scholarly journals Transcriptional and epigenomic landscapes of CNS and non-CNS vascular endothelial cells

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Mark F Sabbagh ◽  
Jacob S Heng ◽  
Chongyuan Luo ◽  
Rosa G Castanon ◽  
Joseph R Nery ◽  
...  
Keyword(s):  
Regulatory Networks ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial Cell ◽  
Regulatory Elements ◽  
Vascular Endothelial ◽  
Organ Specific ◽  
The Central Nervous System ◽  
Tf Gene ◽  
Canonical Wnt ◽  
Tip Cells

Vascular endothelial cell (EC) function depends on appropriate organ-specific molecular and cellular specializations. To explore genomic mechanisms that control this specialization, we have analyzed and compared the transcriptome, accessible chromatin, and DNA methylome landscapes from mouse brain, liver, lung, and kidney ECs. Analysis of transcription factor (TF) gene expression and TF motifs at candidate cis-regulatory elements reveals both shared and organ-specific EC regulatory networks. In the embryo, only those ECs that are adjacent to or within the central nervous system (CNS) exhibit canonical Wnt signaling, which correlates precisely with blood-brain barrier (BBB) differentiation and Zic3 expression. In the early postnatal brain, single-cell RNA-seq of purified ECs reveals (1) close relationships between veins and mitotic cells and between arteries and tip cells, (2) a division of capillary ECs into vein-like and artery-like classes, and (3) new endothelial subtype markers, including new validated tip cell markers.

Alterations in Vascular Endothelial Cell-related Plasma Proteins In Thalassaemic Patients and their Correlation with Clinical Symptoms

1995 ◽  
Vol 74 (04) ◽  
pp. 1045-1049 ◽  
Author(s):  
P Butthep ◽  
A Bunyaratvej ◽  
Y Funahara ◽  
H Kitaguchi ◽  
S Fucharoen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Immunosorbent Assay ◽  
Plasma Proteins ◽  
Clinical Symptoms ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial Cell ◽  
Enzyme Linked Immunosorbent Assay ◽  
Vascular Endothelial ◽  
Leg Ulcers

SummaryAn increased level of plasma thrombomodulin (TM) in α- and β- thalassaemia was demonstrated using an enzyme-linked immunosorbent assay (ELISA). Nonsplenectomized patients with β-thalassaemia/ haemoglobin E (BE) had higher levels of TM than splenectomized cases (BE-S). Patients with leg ulcers (BE-LU) were found to have the highest increase in TM level. Appearance of larger platelets in all types of thalassaemic blood was observed indicating an increase in the number of younger platelets. These data indicate that injury of vascular endothelial cells is present in thalassaemic patients.

scholarly journals Salmonella Typhimurium L Forms Induce Vascular Endothelial Cell Apoptosis via Mitochondrial-dependent Pathway

2021 ◽  
Author(s):  
Jinhai Zhai ◽  
Cuiping Yang ◽  
Tao Zhang ◽  
Dengyu Chen
Keyword(s):  
Endothelial Cells ◽  
Salmonella Typhimurium ◽  
Cell Apoptosis ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial Cell ◽  
Intestinal Lumen ◽  
Vascular Endothelial ◽  
Caspase 9 ◽  
Apoptosis Pathway ◽  
Significant Difference

Abstract BackgroundSalmonella typhimurium is a pathogenic gram-negative bacterium, which is found primarily in the intestinal lumen. It often causes diarrhea in infants and young children and leads to food poisoning, as well as septicemia and septic shock. In this study, we investigated the phenomenon and mechanism of vascular endothelial cells apoptosis induced by Salmonella typhimurium L forms, in order to recognize and control Salmonella typhimurium L-form infection.Methods The apoptosis of vascular endothelial cells at 8 hours after infection with Salmonella typhimurium L forms was determined by flow cytometric assay and fluoroscopy of Annexin V-FITC/PI staining. Caspase-9 was detected by spectrophotometer. Results Salmonella typhimurium L forms can induce apoptosis of vascular endothelial cells, with significant difference in the apoptosis rate compared with the control. Caspase-9 expression is higher than that of the control. Conclusion The ability to induce cell apoptosis of vascular endothelial cells by Salmonella typhimurium L forms may be related to mitochondria apoptosis pathway depending on Caspase-9.

