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3,938 results for “endothelialization”
Data for a publication "Argon plasma-modified bacterial nanocellulose: Cell-specific differences in the interaction with fibroblasts and endothelial cells"
<p>A dataset containing data for the published article "Argon plasma-modified bacterial nanocellulose: Cell-specific differences in the interaction with fibroblasts and endothelial cells".</p> <p> </p> <p>For more details, please read the <strong>README - Description of data and analysis informations.txt</strong> file.</p> <p><strong>Dataset versions:</strong></p> <p><strong>V1:</strong> The first dataset containing a majority of the data.</p> <p><strong>V2:</strong> Dataset contains all the data mentioned in the article in the appropriate file formats for long-term preservation and accessibility.</p>
Data from: Selectivity of Guanine Nucleotide Exchange Factor-mediated Cdc42 activation in primary human endothelial cells
<p>Data that was reported in "Selectivity of Guanine Nucleotide Exchange Factor-mediated Cdc42 activation in primary human endothelial cells" by </p> <p>Nathalie R. Reinhard<sup>1</sup>, Sanne van der Niet<sup>1</sup>, Anna Chertkova<sup>1</sup>, Marten Postma<sup>1</sup>, Theodorus W.J. Gadella Jr.<sup>1</sup>, Peter L. Hordijk<sup>1,2</sup>, and Joachim Goedhart<sup>1*</sup><br> </p> <p><strong>Affiliations:</strong></p> <p><sup>1 </sup>University of Amsterdam, Molecular Cytology, Swammerdam Institute for Life Sciences, van Leeuwenhoek Centre for Advanced Microscopy, Amsterdam, the Netherlands</p> <p><sup>2 </sup>Department of Physiology, Free University Medical Center, Amsterdam, The Netherlands</p> <p> </p> <p>*Correspondence to: j.goedhart@uva.nl</p>
Research data supporting "Pericyte seeded dual peptide scaffold with improved endothelialization for vascular graft tissue engineering"
<p>Raw research data supporting the paper:</p> <p>Campagnolo, P. <em>et al</em>., Pericyte seeded dual peptide scaffold with improved endothelialization for vascular graft tissue engineering, 2016, Advanced Healthcare Materials, 5(23), 3046-3055.</p> <p> </p>
Reference model and embedding for human kidney endothelial cell mapping
<p>Reference model and embedding for human kidney endothelial cell mapping</p><p>The reference model serves as a basis for the mapping of new data to the HLCA using scArches (Lotfollahi et al., https://doi.org/10.1038/s41587-021-01001-7). </p>
Dataset related to: Sirt3 deficiency promotes endothelial dysfunction and aggravates renal injury
<p>The .xlsx file contains raw data related to the article "<i><strong>Sirt3</strong></i><strong> deficiency promotes endothelial dysfunction and aggravates renal injury</strong>. <i>PLOS One</i>. 2023 Oct 10;18(10):e0291909<i>", </i>available at the following <a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0291909">link</a>.</p><p> </p><p><strong>Abstract</strong></p><p>Sirtuin 3 (SIRT3), the main deacetylase of mitochondria, modulates the acetylation levels of substrates governing metabolism and oxidative stress. In the kidney, we showed that SIRT3 affects the proper functioning of high energy-demanding cells, such as tubular cells and podocytes. Less is known about the role of SIRT3 in regulating endothelial cell function and its impact on the progression of kidney disease. Here, we found that whole body <i>Sirt3</i>-deficient mice exhibited reduced renal capillary density, reflecting endothelial dysfunction, and VEGFA expression compared to wild-type mice. This was paralleled by activation of hypoxia signaling, upregulation of HIF-1α and Angiopietin-2, and oxidative stress increase. These alterations did not result in kidney disease. However, when <i>Sirt3</i>-deficient mice were exposed to the nephrotoxic stimulus Adriamycin (ADR) they developed aggravated endothelial rarefaction, altered VEGFA signaling, and higher oxidative stress compared to wild-type mice receiving ADR. As a result, ADR-treated <i>Sirt3</i>-deficient mice experienced a more severe injury with exacerbated albuminuria, podocyte loss and fibrotic lesions. These data suggest that SIRT3 is a crucial regulator of renal vascular homeostasis and its dysregulation is a predisposing factor for kidney disease. By extension, our findings indicate SIRT3 as a pharmacologic target in progressive renal disease whose treatments are still imperfect.</p>
Data from: Hypoxia blunts angiogenic signaling and upregulates the antioxidant system in elephant seal endothelial cells
