | GSE236523 | GEO
Project description:Pulmonary endothelial dysfunction plays an integral role in mediating the initiation and progression of pulmonary vascular remodelling, an important feature of pulmonary arterial hypertension (PAH). Our aim was to decipher the gene expression program of endothelial cells derived from circulating endothelial progenitor (EPCs) to gain insight into the pathological process of PAH associated with systemic sclerosis (SSc), which is the most extreme vascular phenotype of this disease. We used microarrays to investigate the gene expression profile in late outgrowth EPC-derived endothelial cells issued from SSc-PAH patients, in comparison with SSc patients without PAH and healthy controls.
2016-09-30 | GSE73674 | GEO