Arachidonic acid induces brain endothelial cell apoptosis via p38-MAPK and intracellular calcium signaling

2015 ◽  
Vol 98 ◽  
pp. 145-158 ◽  
Author(s):  
Justin Evans ◽  
YooSeung Ko ◽  
Wilmer Mata ◽  
Muhammad Saquib ◽  
Joel Eldridge ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Endothelial Cell ◽  
Calcium Signaling ◽  
Intracellular Calcium ◽  
P38 Mapk ◽  
Cell Apoptosis ◽  
Brain Endothelial Cell ◽  
Endothelial Cell Apoptosis ◽  
Intracellular Calcium Signaling

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 EF1A1/HSC70 Cooperatively Suppress Brain Endothelial Cell Apoptosis via Regulating JNK Activity

2016 ◽  
Vol 22 (10) ◽  
pp. 836-844 ◽  
Author(s):  
Ying Liu ◽  
Shu Jiang ◽  
Peng-Yuan Yang ◽  
Yue-Fan Zhang ◽  
Tie-Jun Li ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Brain Endothelial Cell ◽  
Endothelial Cell Apoptosis

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 Protective Effect of α-Mangostin on High Glucose Induced Endothelial Cell Apoptosis

2017 ◽  
Vol 15 (8) ◽  
pp. 579-587 ◽  
Author(s):  
Kanjana JITTIPORN ◽  
Primchanien MOONGKARNDI ◽  
Jutima SAMER ◽  
Wisuda SUVITAYAVAT
Keyword(s):  
Endothelial Cell ◽  
P38 Mapk ◽  
High Glucose ◽  
Cell Apoptosis ◽  
Umbilical Vein ◽  
Endothelial Cell Apoptosis ◽  
Toxic Dose ◽  
Cell Functions ◽  
Induced Apoptosis ◽  
Umbilical Vein Endothelial Cells

α-mangostin is a phenolic compound from pericarp of mangosteen. It has prominent anti-oxidant properties. Oxidative stress has been shown to be a major factor that disrupts cell functions including endothelium. High glucose (HG) induced ROS production plays a key role in endothelial cell apoptosis. However, the effect of α-mangostin on HG induced apoptosis has not been studied yet. This study demonstrates the effect of α-mangostin in HG induced human umbilical vein endothelial cells (HUVECs) apoptosis. The non-toxic dose of α-mangostin was determined using a MTT assay. Intracellular reactive oxygen species (ROS) and cell apoptosis were evaluated using DCF-DA and TUNEL assays, respectively. The signaling of α-mangostin was elucidated by western blotting. α-mangostin significantly and, dose-dependently, decreased HG induced ROS formation. Also, α-mangostin significantly attenuated HG induced endothelial cell apoptosis. In addition, α-mangostin suppressed HG induced apoptosis via JNK and p38-MAPK. According to our results, α-mangostin attenuated HG induced endothelial cell apoptosis through inhibition of phosphorylation of JNK and p38-MAPK.

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