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Differential miRNA expression profiles of human vascular endothelial cells (VECs) between Type-I pro-proliferative/pro-stenotic VECs and Type-II anti-proliferative/anti-stenotic VECs

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE102207 | GEO | 2020/07/27

REPOSITORIES: GEO

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Differential miRNA expression profiles of human vascular endothelial cells (VECs) between Type-I pro-proliferative/pro-stenotic VECs and Type-II anti-proliferative/anti-stenotic VECs [Agilent-070156]

Project description:Human VECs are categorized into two groups according to their effects on the proliferation of vascular smooth muscle cells (in vitro) and the induction of stenosis in endothelia-removed arteries after transplantation (In vivo): pro-proliferative/pro-stenotic (Type-I) virsus anti-proliferative/anti-stenotic (Type-II) VECs. Since RGS5, which is a master gene responsible for aging- and oxidative stress-dependent Type-II to Type-I conversion, is the only protein-coding gene that shows differential expression profiles between Type-I and Type-II VECs, non-coding RNAs including miRNA should be working at the downstream of RGS5 for quality control of VECs.

2020-07-27 | GSE102206 | GEO

Differential miRNA expression profiles of human vascular endothelial cells (VECs) between Type-I pro-proliferative/pro-stenotic VECs and Type-II anti-proliferative/anti-stenotic VECs [Agilent-046064]

2020-07-27 | GSE102205 | GEO

Differential miRNA expression profiles of human vascular endothelial cells (VECs) between Type-I pro-proliferative/pro-stenotic VECs and Type-II anti-proliferative/anti-stenotic VECs

Project description:Differential miRNA expression profiles of human vascular endothelial cells (VECs) between Type-I pro-proliferative/pro-stenotic VECs and Type-II anti-proliferative/anti-stenotic VECs

| PRJNA397006 | ENA

Comparison between type-I vascular endothelial cells (VECs) and type-II VECs

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

Comparison between type-I vascular endothelial cells (VECs) and type-II VECs

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

Effects of differences in donors and passage numbers of endothelial progenitor cell (EPC)-derived vascular endothelial cells (VECs) on the phenotype determination of VECs (type-I versus type-II).

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

Effects of differences in donors and passage numbers of endothelial progenitor cell (EPC)-derived vascular endothelial cells (VECs) on the phenotype determination of VECs (type-I versus type-II).

2014-09-30 | GSE61000 | GEO

The role of anti-vascular endothelial growth factor (anti-VEGF) in the management of proliferative diabetic retinopathy.

Project description:Diabetes is a major cause of visual impairment among working-age adults in the United States. The proliferative form of diabetic retinopathy is associated with severe vision loss (acuity <5/200). The standard treatment in proliferative diabetic retinopathy (PDR) is panretinal photocoagulation (PRP), which is effective but has established side effects such as peripheral visual-field constraints. Vascular endothelial growth factor (VEGF) is thought to drive the process of vascular proliferation. Drugs targeting VEGF (anti-VEGF) have been studied extensively in diabetic macular edema (DME), and results have shown that diabetic retinopathy regresses with anti-VEGF treatment. Recent studies show that anti-VEGF is not inferior to PRP for PDR while treatment is maintained, though recurrence rate when anti-VEGF treatment is stopped is unclear. In vitreous hemorrhage where PRP cannot be performed, use of anti-VEGF medications can treat underlying PDR and delay or reduce need for vitrectomy. Limitations of anti-VEGF treatment, however, require careful patient selection and monitoring. This review discusses recent clinical trials and guidelines for anti-VEGF use in PDR.

| S-EPMC6113746 | biostudies-literature

Vascular endothelial cells (VECs) and lymphatic endothelial cells (LECs) of small intestines

Project description:Analysis of vascular endothrial cells and lympatic endotherial cells purified from small intestines

2020-09-21 | GSE104979 | GEO

Pro-proliferative factor KLF5 becomes anti-proliferative in epithelial homeostasis upon signaling-mediated modification.

Project description:During epithelial homeostasis, stem cells divide to produce progenitor cells, which not only proliferate to generate the cell mass but also respond to cellular signaling to transition from a proliferative state to a differentiation state. Such a transition involves functional alterations of transcriptional factors, yet the underlying molecular mechanisms are poorly understood. Recent studies have implicated Kruppel-like factors (KLFs) including KLF5 in the renewal and maintenance of stem/progenitor cells. Here we demonstrate that the pro-proliferative factor KLF5 becomes anti-proliferative upon TGFbeta-mediated acetylation in an in vitro model of epithelial homeostasis. In the HaCaT epidermal cell line treated with or without TGFbeta, we found that KLF5 was not only essential for cell proliferation, it was also indispensable for TGFbeta-induced anti-proliferation in these cells. KLF5 inhibited the expression of p15 (CDKN2B), a cell cycle inhibitor, without TGFbeta, but became a coactivator in TGFbeta-induced p15 expression in the same cells. Mechanistically, TGFbeta recruited acetylase p300 to acetylate KLF5, and acetylation in turn altered the binding of KLF5 to p15 promoter, resulting in the reversal of KLF5 function. These studies not only demonstrate that a basic transcription factor can be both pro-proliferation and anti-proliferation in epithelial homeostasis, they also present a unique mechanism for how transcriptional regulation changes during the transition from proliferation to inhibition of proliferation. Furthermore, they establish KLF5 as an essential cofactor for TGFbeta signaling.

| S-EPMC2649083 | biostudies-literature

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