scholarly journals Mitochondrial division inhibitor-1 potentiates cisplatin-induced apoptosis via the mitochondrial death pathway in cholangiocarcinoma cells

2019 ◽  
Vol 111 ◽  
pp. 109-118 ◽  
Author(s):  
Ornanong Tusskorn ◽  
Tueanjai Khunluck ◽  
Auemduan Prawan ◽  
Laddawan Senggunprai ◽  
Veerapol Kukongviriyapan
Keyword(s):  
Mitochondrial Division ◽  
Mitochondrial Death Pathway ◽  
Induced Apoptosis

scholarly journals Involvement of the Mitochondrial Death Pathway in Chemopreventive Benzyl Isothiocyanate-induced Apoptosis

2001 ◽  
Vol 277 (10) ◽  
pp. 8492-8499 ◽  
Author(s):  
Yoshimasa Nakamura ◽  
Makiko Kawakami ◽  
Akira Yoshihiro ◽  
Noriyuki Miyoshi ◽  
Hajime Ohigashi ◽  
...  
Keyword(s):  
Benzyl Isothiocyanate ◽  
Mitochondrial Death Pathway ◽  
Induced Apoptosis

scholarly journals Exogenous ubiquitin attenuates hypoxia/reoxygenation-induced cardiac myocyte apoptosis via the involvement of CXCR4 and modulation of mitochondrial homeostasis

2020 ◽  
Vol 98 (4) ◽  
pp. 492-501 ◽  
Author(s):  
Suman Dalal ◽  
Christopher R. Daniels ◽  
Ying Li ◽  
Gary L. Wright ◽  
Mahipal Singh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Myocyte ◽  
Glycogen Synthase ◽  
Ischemia Reperfusion ◽  
Protective Role ◽  
Mitochondrial Homeostasis ◽  
Myocyte Apoptosis ◽  
Mitochondrial Death Pathway ◽  
Induced Apoptosis ◽  
Hypoxia Reoxygenation

Exogenous ubiquitin (UB) plays a protective role in β-adrenergic receptor-stimulated and ischemia/reperfusion (I/R)-induced myocardial remodeling. Here, we report that UB treatment inhibits hypoxia/reoxygenation (H/R)-induced apoptosis in adult rat ventricular myocytes (ARVMs). The activation of Akt was elevated, whereas the activation of glycogen synthase kinase-3β was reduced in UB-treated cells post-H/R. The level of oxidative stress was lower, whereas the number of ARVMs with polarized mitochondria was significantly greater in the UB-treated samples. ARVMs express CXCR4 with majority of CXCR4 localized in the membrane fraction. CXCR4 antagonism using AMD3100, and siRNA-mediated knockdown of CXCR4 negated the protective effects of UB. Two mutated UB proteins (unable to bind CXCR4) had no effect on H/R-induced apoptosis, activation of Akt and GSK-3β, or oxidative stress. UB treatment enhanced mitochondrial biogenesis, and inhibition of mitochondrial fission using mdivi1 inhibited H/R-induced apoptosis. Ex vivo, UB treatment significantly decreased infarct size and improved functional recovery of the heart following global I/R. Activation of caspase-9, a key player of the mitochondrial death pathway, was significantly lower in UB-treated hearts post-I/R. UB, most likely acting via CXCR4, plays a protective role in H/R-induced myocyte apoptosis and myocardial I/R injury via modulation of mitochondrial homeostasis and the mitochondrial death pathway of apoptosis.

scholarly journals Mitochondrial division inhibitor-1 induces mitochondrial hyperfusion and sensitizes human cancer cells to TRAIL-induced apoptosis