<p><strong><em>Background</em></strong></p> <p>Elephant seals exhibit extreme hypoxemic tolerance derived from repetitive hypoxia/reoxygenation episodes they experience during diving bouts. Real-time assessment of the molecular changes underlying protection against hypoxic injury in seals remains restricted by their at-sea inaccessibility. Hence, we developed a proliferative arterial endothelial cell culture model from elephant seals and used RNA-seq, functional assays, and confocal microscopy to assess the molecular response to prolonged hypoxia.</p> <p><strong><em>Results</em></strong></p> <p>Seal and human endothelial cells exposed to 1% O<sub>2</sub> for up to 6 h respond differently to acute and prolonged hypoxia. Seal cells decouple stabilization of the hypoxia-sensitive transcriptional regulator HIF-1α from angiogenic signaling. Rapid upregulation of genes involved in glutathione (GSH) metabolism supports the maintenance of GSH pools, and intracellular succinate increases in seal but not human cells. High maximal and spare respiratory capacity in seal cells after hypoxia exposure occurs in concert with increasing mitochondrial branch length and independent from major changes in extracellular acidification rate, suggesting that seal cells recover oxidative metabolism without significant glycolytic dependency after hypoxia exposure.</p> <p><strong><em>Conclusions</em></strong></p> <p>We found that the glutathione antioxidant system is upregulated in seal cells during hypoxia, while this system remains static in comparable human cells. Furthermore, we found that in contrast to human cells, hypoxia exposure rapidly activates HIF-1 in seal cells, but this response is decoupled from the canonical HIF-angiogenesis pathway. These results highlight the unique mechanisms that confer extraordinary tolerance to limited oxygen availability in a champion diving mammal.</p>
"Dynamics of Endothelial Engagement and Filopodia Formation in Complex 3D Microscaffolds" : Raw Data
<p>Raw data of the paper "Dynamics of Endothelial Engagement and Filopodia Formation in Complex 3D Microscaffolds", <strong> </strong> International Journal of Molecular Sciences, 2022.</p> <p><strong>Abstract: </strong>The understanding of endothelium–extracellular matrix interactions during the initiation of new blood vessels is of great medical importance; however, the mechanobiological principles governing endothelial protrusive behaviours in 3D microtopographies remain imperfectly understood. In blood capillaries submitted to angiogenic factors (such as vascular endothelial growth factor, VEGF), endothelial cells can transiently transdifferentiate in filopodia-rich cells, named tip cells, from which angiogenesis processes are locally initiated. This protrusive state based on filopodia dynamics contrasts with the lamellipodia-based endothelial cell migration on 2D substrates. Using two-photon polymerization, we generated 3D microstructures triggering endothelial phenotypes evocative of tip cell behaviour. Hexagonal lattices on pillars (“open”), but not “closed” hexagonal lattices, induced engagement from the endothelial monolayer with the generation of numerous filopodia. The development of image analysis tools for filopodia tracking allowed to probe the influence of the microtopography (pore size, regular vs.<em> </em>elongated structures, role of the pillars) on orientations, engagement and filopodia dynamics, and to identify MLCK (myosin light-chain kinase) as a key player for filopodia-based protrusive mode. Importantly, these events occurred independently of VEGF treatment, suggesting that the observed phenotype was induced through microtopography. These microstructures are proposed as a model research tool for understanding endothelial cell behaviour in 3D fibrillary networks.</p>
Long read proteogenomics to characterize protein isoform diversity in human umbilical vein endothelial cells (HUVECs)
<p>Endothelial cells (ECs) comprise the lumenal lining of all blood vessels and are critical for the functioning of the cardiovascular system and their phenotypes can be modulated by protein isoforms. To characterize the isoform landscape within EC, we applied a long read proteogenomics approach to analyze human umbilical vein endothelial cells (HUVECs). Transcripts delineated from PacBio sequencing serve as the basis for a sample-specific protein database used for downstream MS analysis to infer protein isoform expression. We detected 53,836 transcript isoforms from 10,426 genes, with 22,195 of those transcripts being novel. Furthermore, the predominant isoform in HUVECs does not correspond with the accepted “reference isoform” 25% of the time, with vascular pathway-related genes among this group. We found 2,597 protein isoforms supported through unique peptides, with an additional 2,280 isoforms nominated upon incorporation of long-read transcript evidence. We characterized a novel alternative acceptor for endothelial-related gene <em>CDH5</em>, suggesting potential changes in its associated signaling pathways. Finally, we identified novel protein isoforms arising from a diversity of splicing mechanisms supported by uniquely mapped novel peptides. Our results represent a high resolution atlas of known and novel isoforms of potential relevance to endothelial phenotypes and function.</p>
