Role of Hydrophilic Monomers in α ‐Tocopherol‐Based Copolymers in Causing Cell Death by ROS Production

2021 ◽  
pp. 2100099
Author(s):  
Takuya Kitazume ◽  
Ning Gan ◽  
Shin‐Ichi Yusa ◽  
Tooru Ooya
Keyword(s):  
Cell Death ◽  
Ros Production ◽  
Hydrophilic Monomers

scholarly journals Effect of Staurosporine in the Morphology and Viability of Cerebellar Astrocytes: Role of Reactive Oxygen Species and NADPH Oxidase

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Mauricio Olguín-Albuerne ◽  
Guadalupe Domínguez ◽  
Julio Morán
Keyword(s):  
Cell Death ◽  
Nadph Oxidase ◽  
Morphological Changes ◽  
Critical Factor ◽  
Cytoskeletal Proteins ◽  
Ros Production ◽  
Oxygen Species ◽  
Morphological Alterations ◽  
Cerebellar Astrocytes

Cell death implies morphological changes that may contribute to the progression of this process. In astrocytes, the mechanisms involving the cytoskeletal changes during cell death are not well explored. Although NADPH oxidase (NOX) has been described as being a critical factor in the production of ROS, not much information is available about the participation of NOX-derived ROS in the cell death of astrocytes and their role in the alterations of the cytoskeleton during the death of astrocytes. In this study, we have evaluated the participation of ROS in the death of cultured cerebellar astrocytes using staurosporine (St) as death inductor. We found that astrocytes express NOX1, NOX2, and NOX4. Also, St induced an early ROS production and NOX activation that participate in the death of astrocytes. These findings suggest that ROS produced by St is generated through NOX1 and NOX4. Finally, we showed that the reorganization of tubulin and actin induced by St is ROS independent and that St did not change the level of expression of these cytoskeletal proteins. We conclude that ROS produced by a NOX is required for cell death in astrocytes, but not for the morphological alterations induced by St.

Role of the cytoskeleton in Cd2+-induced death of mouse mesangial cellsThis article is one of a selection of papers published in a Special Issue on Oxidative Stress in Health and Disease.

2010 ◽  
Vol 88 (3) ◽  
pp. 341-352 ◽  
Author(s):  
Ying Liu ◽  
Douglas M. Templeton
Keyword(s):  
Cell Death ◽  
Mesangial Cells ◽  
Apoptotic Cell ◽  
Cytochalasin D ◽  
Ros Production ◽  
Filamentous Actin ◽  
P38 Kinase ◽  
Apoptotic Death ◽  
Dependent Cell

Cadmium induces apoptotic cell death in mouse mesangial cells that is in part dependent on reactive oxygen species (ROS). Cadmium also activates multiple kinases in these cells, including the Ca2+/calmodulin-dependent protein kinase II (CaMK-II) and p38 kinase, and also leads to disruption of the filamentous actin cytoskeleton. We investigated the role of the cytoskeleton in Cd2+-induced cell death. Cell viability was decreased by Cd2+and two types of apoptotic death, defined by flow cytometry, were increased. Disruption of actin filaments with cytochalasin D was partially protective, whereas stabilization of the cytoskeleton with jasplakinolide was without effect, indicating that cytoskeletal disruption contributes to, but is not necessary for, induction of apoptosis. Inhibition of CaMK-II and p38 kinase, mitochondrial stabilization with cyclosporine A, and the antioxidant N-acetyl cysteine all protected against apoptosis and prevented disruption of the cytoskeleton. Cytochalasin D decreased Cd2+-dependent ROS production, reduced the decline in mitochondrial membrane potential, and decreased phosphorylation of p38 kinase. We conclude that Cd2+-dependent actin disruption is a downstream event facilitating apoptotic death. Cadmium-dependent cell death involves actin-dependent mitochondrial changes, ROS production, and p38 activation.

scholarly journals Ca2+ Participates in Programmed Cell Death by Modulating ROS During Pollen Cryopreservation

2021 ◽  
Author(s):  
Ruifen Ren ◽  
Hao Zhou ◽  
Lingling Zhang ◽  
Xueru Jiang ◽  
Yan Liu
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Opposite Effect ◽  
Pollen Viability ◽  
Chelating Agent ◽  
Ros Production ◽  
Caspase 9 ◽  
Related Substances ◽  
Intracellular Ros

Abstract Programmed cell death (PCD) is one of the reasons for the decline in pollen viability after cryopreservation. However, the role of calcium ions (Ca2+) in PCD during pollen cryopreservation has not been revealed in the existing studies. In this study, Paeonia lactiflora 'Fen Yu Nu' pollen was used as the research material for investigating the effects of Ca2+ changes on PCD indices and reactive oxygen species (ROS) during pollen cryopreservation. The results showed that after cryopreservation, with the decrease of pollen viability, the Ca2+ content significantly increased. The regulation of Ca2+ content had a significant effect on PCD indices, which showed that the Ca2+ carrier A23187 accelerated the decrease of mitochondrial membrane potential level and increased the activity of caspase-3-like and caspase-9-like proteases and the apoptosis rate. The expression levels of partial pro-PCD genes were upregulated, the anti-PCD gene BI-1 was downregulated, and the addition of Ca2+ chelating agent EGTA had the opposite effect. The addition of the Ca2+ carrier A23187 after cryopreservation significantly increased the ROS content of pollen, the addition of the Ca2+ chelating agent EGTA had the opposite effect, and Ca2+ regulators also had significant effects on the contents of ROS production and clearance-related substances. Ca2+ affected intracellular ROS content by acting on the ROS production and clearance system during the cryopreservation of pollen and is thus involved in the occurrence of PCD.