2014 ◽  
Vol 45 (5) ◽  
pp. 1901-1912 ◽  
Author(s):  
MAMORU AKITA ◽  
MIKI SUZUKI-KARASAKI ◽  
KYOKO FUJIWARA ◽  
CHINATSU NAKAGAWA ◽  
MASAYOSHI SOMA ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Human Cancer ◽  
Mitochondrial Division ◽  
Human Cancer Cells ◽  
Induced Apoptosis

scholarly journals Molecular ordering of hypoxia-induced apoptosis: critical involvement of the mitochondrial death pathway in a FADD/caspase-8 independent manner

Oncogene ◽  
2004 ◽  
Vol 23 (21) ◽  
pp. 3757-3769 ◽  
Author(s):  
Martin Weinmann ◽  
Verena Jendrossek ◽  
Rene Handrick ◽  
Dilek Güner ◽  
Barbara Goecke ◽  
...  
Keyword(s):  
Caspase 8 ◽  
Independent Manner ◽  
Molecular Ordering ◽  
Mitochondrial Death Pathway ◽  
Induced Apoptosis

scholarly journals p38 Mitogen-Activated Protein Kinase Mediates the Fas-Induced Mitochondrial Death Pathway in CD8+ T Cells

2006 ◽  
Vol 26 (6) ◽  
pp. 2118-2129 ◽  
Author(s):  
Nicholas Farley ◽  
Gustavo Pedraza-Alva ◽  
Diego Serrano-Gomez ◽  
Viswas Nagaleekar ◽  
Alexander Aronshtam ◽  
...  
Keyword(s):  
T Cells ◽  
Protein Kinase ◽  
P38 Mapk ◽  
Fas Ligand ◽  
Death Receptor ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Mitogen Activated Protein ◽  
Mitochondrial Death Pathway ◽  
Induced Apoptosis

ABSTRACT The p38 mitogen-activated protein kinase (MAPK) signaling pathway can be activated by a variety of stress stimuli such as UV radiation and osmotic stress. The regulation and role of this pathway in death receptor-induced apoptosis remain unclear and may depend on the specific death receptor and cell type. Here we show that binding of Fas ligand to Fas activates p38 MAPK in CD8+ T cells and that activation of this pathway is required for Fas-mediated CD8+ T-cell death. Active p38 MAPK phosphorylates Bcl-xL and Bcl-2 and prevents the accumulation of these antiapoptotic molecules within the mitochondria. Consequently, a loss of mitochondrial membrane potential and the release of cytochrome c lead to the activation of caspase 9 and, subsequently, caspase 3. Therefore, the activation of p38 MAPK is a critical link between Fas and the mitochondrial death pathway and is required for the Fas-induced apoptosis of CD8+ T cells.

Absence of temporal ordering of apoptotic features in heat-shock treated leukemia and lymphoma cell lines

1996 ◽  
Vol 54 ◽  
pp. 758-759
Author(s):  
D. W. Fairbain ◽  
M.D. Standing ◽  
K.L. O'Neill
Keyword(s):  
Heat Shock ◽  
Cell Lines ◽  
Chromatin Condensation ◽  
Membrane Integrity ◽  
Resistant Cell ◽  
Membrane Blebbing ◽  
Late Loss ◽  
Induced Apoptosis ◽  
Dying Cells ◽  
In Cells

Apoptosis is a genetically defined response to physiological stimuli that results in cellular suicide. Features common to apoptotic cells include chromatin condensation, oligonucleosomal DNA fragmentation, membrane blebbing, nuclear destruction, and late loss of ability to exclude vital dyes. These characteristics contrast markedly from pathological necrosis, in which membrane integrity loss is demonstrated early, and other features of apoptosis, which allow a non-inflammatory removal of dead and dying cells, are absent. Using heat shock-induced apoptosis as a model for examining stress response in cells, we undertook to categorize a variety of human leukemias and lymphomas with regard to their response to heat shock. We were also interested in determining whether a common temporal order was followed in cells dying by apoptosis. In addition, based on our previous results, we investigated whether increasing heat load resulted in increased apoptosis, with particular interest in relatively resistant cell lines, or whether the mode of death changed from apoptosis to necrosis.

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