Dataset and code for paper "An automated quantification tool for angiogenic sprouting from endothelial spheroids"
<p>This repository contains raw data and code for the manuscript with DOI: 10.3389/fphar.2022.883083</p>
TIRF imaging data of neutrophils migrating underneath endothelial cells
<p>This data is used in the publication "Endothelial Focal Adhesions Are Functional Obstacles for Leukocytes During Basolateral Crawling": https://www.frontiersin.org/articles/10.3389/fimmu.2021.667213/full</p> <p> </p> <p><strong>TIRF Microscopy</strong></p> <p>Lentiviral transduction was used to generate an endothelial cell line expressing mNeonGreen-Paxillin (derived from addgene plasmid # 129604). Cells were imaged with a Nikon Ti-E microscope equipped with a motorized TIRF Illuminator unit, a 60x TIRF objective (60x Plan Apo, Oil DIC N2, NA =1.49, WD = 120 um) and Perfect Focus System. Images were acquired with an Andor iXon 897 EMCCD camera and the Nikon NIS elements software. mNeonGreen was imaged using the 488 nm laser line and calcein red-orange was imaged using the 561 nm laser line. A quad split dichroic mirror (405 nm, 488 nm, 561 nm, 640 nm) was used in combination with dual band pass emission filter (515 to 545 nm, 600 to 650 nm). To achieve a larger field of view a 3 x 3 tile scans was acquired with 15% overlap stitching on the GFP channel. Time lapse images were taken every 10 s.</p>
Tyrosine-protein kinase Yes controls endothelial junctional plasticity and barrier integrity by regulating VE-cadherin phosphorylation and endocytosis
<p><strong>Abstract</strong></p> <p>Vascular endothelial (VE)-cadherin in endothelial adherens junctions is an essential component of the vascular barrier, critical for tissue homeostasis and implicated in diseases such as cancer and retinopathies. Inhibitors of Src cytoplasmic tyrosine kinase have been applied to suppress VE-cadherin tyrosine phosphorylation and prevent excessive leakage, edema and high interstitial pressure. Here we show that the Src-related Yes tyrosine kinase, rather than Src, is localized at endothelial cell (EC) junctions where it becomes activated in a flow-dependent manner. EC-specific <em>Yes1</em> deletion suppresses VE-cadherin phosphorylation and arrests VE-cadherin at EC junctions. This is accompanied by loss of EC collective migration and exaggerated agonist-induced macromolecular leakage. Overexpression of <em>Yes1</em> causes ectopic VE-cadherin phosphorylation, while vascular leakage is unaffected. In contrast, in EC-specific Src-deficiency, VE-cadherin internalization is maintained, and leakage is suppressed. In conclusion, Yes-mediated phosphorylation regulates constitutive VE-cadherin turnover, thereby maintaining endothelial junction plasticity and vascular integrity.</p> <p><strong>Method for retinal EC distribution analysis</strong></p> <p>Chimeric recombination was induced in iSuRe-Cre+ mice at P3 by i.p. injection of tamoxifen (100 µg/mouse, Sigma). Retinas were taken at P7 and P15, immunostained for CD31 and flat-mounted. Images were taken by z-stack tile scanning using a 10X objective on a confocal microscope (Leica SP8). Maximum intensity projection images of whole retinas were used for image segmentation, which was performed with ImageJ resources. The maximum projection of the MbTomato channel threshold was established to distinguish MbTomato+ cells from the background. Outliers with a radius between 0.2-1.0 µm were removed. The CD31 channel (after maximum projection) was used to define the outlines of veins and arteries; the optic nerve was used as a mask to define a referential system. For computational analysis, a bespoken Python-based workflow was employed, accessible on GitHub (https://github.com/wgiese/retina-vein-artery-cs). For every pixel in the image, three numbers were computed (using the mask as referential): (1) distance to the nearest vein (d<sub>v</sub>), (2) distance to the nearest artery (d<sub>a</sub>) and (3) radial distance to the optic nerve (r). From these measures, the relative distances by ϕ<sub>v-a</sub> = d<sub>v/</sub>(d<sub>v</sub> + d<sub>a</sub>) were obtained. The EC distribution was computed by performing the operation for all YFP-positive pixels, which were used as a proxy for EC distribution. A kernel density estimation was used to approximate the underlying EC distribution in the 2D coordinate system spanned by ϕ<sub>v-a</sub> and r. </p>