Role of reactive oxygen species in acetylcholine-induced preconditioning in cardiomyocytes

1999 ◽  
Vol 277 (6) ◽  
pp. H2504-H2509 ◽  
Author(s):  
Zhenhai Yao ◽  
Jiankun Tong ◽  
Xiaohui Tan ◽  
Changqing Li ◽  
Zuohui Shao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Ventricular Myocytes ◽  
Reactive Oxygen ◽  
Ros Production ◽  
Oxygen Species ◽  
Intracellular Signals ◽  
Dichlorofluorescin Diacetate ◽  
Flow Through

We examined the ability of ACh to mimic ischemic preconditioning in cardiomyocytes and the role of ATP-sensitive potassium (KATP) channels and mitochondrial reactive oxygen species (ROS) in mediating this effect. Chick embryonic ventricular myocytes were studied in a flow-through chamber while flow rate, pH,[Formula: see text], and[Formula: see text] were controlled. Cell viability was quantified with propidium iodide (5 μM), and production of ROS was measured using 2′,7′-dichlorofluorescin diacetate. Data were expressed as means ± SE. Preconditioning with 10 min of ischemia followed by 10 min of reoxygenation or 10 min of ACh (1 mM) followed by a drug-free period before 1 h of ischemia and 3 h of reoxygenation reduced cell death to the same extent [preconditioning 19 ± 2% ( n = 6, P < 0.05) ACh 21 ± 5% ( n = 6, P < 0.05) vs controls 42 ± 5% ( n = 9)]. Like preconditioning, ACh increased ROS production threefold before ischemia [0.60 ± 0.16 ( n = 7, P< 0.05) vs. controls, 0.16 ± 0.03 ( n = 6); arbitrary units]. Protection and increased ROS production during ACh preconditioning were abolished with 5-hydroxydecanoate (5-HD, 100 μM), a selective mitochondrial KATP channel antagonist, and the thiol reductant 2-mercaptopropionyl glycine (2-MPG, 1 mM), an antioxidant [cell death: 5-HD+ACh 37 ± 7% ( n = 5), 2-MPG+ACh 47 ± 6% ( n = 6); ROS signals: 5-HD+ACh 0.09 ± 0.03 ( n = 5), 2-MPG+ACh 0.01 ± 0.04 ( n = 4)]. In addition, ACh-induced ROS signaling was blocked by the mitochondrial site III electron transport inhibitor myxothiazol (0.02 ± 0.07, n = 5). These results demonstrate that activation of mitochondrial KATPchannels and increased ROS production from mitochondria are important intracellular signals that participate in ACh-induced preconditioning in cardiomyocytes.

The role of programmed cell death ligand-1/ programmed cell death-1 (PD-L1/PD-1) in HPV-induced cervical cancer and potential for their use in blockade therapy

2020 ◽  
Vol 27 ◽  
Author(s):  
Lifang Zhang ◽  
Yu Zhao ◽  
Quanmei Tu ◽  
Xiangyang Xue ◽  
Xueqiong Zhu ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Immune Escape ◽  
Hypoxia Inducible Factor ◽  
Hpv Infection ◽  
Advanced Cervical Cancer ◽  
Cervical Carcinogenesis ◽  
Programmed Cell Death 1

Background: Cervical cancer induced by infection with human papillomavirus (HPV) remains a leading cause of mortality for women worldwide although preventive vaccines and early diagnosis have reduced morbidity and mortality. Advanced cervical cancer can only be treated with either chemotherapy or radiotherapy but outcomes are poor. The median survival for advanced cervical cancer patients is only 16.8 months. Methods: We undertook a structural search of peer-reviewed published studies based on 1). Characteristics of programmed cell death ligand-1/programmed cell death-1(PD-L1/PD-1) expression in cervical cancer and upstream regulatory signals of PD-L1/PD-1 expression, 2). The role of the PD-L1/PD-1 axis in cervical carcinogenesis induced by HPV infection and 3). Whether the PD-L1/PD-1 axis has emerged as a potential target for cervical cancer therapies. Results: One hundred and twenty-six published papers were included in the review, demonstrating that expression of PD-L1/PD-1 is associated with HPV-caused cancer, especially with HPV 16 and 18 which account for approximately 70% of cervical cancer cases. HPV E5/E6/E7 oncogenes activate multiple signaling pathways including PI3K/AKT, MAPK, hypoxia-inducible factor 1α, STAT3/NF-kB and MicroRNAs, which regulate PD-L1/PD-1 axis to promote HPV-induced cervical carcinogenesis. The PD-L1/PD-1 axis plays a crucial role in immune escape of cervical cancer through inhibition of host immune response. creating an "immune-privileged" site for initial viral infection and subsequent adaptive immune resistance, which provides a rationale for therapeutic blockade of this axis in HPV-positive cancers. Currently, Phase I/II clinical trials evaluating the effects of PD-L1/PD-1 targeted therapies are in progress for cervical carcinoma, which provide an important opportunity for the application of anti-PD-L1/anti-PD-1 antibodies in cervical cancer treatment. Conclusion: Recent research developments have led to an entirely new class of drugs using antibodies against the PD-L1/PD-1 thus promoting the body’s immune system to fight the cancer. The expression and roles of the PD-L1/ PD-1 axis in the progression of cervical cancer provide great potential for using PD-L1/PD-1 antibodies as a targeted cancer therapy.

Sign in / Sign up

Export Citation Format

Share Document