scholarly journals RPS4Y1 Promotes High Glucose-Induced Endothelial Cell Apoptosis and Inflammation by Activation of the p38 MAPK Signaling

2021 ◽  
Vol Volume 14 ◽  
pp. 4523-4534
Author(s):  
Yuan Chen ◽  
Yiheng Chen ◽  
Chonghui Tang ◽  
Qian Zhao ◽  
Tailin Xu ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
P38 Mapk ◽  
High Glucose ◽  
Cell Apoptosis ◽  
Mapk Signaling ◽  
Endothelial Cell Apoptosis ◽  
Apoptosis And Inflammation

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.

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 Constant and intermittent high glucose enhances endothelial cell apoptosis through mitochondrial superoxide overproduction

2006 ◽  
Vol 22 (3) ◽  
pp. 198-203 ◽  
Author(s):  
Ludovica Piconi ◽  
Lisa Quagliaro ◽  
Roberta Assaloni ◽  
Roberto Da Ros ◽  
Amabile Maier ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
High Glucose ◽  
Cell Apoptosis ◽  
Endothelial Cell Apoptosis ◽  
Mitochondrial Superoxide ◽  
Intermittent High Glucose

scholarly journals Taurine prevents high-glucose-induced human vascular endothelial cell apoptosis

1999 ◽  
Vol 277 (6) ◽  
pp. C1229-C1238 ◽  
Author(s):  
Qiong di Wu ◽  
Jiang Huai Wang ◽  
Fiona Fennessy ◽  
H. Paul Redmond ◽  
David Bouchier-Hayes
Keyword(s):  
Endothelial Cell ◽  
High Glucose ◽  
Cell Apoptosis ◽  
Umbilical Vein ◽  
Vascular Endothelial Cell ◽  
Microvascular Disease ◽  
Diabetic Microangiopathy ◽  
Critical Event ◽  
Endothelial Cell Apoptosis ◽  
Human Vascular Endothelial Cell

Elevated blood glucose in uncontrolled diabetes is causally correlated with diabetic microangiopathy. Hyperglycemia-triggered accelerated endothelial cell apoptosis is a critical event in the process of diabetes-associated microvascular disease. The conditionally semiessential amino acid taurine has been previously shown to protect against human endothelial cell apoptosis. Therefore, this study was designed to investigate the role of taurine in the prevention of high-glucose-mediated cell apoptosis in human umbilical vein endothelial cells (HUVEC) and the mechanisms involved. Exposure of HUVEC to 30 mM glucose for 48 h (short-term) and 14 days (long-term) resulted in a significant increase in apoptosis, compared with normal glucose (5.5 mM; P < 0.05). High-glucose-induced DNA fragmentation preferentially occurred in the S phase cells. Mannitol (as osmotic control) at 30 mM failed to induce HUVEC apoptosis. Taurine prevented high-glucose-induced HUVEC apoptosis, which correlates with taurine attenuation of high-glucose-mediated increased intracellular reactive oxygen species (ROS) formation and elevated intracellular Ca2+ concentration ([Ca2+]i) level. Antioxidants, DMSO, N-acetyl cysteine, and glutathione, only partly attenuated high-glucose-induced HUVEC apoptosis. Glucose at 30 mM did not cause HUVEC necrosis. However, both glucose and mannitol at 60 mM caused HUVEC necrosis as represented by increased lactate dehydrogenase release and cell lysis. Taurine failed to prevent hyperosmolarity-induced cell necrosis. These results demonstrate that taurine attenuates hyperglycemia-induced HUVEC apoptosis through ROS inhibition and [Ca2+]istabilization and suggest that taurine may exert a beneficial effect in preventing diabetes-associated microangiopathy.

scholarly journals IL-37b alleviates endothelial cell apoptosis and inflammation in Kawasaki disease through IL-1R8 pathway

2021 ◽  
Vol 12 (6) ◽  
Author(s):  
Chang Jia ◽  
Yingzhi Zhuge ◽  
Shuchi Zhang ◽  
Chao Ni ◽  
Linlin Wang ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Kawasaki Disease ◽  
Mouse Model ◽  
Cell Apoptosis ◽  
Developed Countries ◽  
Protective Role ◽  
Potential Candidate ◽  
Endothelial Cell Apoptosis ◽  
Apoptosis And Inflammation

AbstractKawasaki disease (KD) is an acute vasculitis of pediatric populations that may develop coronary artery aneurysms if untreated. It has been regarded as the principal cause of acquired heart disease in children of the developed countries. Interleukin (IL)-37, as one of the IL-1 family members, is a natural suppressor of inflammation that is caused by activation of innate and adaptive immunity. However, detailed roles of IL-37 in KD are largely unclear. Sera from patients with KD displayed that IL-37 level was significantly decreased compared with healthy controls (HCs). QRT-PCR and western blot analyses showed that the expression level of IL-37 variant, IL-37b, was remarkably downregulated in human umbilical vein endothelial cells (HUVECs) exposed to KD sera-treated THP1 cells. Therefore, we researched the role of IL-37b in the context of KD and hypothesized that IL-37b may have a powerful protective effect in KD patients. We first observed and substantiated the protective role of IL-37b in a mouse model of KD induced by Candida albicans cell wall extracts (CAWS). In vitro experiments demonstrated that IL-37b alleviated endothelial cell apoptosis and inflammation via IL-1R8 receptor by inhibiting ERK and NFκB activation, which were also recapitulated in the KD mouse model. Together, our findings suggest that IL-37b play an effective protective role in coronary endothelial damage in KD, providing new evidence that IL-37b is a potential candidate drug to treat KD.

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