The Role of Endogenous Nitric Oxide in Endothelial Cell Apoptosis Studied using Anti-sense Technology

2000 ◽  
Vol 28 (5) ◽  
pp. A376-A376
Author(s):  
C. R. Da Costa ◽  
A. P. Johnstone ◽  
J. E. Cartwright ◽  
G. StJ. Whitley ◽  
G. T. Williams
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Endothelial Cell Apoptosis ◽  
Endogenous Nitric Oxide

scholarly journals LncRNA LUADT1 sponges miR-195 to prevent cardiac endothelial cell apoptosis in sepsis

2020 ◽  
Vol 26 (1) ◽  
Author(s):  
Zhimin Zhang ◽  
Mingzhu Lv ◽  
Xiang Wang ◽  
Zheng Zhao ◽  
Daolong Jiang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Critical Role ◽  
Potential Interaction ◽  
Luciferase Reporter ◽  
Endothelial Cell Apoptosis ◽  
Luciferase Activity Assay ◽  
Apoptosis Related Protein

Abstract Background The oncogenic role of the newly identified lncRNA LUADT1 has been revealed in lung adenocarcinoma. It was reported that LUADT1 plays a critical role in multiple human diseases. This study was carried out to investigate the role of LUADT1 in sepsis. Methods Sixty patients with sepsis and sixty healthy volunteers were recruited for this study. Plasma samples were collected from all participants. Human primary coronary artery endothelial cells were also used in this study. The expression of Pim-1, miR-195 and LUADT1 were detected by RT-qPCR. The interaction between miR-195 and LUADT1 was determined by overexpression experiments and luciferase activity assay. Cell apoptosis was detected by flow cytometry. The expression of apoptosis-related protein was detected by Western blotting. Results Bioinformatics analysis revealed the potential interaction between LUADT1 and miR-195, which was confirmed by dual luciferase reporter assay. LUADT1 was downregulated in patients with sepsis. Moreover, LPS treatment downregulated the expression of LUADT1 in primary cardiac endothelial cells. Overexpression of LUADT1 and miR-195 did not affect the expression of each other in primary cardiac endothelial cells. Interestingly, overexpression of LUADT1 was found to upregulate the expression of Pim-1, a target of miR-195. In addition, it was found that overexpression of LUADT1 and Pim-1 reduced the enhancement effects of miR-195 on LPS-induced cardiac endothelial cell apoptosis. Conclusion In summary, LUADT1 may protect cardiac endothelial cells against apoptosis in sepsis by regulating the miR-195/Pim-1 axis.

Oxidized LDL-induced endothelial cell apoptosis: Role of mediator phospholipids and bFGF

2000 ◽  
Vol 151 (1) ◽  
pp. 215-216
Author(s):  
C. Chen ◽  
J. Yang ◽  
S. Luo ◽  
P. Chang ◽  
R. Gross ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Oxidized Ldl ◽  
Endothelial Cell Apoptosis

Cytosolic phospholipase A2-α is an early apoptotic activator in PEDF-induced endothelial cell apoptosis

2009 ◽  
Vol 296 (2) ◽  
pp. C273-C284 ◽  
Author(s):  
Tsung-Chuan Ho ◽  
Show-Li Chen ◽  
Yuh-Cheng Yang ◽  
Tzu-Hsiu Lo ◽  
Jui-Wen Hsieh ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
P38 Mapk ◽  
Cell Apoptosis ◽  
Nuclear Translocation ◽  
Mitogen Activated Protein Kinase ◽  
Endothelial Cell Apoptosis ◽  
P53 Expression ◽  
Ppar Γ