Therapeutic activation of endothelial sphingosine 1-phosphate receptor-1 by chaperone-bound S1P suppresses proliferative retinal neovascularization
<p>Sphingosine-1-phosphate (S1P), the circulating HDL-bound lipid mediator that acts via S1P receptors (S1PR), is required for normal vascular development. The role of this signaling axis in vascular retinopathies is unclear. Here we show in a mouse model of oxygen-induced retinopathy (OIR) that endothelial overexpression of <em>S1pr1</em> suppresses while endothelial knockout of <em>S1pr1</em> worsens neovascular tuft formation. Furthermore, neovascular tufts are increased in <em>Apom<sup>-/-</sup> </em>mice which lack HDL-bound S1P while they are suppressed in <em>Apom<sup>TG</sup> </em>mice which has more circulating HDL-S1P. These results suggest that circulating HDL-S1P activation of endothelial S1PR1 suppresses neovascular pathology in OIR. Additionally, systemic administration of ApoM-Fc-bound S1P or a small molecule Gi-biased S1PR1 agonist suppressed neovascular tuft formation. Circulating HDL-S1P activation of endothelial S1PR1 may be a key protective mechanism to guard against neovascular retinopathies that occur not only in premature infants but also in diabetes and aging.</p>
Dataset related to: Empagliflozin protects glomerular endothelial cell architecture in experimental diabetes through the VEGF-A/caveolin-1/PV-1 signaling pathway
<p>The files contain all the dataset included in the manuscript divided by figures.</p> <p>Abstract<br> In addition to having blood glucose-lowering effects, inhibitors of sodium glucose cotransporter 2 (SGLT2) afford renoprotection in diabetes. We sought to investigate which components of the glomerular filtration barrier could be involved in the antiproteinuric and renoprotective effects of SGLT2 inhibition in diabetes. BTBR (black and tan, brachyuric) <em>ob/ob</em> mice that develop a type 2 diabetic nephropathy received a standard diet with or without empagliflozin for 10 weeks, starting at 8 weeks of age, when animals had developed albuminuria. Empagliflozin caused marked decreases in blood glucose levels and albuminuria but did not correct glomerular hyperfiltration. The protective effect of empagliflozin against albuminuria was not due to a reduction in podocyte damage as empagliflozin did not affect the larger podocyte filtration slit pore size nor the defective expression of nephrin and nestin. Empagliflozin<br> did not reduce the thickening of the glomerular basement membrane. In BTBR <em>ob/ob</em> mice, the most profound abnormality seen using electron microscopy was in the endothelial aspect of the glomerular capillary, with significant loss of endothelial fenestrations. Remarkably, empagliflozin ameliorated the subverted microvascular endothelial ultrastructure. Caveolae and bridging diaphragms between adjacent endothelial fenestrae were seen in diabetic mice and associated with increased expression of caveolin-1 and the appearance of PV-1. These endothelial abnormalities were limited by the SGLT2 inhibitor. Although no expression of SGLT2 was found in glomerular endothelial cells, SGLT2 was expressed in the podocytes of diabetic mice. VEGF-A, which is a known stimulus for endothelial caveolin-1 and PV-1, was increased in podocytes of BTBR <em>ob/ob</em> mice and normalized by SGLT2 inhibitor treatment.<br> Thus, empagliflozin’s protective effect on the glomerular endothelium of diabetic mice could be due to a limitation of the paracrine signaling of podocyte-derived VEGF-A that resulted in a reduction of the abnormal endothelial caveolin-1 and PV-1, with the consequent preservation of glomerular endothelial function and permeability.</p>
Vascular Endothelial Growth Factor-B (VEGF-B) Blockade With the Monoclonal Antibody CSL346 in Subjects With Diabetic Kidney Disease
ClinicalTrials.gov study NCT04419467. IPD Sharing: YES. Countries: 6. Publications: 1.
Impact of Donor Diabetes on DMEK Success and Endothelial Cell Loss
ClinicalTrials.gov study NCT05134480. IPD Sharing: YES. Countries: 1. Publications: 3.