scholarly journals Immobilized DNA aptamers used as potent attractors for vascular endothelial cell: in vitro study of female rat

2020 ◽  
Vol 40 (1) ◽  
Author(s):  
Jung-Joon Cha ◽  
Hoyeon Lee ◽  
Miyoung Kim ◽  
Juyoung Kang ◽  
Hanlim Song ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Function ◽  
Therapeutic Potential ◽  
Vascular Endothelial Cells ◽  
Specific Binding ◽  
Vascular Endothelial Cell ◽  
Dna Aptamers ◽  
Female Rat ◽  
Vascular Endothelial

Abstract Vascular endothelial cells are essential to vascular function and maintenance. Dysfunction of these cells can lead to the development of cardiovascular disease or contribute to tumorigenesis. As such, the therapeutic modulation and monitoring of vascular endothelial cells are of significant clinical interest, and several endothelial-specific ligands have been developed for drug delivery and the monitoring of endothelial function. However, the application of these ligands has been limited by their high cost and tendency to induce immune responses, highlighting a need for alternate methods of targeting vascular endothelial cells. In the present study, we explore the therapeutic potential of DNA aptamers. Using cell-SELEX technology, we identified two aptamers with specific binding affinity for vascular endothelial cells and propose that these molecules show potential for use as new ligands for drug and biomarker research concerning vascular endothelial cells.

Estrogens modulate bovine vascular endothelial cell permeability and HSP 25 expression concomitantly

1998 ◽  
Vol 275 (3) ◽  
pp. H1011-H1015 ◽  
Author(s):  
F. Delarue ◽  
S. Daunes ◽  
R. Elhage ◽  
A. Garcia ◽  
F. Bayard ◽  
...  
Keyword(s):  
Vascular Endothelial Cells ◽  
Low Density Lipoprotein ◽  
Vascular Endothelial Cell ◽  
Density Lipoprotein ◽  
Endothelial Permeability ◽  
Fluid Phase ◽  
Cell Permeability ◽  
Vascular Endothelial ◽  
Macromolecular Transport

The atheroprotective properties of estrogens are supported by clinical data from postmenopausal women who use estrogen replacement therapy. However, the mechanisms mediating activity remain unknown, and it has been suggested that estrogens may help to modulate endothelial permeability to atherogenic lipoproteins. In these studies we used bovine vascular endothelial cells as an in vitro model to show that estrogens were able to regulate low-density lipoprotein transport and permeability of the endothelial monolayer. Macromolecular transport was observed to be a second-order polynomial function of estrogen concentration. Moreover, this regulation was correlated with expression of heat shock protein (HSP) 25, which is known to influence fluid phase pinocytosis and cytoskeleton remodeling, thus suggesting a role for HSP 25 in the estrogenic control of transcellular permeability of the endothelium monolayer.

Calcium and Calmodulin Regulate Mercury-induced Phospholipase D Activation in Vascular Endothelial Cells

2009 ◽  
Vol 28 (3) ◽  
pp. 190-206 ◽  
Author(s):  
Alon Peltz ◽  
Shariq I. Sherwani ◽  
Sainath R. Kotha ◽  
Jessica N. Mazerik ◽  
Elizabeth S. O’Connor Butler ◽  
...  
Keyword(s):  
Cardiovascular Diseases ◽  
Phospholipase D ◽  
Vascular Endothelial Cells ◽  
Protective Action ◽  
Vascular Endothelial Cell ◽  
Mercury Chloride ◽  
Channel Blockers ◽  
Significant Finding ◽  
Vascular Endothelial ◽  
The Novel

Earlier, we reported that mercury, the environmental risk factor for cardiovascular diseases, activates vascular endothelial cell (EC) phospholipase D (PLD). Here, we report the novel and significant finding that calcium and calmodulin regulated mercury-induced PLD activation in bovine pulmonary artery ECs (BPAECs). Mercury (mercury chloride, 25 μM; thimerosal, 25 μM; methylmercury, 10 μM) significantly activated PLD in BPAECs. Calcium chelating agents and calcium depletion of the medium completely attenuated the mercury-induced PLD activation in ECs. Calmodulin inhibitors significantly attenuated mercury-induced PLD activation in BPAECs. Despite the absence of L-type calcium channels in ECs, nifedipine, nimodipine, and diltiazem significantly attenuated mercury-induced PLD activation and cytotoxicity in BPAECs. This study demonstrated the importance of calcium and calmodulin in the regulation of mercury-induced PLD activation and the protective action of L-type calcium channel blockers against mercury cytotoxicity in vascular ECs, suggesting mechanisms of mercury vasculotoxicity and mercury-induced cardiovascular diseases.

