The Role of STAT1/IRF-1 on Synergistic ROS Production and Loss of Mitochondrial Transmembrane Potential during Hepatic Cell Death Induced by LPS/d-GalN

2007 ◽  
Vol 369 (4) ◽  
pp. 967-984 ◽  
Author(s):  
Hyun Jung Lee ◽  
Yeo Kyoung Oh ◽  
Marie Rhee ◽  
Joong-Yeon Lim ◽  
Ji-Young Hwang ◽  
...  
Keyword(s):  
Cell Death ◽  
Transmembrane Potential ◽  
Hepatic Cell ◽  
Mitochondrial Transmembrane Potential ◽  
Ros Production

The role of microRNAs in liver injury at the crossroad between hepatic cell death and regeneration

2017 ◽  
Vol 482 (3) ◽  
pp. 399-407 ◽  
Author(s):  
Volker M. Lauschke ◽  
Souren Mkrtchian ◽  
Magnus Ingelman-Sundberg
Keyword(s):  
Cell Death ◽  
Liver Injury ◽  
Hepatic Cell

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.

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