Data from: Hypoxia blunts angiogenic signaling and upregulates the antioxidant system in elephant seal endothelial cells
Open the record for dataset details and reuse information.
Data from: Acute cytotoxicity and increased vascular endothelial growth factor after in vitro nitrogen mustard vapor exposure
<p>RATIONALE: Nitrogen mustard (NM) is a highly toxic alkylating agent. It is classified as chemical threat due to its potential use as a warfare agent. When inhaled, mustard exposure can cause both acute and chronic lung injury. The aims of this study are to develop an in vitro culture system for modeling mustard-induced airway injury and to identify growth factors contributing to airway pathology.</p> <p><br> METHODS: Primary human bronchial epithelial cells co-cultured with primary human pulmonary endothelial cells were exposed to NM (25, 50, 100, 250 or 500 µM) or PBS (control) for 1 hour. Lactate dehydrogenase (LDH) and trans-epithelial electrical resistance (TEER) were measured prior to and 24 hours after NM exposure. Endothelial cultures were then stained for live/dead staining. Exposed airway media was also analyzed for growth factors using Luminex multiplex technology. </p> <p><br> RESULTS: A one-hour NM vapor exposure increased supernatant LDH and decreased TEER at 24 hours for all cultures exposed to NM concentrations greater than or equal to 50 µM. Evidence of endothelial cell death occurred at NM concentrations of 250 and 500 µM. Vascular endothelial growth factor (VEGF) signaling, specifically VEGF-A and placental growth factor (PlGF), increased in NM-exposed co-culture media compared to PBS controls. </p> <p><br> CONCLUSIONS: NM vapor exposure causes significant airway epithelial and endothelial injury. Increased VEGF signaling occurred in airway co-cultures exposed to higher NM concentrations with concurrent endothelial cell death. Future studies are required to validate the role of VEGF signaling in both acute and chronic mustard-induced airway pathology. </p>
Characterization of photorecruitable Guanine Exchange Factors for the study of Rho GTPases in endothelial cells
<p>Time lapses of respective figures belonging to the report titled "<strong>Characterization of photorecruitable Guanine Exchange Factors for the study of Rho GTPases in endothelial cells"</strong>. This report was written as part of the Msc programe in Biomedical Science of the University of Amsterdam. </p>
Influence of polymorphisms in the vascular endothelial growth factor gene on allograft rejection after kidney transplantation: a meta-analysis
<p><span><b><i>Purpose</i></b><i> </i>Reported associations of allograft rejection in kidney transplant patients with <i>VEGF</i> single nucleotide polymorphisms (SNPs) have been inconsistent between studies, which prompted a meta-analysis to obtain more precise estimates.</span></p> <p><span><b><i>Methods</i></b><i> </i>Using the PICO elements, kidney transplant patients (P) were compared by genotype data between rejectors (I) and non-rejectors (C) in order to determine the risk of allograft rejection (O) attributed to the <i>VEGF</i> SNPs. Literature search of four databases yielded seven articles. To calculate risks for allograft rejection, four SNPs were examined. Meta-analysis treatments included outlier and subgroup analyses, the latter was based on ethnicity (Indians/Caucasians) and rejection type (acute/chronic). Multiple comparisons were corrected with the Bonferroni test. </span></p> <p><span><span><b><i>Results</i></b> Five highly significant outcomes (P<sup>a</sup> < 0.01) survived Bonferroni correction, one of which showed reduced risk for the <i>var</i> allele (OR 0.61, 95% CI 0.45-0.82). The remaining four indicated increased risk for the <i>wt</i> allele where the chronic rejection (OR 2.10, 95% CI 1.36-3.24) and Indian (OR 1.44, 95% CI 1.13-1.84) subgroups were accorded susceptibility status. </span></span></p> <p><span><b><i>Conclusions</i></b> Risk associations for renal allograft rejection were increased and reduced on account of the <i>wt</i> and <i>var</i> alleles, respectively. These findings could render the <i>VEGF</i> polymorphisms useful in the clinical genetics of kidney transplantation. </span></p>
Assessment of endothelial cell function and physiological microcirculatory reserve by video microscopy using a topical acetylcholine and nitroglycerin challenge - Individual subject data
<p>This dataset contains individual subject data for microcirculatory parameters assessed in the present study. Macrocirculatory parameters are not included at this time due to the present study being part of a larger, partially unpublished project.</p>
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.