CYLD regulates angiogenesis by mediating vascular endothelial cell migration

Blood ◽  
2010 ◽  
Vol 115 (20) ◽  
pp. 4130-4137 ◽  
Author(s):  
Jinmin Gao ◽  
Lei Sun ◽  
Lihong Huo ◽  
Min Liu ◽  
Dengwen Li ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Migration ◽  
Endothelial Cell ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial Cell ◽  
Tube Formation ◽  
Endothelial Cell Migration ◽  
Vascular Endothelial

Cylindromatosis (CYLD) is a deubiquitinase that was initially identified as a tumor suppressor and has recently been implicated in diverse normal physiologic processes. In this study, we have investigated the involvement of CYLD in angiogenesis, the formation of new blood vessels from preexisting ones. We find that knockdown of CYLD expression significantly impairs angiogenesis in vitro in both matrigel-based tube formation assay and collagen-based 3-dimensional capillary sprouting assay. Disruption of CYLD also remarkably inhibits angiogenic response in vivo, as evidenced by diminished blood vessel growth into the angioreactors implanted in mice. Mechanistic studies show that CYLD regulates angiogenesis by mediating the spreading and migration of vascular endothelial cells. Silencing of CYLD dramatically decreases microtubule dynamics in endothelial cells and inhibits endothelial cell migration by blocking the polarization process. Furthermore, we identify Rac1 activation as an important factor contributing to the action of CYLD in regulating endothelial cell migration and angiogenesis. Our findings thus uncover a previously unrecognized role for CYLD in the angiogenic process and provide a novel mechanism for Rac1 activation during endothelial cell migration and angiogenesis.

scholarly journals CD34 marks angiogenic tip cells in human vascular endothelial cell cultures

Angiogenesis ◽  
2012 ◽  
Vol 15 (1) ◽  
pp. 151-163 ◽  
Author(s):  
Martin J. Siemerink ◽  
Ingeborg Klaassen ◽  
Ilse M. C. Vogels ◽  
Arjan W. Griffioen ◽  
Cornelis J. F. Van Noorden ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Cultures ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Human Vascular Endothelial Cell ◽  
Endothelial Cell Cultures ◽  
Tip Cells

scholarly journals Endothelial HIF signaling regulates pulmonary fibrosis-associated pulmonary hypertension

2016 ◽  
Vol 310 (3) ◽  
pp. L249-L262 ◽  
Author(s):  
Andrew J. Bryant ◽  
Ryan P. Carrick ◽  
Melinda E. McConaha ◽  
Brittany R. Jones ◽  
Sheila D. Shay ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Pulmonary Hypertension ◽  
Endothelial Cell ◽  
Pulmonary Fibrosis ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial Cell ◽  
Tissue Growth ◽  
Vascular Endothelial ◽  
Pulmonary Vessel ◽  
Deficient Mice

Pulmonary hypertension (PH) complicating chronic parenchymal lung disease, such as idiopathic pulmonary fibrosis, results in significant morbidity and mortality. Since the hypoxia-inducible factor (HIF) signaling pathway is important for development of pulmonary hypertension in chronic hypoxia, we investigated whether HIF signaling in vascular endothelium regulates development of PH related to pulmonary fibrosis. We generated a transgenic model in which HIF is deleted within vascular endothelial cells and then exposed these mice to chronic intraperitoneal bleomycin to induce PH associated with lung fibrosis. Although no differences in the degree of fibrotic remodeling were observed, we found that endothelial HIF-deficient mice were protected against development of PH, including right ventricle and pulmonary vessel remodeling. Similarly, endothelial HIF-deficient mice were protected from PH after a 4-wk exposure to normobaric hypoxia. In vitro studies of pulmonary vascular endothelial cells isolated from the HIF-targeted mice and controls revealed that endothelial HIF signaling increases endothelial cell expression of connective tissue growth factor, enhances vascular permeability, and promotes pulmonary artery smooth muscle cell proliferation and wound healing ability, all of which have the potential to impact the development of PH in vivo. Taken together, these studies demonstrate that vascular endothelial cell HIF signaling is necessary for development of hypoxia and pulmonary fibrosis associated PH. As such, HIF and HIF-regulated targets represent a therapeutic target in these conditions.

