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CD34 marks angiogenic tip cells in human vascular endothelial cell cultures.

ABSTRACT: The functional shift of quiescent endothelial cells into tip cells that migrate and stalk cells that proliferate is a key event during sprouting angiogenesis. We previously showed that the sialomucin CD34 is expressed in a small subset of cultured endothelial cells and that these cells extend filopodia: a hallmark of tip cells in vivo. In the present study, we characterized endothelial cells expressing CD34 in endothelial monolayers in vitro. We found that CD34-positive human umbilical vein endothelial cells show low proliferation activity and increased mRNA expression of all known tip cell markers, as compared to CD34- negative cells. Genome-wide mRNA profiling analysis of CD34-positive endothelial cells demonstrated enrichment for biological functions related to angiogenesis and migration, whereas CD34-negative cells were enriched for functions related to proliferation. In addition, we found an increase or decrease of CD34-positive cells in vitro upon exposure to stimuli that enhance or limit the number of tip cells in vivo, respectively. Our findings suggest cells with virtually all known properties of tip cells are present in vascular endothelial cell cultures and that they can be isolated based on expression of CD34. This novel strategy may open alternative avenues for future studies of molecular processes and functions in tip cells in angiogenesis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE34850 | GEO | 2012/01/05

SECONDARY ACCESSION(S): PRJNA150137

REPOSITORIES: GEO

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CD34 marks angiogenic tip cells in human vascular endothelial cell cultures.

Project description:The functional shift of quiescent endothelial cells into tip cells that migrate and stalk cells that proliferate is a key event during sprouting angiogenesis. We previously showed that the sialomucin CD34 is expressed in a small subset of cultured endothelial cells and that these cells extend filopodia: a hallmark of tip cells in vivo. In the present study, we characterized endothelial cells expressing CD34 in endothelial monolayers in vitro. We found that CD34-positive human umbilical vein endothelial cells show low proliferation activity and increased mRNA expression of all known tip cell markers, as compared to CD34- negative cells. Genome-wide mRNA profiling analysis of CD34-positive endothelial cells demonstrated enrichment for biological functions related to angiogenesis and migration, whereas CD34-negative cells were enriched for functions related to proliferation. In addition, we found an increase or decrease of CD34-positive cells in vitro upon exposure to stimuli that enhance or limit the number of tip cells in vivo, respectively. Our findings suggest cells with virtually all known properties of tip cells are present in vascular endothelial cell cultures and that they can be isolated based on expression of CD34. This novel strategy may open alternative avenues for future studies of molecular processes and functions in tip cells in angiogenesis. Four HUVEC donors were FACS-sorted by CD34 and divided in CD34-positive and CD34-negative fractions.

2012-01-05 | E-GEOD-34850 | biostudies-arrayexpress

Identification of the RNA-bound proteome in endothelial cells

Project description:Most new blood vessels emerge through sprouting angiogenesis, an intricate biological process that entails the coordinated migration of groups of endothelial cells branching from parental vessels. Critical guidance cues such as the Vascular Endothelial Growth Factor secreted by the surrounding tissues regulate the molecular and cellular responses triggered during angiogenesis. Similarly to other collective cell migration systems, endothelial cells within sprouting vessels are hierarchically organised into leader tip cells and follower stalk cells. Endothelial tip cells are highly polarised, exhibiting a leading edge that extends filopodia-containing protrusions and that interacts with the extracellular matrix, whilst their rear engages in cell-to-cell contacts with stalk cells. Polarisation of cytoplasmic components contributes to dynamic membrane remodelling phenomena that are constrained to the cell-leading front during migration. Amongst other factors, asymmetric distribution of mRNA is a well-established and crucial determinant of cell polarity. The active transport of transcripts is mediated by mRNA-binding proteins (mRBPs). Subcellular distribution of transcript messages results in restricted synthesis of the proteins they encode to particular compartments within the cell. This mode of post-transcriptional control of gene expression contributes to rapid and localised cellular responses to dynamic environmental stimuli with implications in development and disease. Although the involvement of RNA interacting proteins in angiogenesis has been previously reported, whether mRBPs play a role in asymmetric transcript localisation crucial for endothelial cell migration is yet to be fully explored.

2024-03-28 | PXD046994 | Pride

Effect of VEGF on expressions of C2H2 zinc finger proteins in human umbilical vein endothelial cells.

Project description:Angiogenic homeostasis is maintained by a balance between vascular endothelial growth factor (VEGF) and Notch signalling in endothelial cells (ECs). We screened for molecules that might mediate the coupling of VEGF signal transduction with down-regulation of Notch signalling, and identified B-cell chronic lymphocytic leukemia/lymphoma6-associated zinc finger protein (BAZF). BAZF was induced by VEGF-A in ECs to bind to the Notch signalling factor CBF1, and to promote the degradation of CBF1 through polyubiquitination in a CBF1-cullin3 (CUL3) E3 ligase complex. BAZF disruption in vivo decreased endothelial tip cell number and filopodia protrusion, and markedly abrogated vascular plexus formation in the mouse retina, overlapping the retinal phenotype seen in response to Notch activation. Further, impaired angiogenesis and capillary remodeling were observed in skin-wounded BAZF-/- mice. We therefore propose that BAZF supports angiogenic sprouting via BAZF-CUL3-based polyubiquitination-dependent degradation of CBF1 to down-regulate Notch signalling. Human umbilical vein endothelial cells were stimulated with recombinant human VEGF165 for 0, 1, 2, 6, 12, 24 and 48 hours.

