scholarly journals Effects of down-regulation of microRNA-23a on TNF-α-induced endothelial cell apoptosis through caspase-dependent pathways

2011 ◽  
Vol 93 (4) ◽  
pp. 623-632 ◽  
Author(s):  
Wei Ruan ◽  
Jun-mei Xu ◽  
Suo-bei Li ◽  
Ling-qing Yuan ◽  
Ru-ping Dai
Keyword(s):  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Endothelial Cell Apoptosis ◽  
Down Regulation ◽  
Tnf Α

scholarly journals Atherosclerosis-Associated Endothelial Cell Apoptosis by MiR-429-Mediated Down Regulation of Bcl-2

2015 ◽  
Vol 37 (4) ◽  
pp. 1421-1430 ◽  
Author(s):  
Tao Zhang ◽  
Feng Tian ◽  
Jing Wang ◽  
Jing Jing ◽  
Shan-Shan Zhou ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Cell Injury ◽  
Luciferase Reporter ◽  
Lower Percentage ◽  
Endothelial Cell Apoptosis ◽  
Down Regulation ◽  
Bioinformatics Analyses

Background/Aims: Endothelial cell injury and subsequent apoptosis play a key role in the development and pathogenesis of atherosclerosis, which is hallmarked by dysregulated lipid homeostasis, aberrant immunity and inflammation, and plaque-instability-associated coronary occlusion. Nevertheless, our understanding of the mechanisms underlying endothelial cell apoptosis is still limited. MicroRNA-429 (miR-29) is a known cancer suppressor that promotes cancer cell apoptosis. However, it is unknown whether miR-429 may be involved in the development of atherosclerosis through similar mechanisms. We addressed these questions in the current study. Methods: We examined the levels of endothelial cell apoptosis in ApoE (-/-) mice suppled with high-fat diet (HFD), a mouse model for atherosclerosis (simplified as HFD mice). We analyzed the levels of anti-apoptotic protein Bcl-2 and the levels of miR-429 in the purified CD31+ endothelial cells from mouse aorta. Prediction of the binding between miR-429 and 3'-UTR of Bcl-2 mRNA was performed by bioinformatics analyses and confirmed by a dual luciferase reporter assay. The effects of miR-429 were further analyzed in an in vitro model using oxidized low-density lipoprotein (ox-LDL)-treated human aortic endothelial cells (HAECs). Results: HFD mice developed atherosclerosis in 12 weeks, while the control ApoE (-/-) mice that had received normal diet (simplified as NOR mice) did not. HFD mice had significantly lower percentage of endothelial cells and significantly higher percentage of mesenchymal cells in the aorta than NOR mice. Significantly higher levels of endothelial cell apoptosis were detected in HFD mice, resulting from decreases in Bcl-2 protein, but not mRNA. The decreases in Bcl-2 in endothelial cells were due to increased levels of miR-429, which suppressed the translation of Bcl-2 mRNA via 3'-UTR binding. These in vivo findings were reproduced in vitro on ox-LDL-treated HAECs. Conclusion: Atherosclerosis-associated endothelial cell apoptosis may result from down regulation of Bcl-2, through increased miR-429 that binds and suppresses translation of Bcl-2 mRNA.

scholarly journals Endothelial cell apoptosis in brown adipose tissue of rats induced by hyperinsulinaemia: the possible role of TNF-α

2011 ◽  
Vol 55 (4) ◽  
pp. 34 ◽  
Author(s):  
M. Markelic ◽  
K. Velickovic ◽  
I. Golic ◽  
V. Otasevic ◽  
A. Stancic ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Endothelial Cell ◽  
Brown Adipose Tissue ◽  
Cell Apoptosis ◽  
Endothelial Cell Apoptosis ◽  
Brown Adipose ◽  
Tnf Α

Regulation of nicotine-induced apoptosis of pulmonary artery endothelial cells by treatment of N-acetylcysteine and vitamin E

2007 ◽  
Vol 26 (7) ◽  
pp. 595-602 ◽  
Author(s):  
R. Demiralay ◽  
N. Gürsan ◽  
H. Erdem
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Vitamin E ◽  
Pulmonary Artery ◽  
Cell Apoptosis ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Control Group ◽  
Endothelial Cell Apoptosis ◽  
Antioxidant Agents ◽  
Tnf Α