scholarly journals Inhibition of vascular endothelial cell prostacyclin synthesis by plasmin

Blood ◽  
1989 ◽  
Vol 74 (3) ◽  
pp. 1015-1020 ◽  
Author(s):  
AI Schafer ◽  
R Rodriguez ◽  
J Loscalzo ◽  
MA Jr Gimbrone
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial Cell ◽  
Fibrinolytic System ◽  
Pharmacologic Therapy ◽  
Ionophore A23187 ◽  
Vascular Endothelial ◽  
Plasmin Activity ◽  
Dependent Inhibition ◽  
Dose Dependent

Vascular endothelial cells (EC) play an active role in the synthesis and assembly of components of the fibrinolytic system and the generation of the major fibrinolytic protease plasmin. However, the reciprocal effects of plasmin on EC function have not been previously examined. We have studied the actions of plasmin on the production of prostacyclin (PGI2) by cultured human umbilical vein (HUVEC) and bovine aortic (BAEC) endothelial cells. Plasmin causes little or no direct stimulation of PGI2 formation by EC. Preincubation of EC with plasmin, however, produces a time- and concentration-dependent inhibition of ionophore A23187-, thrombin-, and histamine-induced PGI2 synthesis; a smaller inhibitory effect on arachidonate- and PGH2-induced PGI2 synthesis is found. Incubation of HUVEC or BAEC with a physiologic concentration of plasminogen (180 micrograms/mL) and recombinant tissue plasminogen activator (tPA) generates tPA dose-dependent plasmin activity that exceeds that generated in the absence of EC. In the presence of plasminogen, tPA also causes a tPA dose-dependent inhibition of thrombin- and ionophore A23187-stimulated PGI2 production. PGI2 inhibitory plasmin activity is generated within the concentration range of tPA achieved in plasma during pharmacologic therapy with tPA. These findings suggest that vascular endothelial cells not only regulate activation of the fibrinolytic system but may also be targets of plasmin action on PGI2 synthesis in the modulation of hemostasis and thrombosis.

scholarly journals Early Ascorbic Acid Administration Prevents Vascular Endothelial Cell Damage In Septic Mice

2021 ◽  
Author(s):  
Yutaro Madokoro ◽  
Chinatsu Kamikokuryo ◽  
Shuhei Niiyama ◽  
Takashi Ito ◽  
Satoshi Hara ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Treatment Group ◽  
Vascular Endothelial Cells ◽  
Cell Damage ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Endothelial Cell Dysfunction ◽  
Endothelial Cell Damage ◽  
Cell Dysfunction ◽  
Late Group

Abstract Ascorbic acid (AsA) therapy for sepsis is thought to have a protective effect on vascular endothelial cells, but the effect of AsA therapy on endothelial cell dysfunction over time and the appropriate timing for AsA administration to demonstrate efficacy is unclear. Septic mice, induced by cecal ligation and puncture (CLP), were examined for the effect of AsA administration (200 mg/kg) on vascular endothelial cell dysfunction at two administration timings: early group (AsA was administered immediately after CLP) and late group (AsA was administered 12 h after CLP). Survival rates were compared between the early and late administration groups, and vascular endothelial cell damage, indicated by the dihydrobiopterin/tetrahydrobiopterin ratio, serum syndecan-1, and endothelial nitric oxide synthase, as well as liver damage, were examined. The early group showed significantly improved survival compared to the non-treatment group (p < 0.05), while the late group showed no improved survival compared to the non-treatment group. Early AsA administration suppressed damage to the vascular endothelial system and liver compared to the non-treatment group. In septic mice, early AsA administration immediately after CLP may have protective effects on vascular endothelial cells, resulting in reduced organ dysfunction and improved survival.

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