2012-03-25 | E-GEOD-35171 | biostudies-arrayexpress

Endothelial CD34 expression and regulation of immune cell response in-vitro

Project description:Endothelial cells cover the lining of different blood vessels and lymph nodes, and have major functions including the transport of blood, homeostasis, inflammatory responses, control of infiltration of circulating cells into the tissues, and formation of new blood vessels. Therefore, understanding these cells is of major interest. The morphological features, phenotype and function of endothelial cells varies according to the vascular bed examined. The sialomucin, CD34, is widely used as an endothelial marker. However, CD34 is differentially expressed on endothelial cells in different organs and in pathological conditions. Little is known about regulation of endothelial CD34 expression or function. This marker is also strongly modified in-vitro in endothelial cell models, including human umbilical vein endothelial cells (HUVEC) and endothelial progenitor cells (EPC). We have therefore selected CD34high and CD34low endothelial cell subpopulations and examined their CD34 expression and function. Results: Transcriptomic analysis showed that CD34 gene and protein expressions are highly correlated, that CD34high cells are less proliferative, and have a stronger expression of IL-33 and Angiopoietin 2, compared to CD34low cells. Higher secretion levels of IL-33 by CD34high HUVECs was confirmed by ELISA. Finally, when endothelial cells were allowed to interact with peripheral blood mononuclear cells (PBMCs), CD34high endothelial cells induced a stronger proliferation of regulatory T lymphocytes (Tregs) compared to CD34low cells whereas expansion of other CD4+-T cell subsets was equivalent. These results suggest that CD34 expression by endothelial cells in-vitro associates with their ability to proliferate and with an immunogenic ability that favours the tolerogenic response.

2023-07-04 | GSE236137 | GEO

miR-221 is required for endothelial tip cell behaviors during vascular development

Project description:Through deep sequencing and functional screening in zebrafish, we find that miR-221 is essential for angiogenesis. miR-221 knockdown phenocopied defects associated with loss of the tip cell-expressed Flt4 receptor. Furthermore, miR-221 was required for tip cell proliferation and migration, as well as tip cell potential in mosaic blood vessels. miR-221 knockdown also prevented “hyper-angiogenesis” defects associated with Notch deficiency and miR-221 expression was inhibited by Notch signaling. Finally, miR-221 promoted tip cell behavior through repression of two targets: cyclin-dependent kinase inhibitor 1b (cdkn1b) and phosphoinositide-3-kinase regulatory subunit 1 (pik3r1). These results identify miR-221 as an important regulatory node through which tip cell migration and proliferation are controlled during angiogenesis. Identification of endothelial-expressed microRNA from FACS-isolated zebrafish endothelial cells.

2012-02-28 | E-GEOD-35078 | biostudies-arrayexpress

FACS-array profiling in retinal endothelial cells from living mouse retinas

Project description:Deregulated retinal angiogenesis directly cause vision loss in many ocular diseases, such as diabetic retinopathy and retinopathy of prematurity. To identify endothelial-specific genes expressed in angiogenic retinal vessels, we purified genetically labeled endothelial cells from Tie2-GFP transgenic mice and performed gene expression profiling using DNA microarray. To find out genes associated with angiogenesis, comparisons of microarray data were carried out between GFP-negative non-endothelial retinal cells and GFP-positive retinal endothelial cells in angiogenic P8 retina. Eighteen arrays are included. Utilizing fluorescence-activated cell sorting (FACS), we isolated endothelial cells as GFP-positive cells from P8 retina in homozygous Tie2-GFP transgenic mice. GFP-negative cells were served as non-endothelial control. RNA extracts from sorted cells were amplified and then hybridized to Affymetrix MGU74v2 series arrays in triplicate.

2011-04-17 | E-GEOD-27238 | biostudies-arrayexpress

Effect of VEGF on expressions of C2H2 zinc finger proteins in human umbilical vein endothelial cells.

2012-03-25 | GSE35171 | GEO

FACS-array profiling in retinal endothelial cells from living mouse retinas

2011-04-17 | GSE27238 | GEO

Endothelin2 signaling in the neural retina promotes the endothelial tip cell state and inhibits angiogenesis

Project description:Endothelin signaling is required for neural crest migration and homeostatic regulation of blood pressure. Here we report that constitutive over-expression of Endothelin-2 (Edn2) in the mouse retina perturbs vascular development by inhibiting endothelial cell (EC) migration across the retinal surface and subsequent EC invasion into the retina. Developing endothelial cells exist in one of two states: tip cells at the growing front, and stalk cells in the vascular plexus behind the front. This division of endothelial cell states is one of the central organizing principle of angiogenesis. In the developing retina, Edn2 over-expression leads to over-production of endothelial tip cells by both morphologic and molecular criteria. Spatially localized over-expression of Edn2 produces a correspondingly localized endothelial response. Edn2 over-expression in the early embryo inhibits vascular development at mid-gestation, but Edn2 over-expression in developing skin and brain has no discernable effect on vascular structure. Inhibition of retinal angiogenesis by Edn2 requires expression of Endothelin receptor A (Ednra) but not Ednrb in the neural retina. Taken together, these observations imply that the neural retina responds to Edn2 by synthesizing one or more factors that promote the endothelial tip cell state and inhibit angiogenesis. The response to Edn2 is sufficiently potent that it over-rides the activities of other homeostatic regulators of angiogenesis, such as vascular endothelial growth factor.

2014-01-01 | GSE50059 | GEO

Endothelin2 signaling in the neural retina promotes the endothelial tip cell state and inhibits angiogenesis

2014-01-01 | E-GEOD-50059 | biostudies-arrayexpress

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