Rac1 inhibits TNF‐α‐induced endothelial cell apoptosis: dual regulation by reactive oxygen species

2000 ◽  
Vol 14 (12) ◽  
pp. 1705-1714 ◽  
Author(s):  
Shailesh S. Deshpande ◽  
Piamsook Angkeow ◽  
Jianping Huang ◽  
Michitaka Ozaki ◽  
Kaikobad Irani
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Endothelial Cell Apoptosis ◽  
Tnf Α

Tumor-induced endothelial cell apoptosis: Roles of NAD(P)H oxidase-derived reactive oxygen species

2011 ◽  
Vol 226 (7) ◽  
pp. 1750-1762 ◽  
Author(s):  
Ruei-Zeng Lin ◽  
Tsung-Pao Wang ◽  
Ruei-Jiun Hung ◽  
Yung-Jen Chuang ◽  
Chi-Chen Michae Chien ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Endothelial Cell Apoptosis

Endothelial cell apoptosis induced by bacteria-activated platelets requires caspase-8 and -9 and generation of reactive oxygen species

2008 ◽  
Vol 99 (02) ◽  
pp. 363-372 ◽  
Author(s):  
Christopher J. Kuckleburg ◽  
Raksha Tiwari ◽  
Charles J. Czuprynski
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Vascular Inflammation ◽  
Reactive Oxygen ◽  
Caspase 8 ◽  
Oxygen Species ◽  
Endothelial Cell Apoptosis ◽  
Activated Platelets

SummaryA common feature of severe sepsis is vascular inflammation and damage to the endothelium. Because platelets can be directly activated by bacteria and endotoxin, these cells may play an important role in determining the outcome of sepsis. For example, inhibiting platelet interactions with the endothelium has been shown to attenuate endothelial cell damage and improve survival during sepsis. Although not entirely understood, the interactions between bacteria-activated platelets and the endothelium may play a key role in the vascular pathology of bacterial sepsis. Haemophilus somnus is a bacterial pathogen that causes diffuse vascular inflammation and endothelial damage. In some cases H.somnus infection results in an acute and fatal form of vasculitis in the cerebral microvasculature known as thrombotic meningoencephalitis (TME). In this study, we have characterized the mechanisms involved in endothelial cell apoptosis induced by activated platelets. We observed that direct contact between H.somnus-activated platelets and endothelial cells induced significant levels of apoptosis; however, Fas receptor activation on bovine endothelial cells was not able to induce apoptosis unless protein synthesis was disrupted. Endothelial cell apoptosis by H.somnus-activated platelets required activation of both caspase-8 and caspase-9, as inhibitors of either caspase inhibited apoptosis. Furthermore, activated platelets induced endothelial cell production of reactive oxygen species (ROS) and disrupting ROS activity in endothelial cells significantly inhibited apoptosis. These findings suggest that bacterial activation of platelets may contribute to endothelial cell dysfunction observed during sepsis, specifically by inducing endothelial cell apoptosis.

scholarly journals Endothelial-cell apoptosis induced by cleaved high-molecular-weight kininogen (HKa) is matrix dependent and requires the generation of reactive oxygen species

Blood ◽  
2006 ◽  
Vol 107 (12) ◽  
pp. 4714-4720 ◽  
Author(s):  
Danyu Sun ◽  
Keith R. McCrae
Keyword(s):  
Reactive Oxygen Species ◽  
Molecular Weight ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
High Molecular Weight ◽  
Cell Apoptosis ◽  
Oxygen Species ◽  
High Molecular Weight Kininogen ◽  
Endothelial Cell Apoptosis ◽  
Cells Cultured

