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 Salmonella Typhimurium L Forms Induce Vascular Endothelial Cell Apoptosis via Mitochondrial-Dependent Pathway

2020 ◽  
Author(s):  
Jinhai Zhai ◽  
Tao Zhang ◽  
Cuiping Yang ◽  
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 Background Salmonella 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.

Role of protein kinase C β2 activation in TNF-α-induced human vascular endothelial cell apoptosis

2009 ◽  
Vol 87 (3) ◽  
pp. 221-229 ◽  
Author(s):  
Fang Wang ◽  
Hui-min Liu ◽  
Michael G. Irwin ◽  
Zhong-yuan Xia ◽  
Zhiyong Huang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Endothelial Cell Apoptosis ◽  
Human Vascular Endothelial Cell ◽  
Kinase C ◽  
Tnf Α

The circulatory inflammatory cytokine tumor necrosis factor alpha (TNF-α) is increased in pathologic conditions that initiate or exacerbate vascular endothelial injury, such as diabetes. Protein kinase C (PKC) has been shown to play a critical role in TNF-α-induced human endothelial cell apoptosis. However, the relative roles played by specific isoforms of PKC in TNF-α-induced human endothelial cell apoptosis have not been addressed. We investigated the effects of a selective PKCβ2 inhibitor (CGP53353) on TNF-α-induced apoptosis in human vascular endothelial cells (cell line ECV304) and on the production of reactive oxygen species and nitric oxide, and compared its effects with rottlerin, a reagent that has been shown to reduce PKCδ protein levels. Cultured human vascular endothelial cells (ECV304) were treated for 24 h with one of 4 regimes: 40 ng/mL TNF-α alone (TNF-α), TNF-α with 10 µmol/L rottlerin (T+rottlerin), TNF-α with 1 µmol/L CGP53353 (T+CGP), or untreated (control). Cell viability was measured by MTT assay, and cell apoptosis was assessed by flow cytometry. TNF-α-induced endothelial cell apoptosis was associated with dramatic increases in production of intracellular hydrogen peroxide (approximately 20 times greater than control) and superoxide (approximately 16 times greater than control), as measured by dichlorofluorescein and dihydroethidium fluorescent staining, respectively. This increase was accompanied by reduced activity of superoxide dismutase and glutathione peroxidase and, subsequently, an increase in the lipid peroxidation product malondialdehyde. CGP53353, but not rottlerin, abolished or attenuated all these changes. We conclude that PKCβ2 plays a major role in TNF-α-induced human vascular endothelial cell apoptosis.

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 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.

scholarly journals L-Cystathionine Protects against Homocysteine-Induced Mitochondria-Dependent Apoptosis of Vascular Endothelial Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Xiuli Wang ◽  
Yi Wang ◽  
Lulu Zhang ◽  
Da Zhang ◽  
Lu Bai ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Caspase 3 ◽  
Mitochondrial Permeability Transition ◽  
Vascular Endothelial Cells ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Vascular Endothelial ◽  
Caspase 9 ◽  
Mitochondrial Superoxide ◽  
Mptp Opening

The study was aimed at investigating the effects of L-cystathionine on vascular endothelial cell apoptosis and its mechanisms. Cultured human umbilical vein endothelial cells (HUVECs) were used in the study. Apoptosis of vascular endothelial cells was induced by homocysteine. Apoptosis, mitochondrial superoxide anion, mitochondrial membrane potential, mitochondrial permeability transition pore (MPTP) opening, and caspase-9 and caspase-3 activities were examined. Expression of Bax, Bcl-2, and cleaved caspase-3 was tested and BTSA1, a Bax agonist, and HUVEC Bax overexpression was used in the study. Results showed that homocysteine obviously induced the apoptosis of HUVECs, and this effect was significantly attenuated by the pretreatment with L-cystathionine. Furthermore, L-cystathionine decreased the production of mitochondrial superoxide anion and the expression of Bax and restrained its translocation to mitochondria, increased mitochondrial membrane potential, inhibited mitochondrial permeability transition pore (MPTP) opening, suppressed the leakage of cytochrome c from mitochondria into the cytoplasm, and downregulated activities of caspase-9 and caspase-3. However, BTSA1, a Bax agonist, or Bax overexpression successfully abolished the inhibitory effect of L-cystathionine on Hcy-induced MPTP opening, caspase-9 and caspase-3 activation, and HUVEC apoptosis. Taken together, our results indicated that L-cystathionine could protect against homocysteine-induced mitochondria-dependent apoptosis of HUVECs.

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 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 Proteome-Scale Profiling Reveals MAFG and MAFF as Two Novel Candidate Key Transcription Factors Involved in Palmitic acid Induced Umbilical Vein Endothelial Cells Apoptosis

2020 ◽  
Author(s):  
Mangyuan Wang ◽  
Fen Liu ◽  
Binbin Fang ◽  
Qiang Huo ◽  
Yining Yang
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Umbilical Vein ◽  
Vascular Endothelial Cell ◽  
P Value ◽  
Vascular Endothelial ◽  
Endothelial Cell Apoptosis ◽  
Family Protein ◽  
Umbilical Vein Endothelial Cells

Abstract Backgrounds: Vascular endothelial cell apoptosis is the first risk factor of atherosclerosis (AS), and it can be induced by high doses of glucose and palmitic acid (PA). The purpose of our study is to use a new generation of high-throughput transcription factors (TFs) detecting method to identify novel candidate key TFs involved in PA-induced vascular endothelial cell apoptosis.Methods: Human umbilical vein endothelial cells (HUVECs) were treated with 0µM PA (control group), 250µM PA (group 1), or 500µM PA (group 2). Candidate TFs among the three groups were determined by significant changes according to t-test, and pathway enrichment, western blot (WB) and RT-qPCR were then performed.Results: Fifty-one TFs showing with significant p value were identified, and 24 TFs with significant p value plus fold change > 2 and with dose-dependence were identified with 12 TFs biologically validated in former studies. Two of the remaining 12 novel TFs, v-maf musculoaponeurotic fibrosarcoma oncogene family protein G (MAFG) and v-maf musculoaponeurotic fibrosarcoma oncogene family protein F (MAFF), were matched to AS known signalling pathways and were validated by WB and RT-qPCR in our study.Conclusions: We identified MAFG and MAFF as novel candidate key TFs in vascular endothelial cell apoptosis, which is the key initial process of AS.

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