Pigment epithelium-derived factor (PEDF) is an intrinsic antiangiogenic factor and a potential therapeutic agent. Previously, we discovered the mechanism of PEDF-induced apoptosis of human umbilical vein endothelial cells (HUVECs) as sequential induction/activation of p38 mitogen-activated protein kinase (MAPK), peroxisome proliferator-activated receptor gamma (PPAR-γ), and p53. In the present study, we investigated the signaling role of cytosolic calcium-dependent phospholipase A2-α (cPLA2-α) to bridge p38 MAPK and PPAR-γ activation. PEDF induced cPLA2-α activation in HUVECs and in endothelial cells in chemical burn-induced vessels on mouse cornea. The cPLA2-α activation is evident from the phosphorylation and nuclear translocation of cPLA2-α as well as arachidonic acid release and the cleavage of PED6, a synthetic PLA2 substrate. Such activation can be abolished by p38 MAPK inhibitor. The PEDF-induced PPAR-γ activation, p53 expression, caspase-3 activity, and apoptosis can be abolished by both cPLA2 inhibitor and small interfering RNA targeting cPLA2-α. Our observation not only establishes the signaling role of cPLA2-α but also for the first time demonstrates the sequential activation of p38 MAPK, cPLA2-α, PPAR-γ, and p53 as the mechanism of PEDF-induced endothelial cell apoptosis.

scholarly journals Congestive heart failure induces endothelial cell apoptosis: protective role of carvedilol

2000 ◽  
Vol 36 (7) ◽  
pp. 2081-2089 ◽  
Author(s):  
Lothar Rössig ◽  
Judith Haendeler ◽  
Ziad Mallat ◽  
Benedicte Hugel ◽  
Jean-Marie Freyssinet ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Protective Role ◽  
Endothelial Cell Apoptosis

scholarly journals Role of VPO1, a newly identified heme-containing peroxidase, in ox-LDL induced endothelial cell apoptosis

2011 ◽  
Vol 51 (8) ◽  
pp. 1492-1500 ◽  
Author(s):  
Yong-Ping Bai ◽  
Chang-Ping Hu ◽  
Qiong Yuan ◽  
Jun Peng ◽  
Rui-Zheng Shi ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Endothelial Cell Apoptosis

scholarly journals MicroRNA-1185 Induces Endothelial Cell Apoptosis by Targeting UVRAG and KRIT1

2017 ◽  
Vol 41 (6) ◽  
pp. 2171-2182 ◽  
Author(s):  
Haoyuan Deng ◽  
Xia Chu ◽  
Zhenfeng Song ◽  
Xinrui Deng ◽  
Huan Xu ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Cell Injury ◽  
Luciferase Reporter ◽  
Endothelial Cell Apoptosis ◽  
Endothelial Apoptosis ◽  
Mechanistic Analysis ◽  
Interfering Rna ◽  
The Impact

Background/Aims: Atherosclerosis is a multifactorial chronic disease and is the main cause of death and impairment in the world. Endothelial injury and apoptosis play a crucial role in the onset and development of atherosclerosis. MicroRNAs (miRNAs) have been proven to be involved in the pathogenesis of atherosclerosis. However, studies of the functional role of apoptosis-related miRNAs in the endothelium during atherogenesis are limited. Methods: Cell injury and apoptosis were measured in five types of cells transfected with miR-1185 or co-transfected with miR-1185 and its inhibitor. Bioinformatics analysis and a luciferase reporter assay were used to confirm the targets of miR-1185. The effects of the targets of miR-1185 on endothelial apoptosis were determined using small-interfering RNA. Results: In this study, we first report that miR-1185 significantly promoted apoptosis in endothelial cells but not in vascular smooth muscle cells and macrophages. A mechanistic analysis showed that ultraviolet irradiation resistance-associated gene (UVRAG) and krev1 interaction trapped gene 1 (KRIT1), targets of miR-1185, mediated miR-1185-induced endothelial cell apoptosis. Conclusion: The results revealed the impact of miR-1185 on endothelial apoptosis, suggesting that miR-1185 may be a potential target for the prevention and treatment of atherosclerosis.

scholarly journals Endothelial Cell Apoptosis Induced by Antibodies Against Dengue Virus Nonstructural Protein 1 Via Production of Nitric Oxide

2002 ◽  
Vol 169 (4) ◽  
pp. 2215-2215 ◽  
Author(s):  
Chiou-Feng Lin ◽  
Huan-Yao Lei ◽  
Ai-Li Shiau ◽  
Hsiao-Sheng Liu ◽  
Trai-Ming Yeh ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cell ◽  
Dengue Virus ◽  
Cell Apoptosis ◽  
Nonstructural Protein ◽  
Endothelial Cell Apoptosis ◽  
Nonstructural Protein 1
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