AbstractHigh–molecular-weight kininogen (HK) is an abundant plasma protein that plays a central role in activation of the kallikrein-kinin system. Cleavage of HK by plasma kallikrein results in release of the nonapeptide bradykinin (BK), leaving behind cleaved high–molecular-weight kininogen (HKa). Previous studies have demonstrated that HKa induces apoptosis of proliferating endothelial cells and inhibits angiogenesis in vivo, activities mediated primarily through its domain 5. However, the mechanisms by which these effects occur are not well understood. Here, we demonstrate that HKa induces apoptosis of endothelial cells cultured on gelatin, vitronectin, fibronectin, or laminin but not collagen type I or IV. The ability of HKa to induce endothelial-cell apoptosis is dependent on the generation of intracellular reactive oxygen species and associated with depletion of glutathione and peroxidation of endothelial-cell lipids, effects that occur only in cells cultured on matrix proteins permissive for HKa-induced apoptosis. Finally, the ability of HKa to induce endothelial-cell apoptosis is blocked by the addition of reduced glutathione or N-acetylcysteine. These studies demonstrate a unique role for oxidant stress in mediating the activity of an antiangiogenic polypeptide and highlight the importance of the extracellular matrix in regulating endothelial-cell survival.

A Novel pH-responsive Fe-MOF System for Enhanced Cancer Treatment Mediated by Fenton Reaction

2021 ◽  
Author(s):  
Senlin Wang ◽  
Hong-Shuai Wu ◽  
Kai Sun ◽  
Jinzhong Hu ◽  
Fanghui Chen ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Hydroxyl Radical ◽  
Cancer Treatment ◽  
Cell Apoptosis ◽  
Fenton Reaction ◽  
Reactive Oxygen ◽  
Cationic Polymer ◽  
Intracellular Reactive Oxygen Species ◽  
Oxygen Species ◽  
Ph Responsive

Recently, the toxic hydroxyl radical (·OH) has received wide interest in inducing cell apoptosis by increasing the intracellular reactive oxygen species (ROS) levels. Herein, a cationic polymer (MV-PAH) was rationally...

Altered composition of high-lipid diet may generate reactive oxygen species by disturbing the balance of antioxidant and free radicals

2020 ◽  
Vol 31 (3) ◽  
Author(s):  
Arnab Banerjee ◽  
Debasmita Das ◽  
Rajarshi Paul ◽  
Sandipan Roy ◽  
Ankita Bhattacharjee ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Reactive Oxygen ◽  
Control Group ◽  
Preliminary Evaluation ◽  
Oxygen Species ◽  
High Lipid ◽  
Tnf Α ◽  
High Lipid Diet ◽  
Lipid Diet

AbstractBackgroundIn the present era, obesity is increasing rapidly, and high dietary intake of lipid could be a noteworthy risk factor for the occasion of obesity, as well as nonalcoholic fatty liver disease, which is the independent risk factor for type 2 diabetes and cardiovascular disease. For a long time, high-lipid diet (HLD) in “fast food” is turning into part of our everyday life. So, we were interested in fulfilling the paucity of studies by means of preliminary evaluation of these three alternative doses of HLD on a rat model and elucidating the possible mechanism of these effects and divulging the most alarming dose.MethodsThirty-two rats were taken, and of these, 24 were fed with HLD in three distinctive compositions of edible coconut oil and vanaspati ghee in a ratio of 2:3, 3:2 and 1:1 (n = 8), orally through gavage at a dose of 10 mL/kg body weight for a period of 28 days, whereas the other eight were selected to comprise the control group.ResultsAfter completion of the experiment, followed by analysis of data it was revealed that hyperlipidemia with increased liver and cardiac marker enzymes, are associated with hepatocellular injury and cardiac damage. The data also supported increased proinflammatory cytokines such as interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α). As oxidative stress parameter increased in both liver and heart, there is also an increased in TNF-α due to an increased expression of inducible nitric oxide (NO) synthase, which led to a high production of NO. Moreover, HLD treatment explicitly weakens reasonability of hepatocytes and cardiomyocytes conceivably through G0/G1 or S stage capture or perhaps by means of enlistment of sub-G0/G1 DNA fragmentation and a sign of apoptosis.ConclusionsBased on the outcomes, it tends to be inferred that consequences of the present examination uncovered HLD in combination of 2:3 applies most encouraging systemic damage by reactive oxygen species generation and hyperlipidemia and necroapoptosis of the liver and heart. Hence, outcome of this study may help to formulate health care strategy and warns about the food habit in universal population regarding the use of hydrogenated and saturated fats (vanaspati ghee) in diet.

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