This study investigated the frequency of apoptosis in rat pulmonary artery endothelial cells after intraperitoneal nicotine injection, examining the roles of the inflammatory markers myeloperoxidase (MPO), tumour necrosis factor alpha (TNF-α ), and vascular endothelial growth factor (VEGF) in nicotine-induced vascular damage and the protective effects of two known antioxidant agents, N-acetylcysteine (NAC) and vitamin E. Female Wistar rats were divided into four groups, each composed of nine rats: negative control group, positive control group, NACtreated group (500 mg/kg), and vitamin E-treated group (500 mg/kg). Nicotine was intraperitoneally injected at a dosage of 0.6 mg/kg for 21 days. Following nicotine injection, the antioxidants were administered orally; treatment was continued until the rats were killed. Lung tissue samples were stained with hematoxylin-eosin (H&E) for histopathological assessments. Apoptosis level in endothelial cells was determined by using TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick endlabelling) method. Staining of cytoplasmic TNF-α and VEGF in endothelial cells, and perivascular MPO activity were evaluated by immunohistochemistry. The treatments with NAC and vitamin E significantly reduced the rate of nicotine-induced endothelial cell apoptosis. NAC and vitamin E significantly reduced the increases in the local production of TNF-α and VEGF, and perivascular MPO activity. This findings suggest that NAC can be as effective as vitamin E in protecting against nicotine-induced endothelial cell apoptosis. Human & Experimental Toxicology (2007) 26: 595—602.

Differential effect of MLC kinase in TNF-α-induced endothelial cell apoptosis and barrier dysfunction

2001 ◽  
Vol 280 (6) ◽  
pp. L1168-L1178 ◽  
Author(s):  
Irina Petrache ◽  
Alexander D. Verin ◽  
Michael T. Crow ◽  
Anna Birukova ◽  
Feng Liu ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Electrical Resistance ◽  
Stress Fiber ◽  
Fiber Formation ◽  
Endothelial Cell Apoptosis ◽  
Gap Formation ◽  
Barrier Dysfunction ◽  
Tnf Α ◽  
Mlc Phosphorylation

Tumor necrosis factor (TNF)-α is released in acute inflammatory lung syndromes linked to the extensive vascular dysfunction associated with increased permeability and endothelial cell apoptosis. TNF-α induced significant decreases in transcellular electrical resistance across pulmonary endothelial cell monolayers, reflecting vascular barrier dysfunction (beginning at 4 h and persisting for 48 h). TNF-α also triggered endothelial cell apoptosis beginning at 4 h, which was attenuated by the caspase inhibitor Z-Val-Ala-Asp-fluoromethylketone. Exploring the involvement of the actomyosin cytoskeleton in these important endothelial cell responses, we determined that TNF-α significantly increased myosin light chain (MLC) phosphorylation, with prominent stress fiber and paracellular gap formation, which paralleled the onset of decreases in transcellular electrical resistance and enhanced apoptosis. Reductions in MLC phosphorylation by the inhibition of either MLC kinase (ML-7, cholera toxin) or Rho kinase (Y-27632) dramatically attenuated TNF-α-induced stress fiber formation, indexes of apoptosis, and caspase-8 activity but not TNF-α-induced barrier dysfunction. These studies indicate a central role for the endothelial cell cytoskeleton in TNF-α-mediated apoptosis, whereas TNF-α-induced vascular permeability appears to evolve independently of contractile tension generation.

Effects and mechanism of arachidonic acid against TNF-α induced apoptosis of endothelial cells

2020 ◽  
pp. 1-7
Author(s):  
Ji-Xiong Chen ◽  
Xiao-Yan Huang ◽  
Ping Wang ◽  
Wen-Ting Lin ◽  
Wen-Xing Xu ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Endothelial Cells ◽  
Arachidonic Acid ◽  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Umbilical Vein ◽  
Arachidonic Acid Metabolite ◽  
Apoptotic Cells ◽  
Endothelial Cell Apoptosis ◽  
Tnf Α

This study aimed to investigate the effects of arachidonic acid metabolite epoxyeicosatrienoic acid (EETs) in the apoptosis of endothelial cells induced by tumor necrosis factor-alpha (TNF-α). After human umbilical vein endothelial cells were cultured, TNF-α/ActD, 14, 15-EET, and HMR-1098 were added, respectively, into the culture medium. The apoptosis level of endothelial cells was detected by flow cytometry. After TNF-α/ActD induced endothelial cell apoptosis, flow cytometry staining showed that endothelial cell apoptosis increased significantly, and the apoptotic cells were significantly reduced after the addition of 14, 15-EET. However, the apoptotic cells significantly increased after the addition of HMR-1098. Western Blot results showed that the phosphorylation levels of LC3-II and AMPK were increased after TNF-α/ActD induction, and the increase was noticeable after the addition of 14, 15-EET. However, the phosphorylation levels of LC3-II and AMPK significantly decreased after the addition of HMR-1098. The activity of Caspase-8 and -9 decreased significantly after the addition of 14, 15-EET but increased after the addition of HMR-1098. Arachidonic acid can inhibit TNF-α induced endothelial cell apoptosis by upregulating autophagy.

scholarly journals IGFBP-3 and TNF-α Regulate Retinal Endothelial Cell Apoptosis

2013 ◽  
Vol 54 (8) ◽  
pp. 5376 ◽  
Author(s):  
Qiuhua Zhang ◽  
Youde Jiang ◽  
Matthew J. Miller ◽  
Bonnie Peng ◽  
Li Liu ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Endothelial Cell Apoptosis ◽  
Tnf Α ◽  
Retinal Endothelial Cell ◽  
Igfbp 3
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