In Vitro Cytotoxicity of Mokko Lactone in Human Leukemia HL‐60 Cells: Induction of Apoptotic Cell Death by Mitochondrial Membrane Potential Collapse

2004 ◽  
Vol 26 (3) ◽  
pp. 343-353 ◽  
Author(s):  
Y. G. Yun ◽  
H. Oh ◽  
G. S. Oh ◽  
H. O. Pae ◽  
B. M. Choi ◽  
...  
Keyword(s):  
Cell Death ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Apoptotic Cell ◽  
In Vitro Cytotoxicity ◽  
Apoptotic Cell Death ◽  
Human Leukemia

scholarly journals Neuroprotective Effect of Tricyclic Pyridine Alkaloids from Fusarium lateritium SSF2, against Glutamate-Induced Oxidative Stress and Apoptosis in the HT22 Hippocampal Neuronal Cell Line

Antioxidants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1115
Author(s):  
Dahae Lee ◽  
Hyun Gyu Choi ◽  
Ji Hye Hwang ◽  
Sang Hee Shim ◽  
Ki Sung Kang
Keyword(s):  
Cell Death ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Cytochrome C Release ◽  
Ht22 Cells ◽  
Superoxide Anion Production ◽  
Fusarium Lateritium

Excessive glutamate damages neuronal cells via the accumulation of intracellular reactive oxygen species (ROS), calcium ion (Ca2+) influx, depolarization of mitochondrial membrane potential, and apoptosis, which may result in the development of chronic neurodegenerative diseases. In this study, we evaluated the effects of 4,6′-anhydrooxysporidinone isolated from endophytic fungus Fusarium lateritium SSF2 on glutamate-induced cytotoxicity, accumulation of intracellular ROS, increases in superoxide anion production, Ca2+, depolarization of mitochondrial membrane potential, and apoptotic cell death in hippocampal HT22 cells. 2′,7′-Dichlorofluorescin diacetate (H2DCFDA) staining was used to determine the intracellular reactive oxygen species concentration and dihydroethidine (DHE) staining was used to determine the superoxide radical. Expression of the nuclear factor-erythroid-2–related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) was analyzed by Western blot. Fluo-4 staining was used to determine the intracellular Ca2+ levels. In order to explore mitochondrial membrane potential, tetramethylrhodamine methyl ester (TMRM) staining was used. Apoptotic cell death was evaluated using Annexin-V/propidium iodide (PI) staining and TUNEL staining. Expression of the cytochrome c release and cleaved caspase-9, -3 was analyzed by Western blot. Here, we were able to isolate 4,6′-anhydrooxysporidinone from endophytic fungus, Fusarium lateritium SSF2, which was shown to protect HT22 cells from glutamate-induced cytotoxicity, accumulation of intracellular ROS, increases in superoxide anion production, Ca2+, and depolarization of mitochondrial membrane potential. In addition, 4,6′-anhydrooxysporidinone enhanced the expressions of Nrf2 and HO-1. It also inhibited the apoptotic cell death through the inhibition of cytochrome c release and cleaved caspase-9, -3 in glutamate-treated HT22 cells. Therefore, our results provide ample evidence of the neuroprotective properties of 4,6′-anhydrooxysporidinone.

Anti-Glycophorin C Induces a Loss of Mitochondrial Membrane Potential but Fails To Activate Apoptotic Caspases.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4097-4097
Author(s):  
Gregory A. Denomme ◽  
Jonathan Micieli ◽  
Jenny Shu ◽  
Dan Wang ◽  
Bernard J. Fernandes
Keyword(s):  
Cell Death ◽  
Membrane Potential ◽  
Growth Inhibition ◽  
Mitochondrial Membrane Potential ◽  
K562 Cell ◽  
Mitochondrial Membrane ◽  
K562 Cells ◽  
Suppressive Effect ◽  
Glycophorin C

Abstract The human erythrocyte transmembrane sialoglycoprotein, glycophorin C (GYPC), plays a functional role in regulating red cell shape and mechanical stability. Antibodies to GYPC cause hemolytic disease of the fetus and newborn (HDFN) that is associated with classical Fcγ receptor-mediated phagocytosis. However, in vitro clonogenic studies with cord blood progenitor cells suggest that anti-GYPC also suppresses erythropoiesis, which is consistent with the observations of severe and early fetal anemia and late onset neonatal anemia [Transfus Med2005;15:125–32]. The mechanism of the suppressive effect on erythropoiesis is unknown. The K562 erythroleukemic cell line treated with anti-GYPC is a potential model system to study the suppressive effect of anti-GYPC. The present in vitro studies were designed to confirm the effect of anti-GYPC on K562 cell growth and viability, and to evaluate changes in mitochondrial membrane potential, phosphatidylserine (PS) expression, propidium iodide (PI) binding, and caspase activation. K562 cells fail to grow in the presence of anti-GYPC confirming earlier CFU-E/BFU-E studies [Brit J Haematol2006;133:443–4], and increased the exofacial expression of PS/PI over time. This process was caspase-independent as demonstrated by the failure of Z-VAD, a caspase inhibitor, to reverse growth inhibition and PS/PI expression. A loss of mitochondrial membrane potential was demonstrated using JC-1, a cationic dye that is sensitive to potential-dependent accumulation or loss in mitochondria. There was a 50% increase in K562 cell mitochondrial membrane potential disruption after 2 days of culture with anti-GYPC (see figure). Morphological examination of May Grunwalde Giemsa-stained K562 cells treated with anti-GYPC for 2 days showed a decrease in mitotic activity compared to isotype treated cells. By day 4, the anti-GYPC treated cells were showing evidence of plasma membrane damage and cell death resulting from fragmentation and dissolution of the cytoplasm. The addition of hemin, an oxidative form of iron protoporphyrin IX known to induce erythroid differentiation of K562 cells, to anti-GYPC treated cells reversed growth inhibition by 45% but did not prevent the loss of mitochondrial membrane potential. Overall, although caspases appear to be unimportant in anti-GYPC induced cell death, the mitchondria play an important role as the early events leading to antibody-mediated suppression of erythropoiesis. Mitochondrial Membrane Potential Disruption by Anti-GYPC Mitochondrial Membrane Potential Disruption by Anti-GYPC

scholarly journals In vitro activity of 1H-phenalen-1-one derivatives against Leishmania spp. and evidence of programmed cell death

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Atteneri López-Arencibia ◽  
María Reyes-Batlle ◽  
Mónica B. Freijo ◽  
Ines Sifaoui ◽  
Carlos J. Bethencourt-Estrella ◽  
...  
Keyword(s):  
Cell Death ◽  
Membrane Potential ◽  
Programmed Cell Death ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Chromatin Condensation ◽  
Death Process ◽  
Leishmania Spp ◽  
Characteristic Features

Abstract Background The in vitro activity against Leishmania spp. of a novel group of compounds, phenalenone derivatives, is described in this study. Previous studies have shown that some phenalenones present leishmanicidal activity, and induce a decrease in the mitochondrial membrane potential in L. amazonensis parasites, so in order to elucidate the evidence of programmed cell death occurring inside the promastigote stage, different assays were performed in two different species of Leishmania. Methods We focused on the determination of the programmed cell death evidence by detecting the characteristic features of the apoptosis-like process, such as phosphatidylserine exposure, mitochondrial membrane potential, and chromatin condensation among others. Results The results showed that four molecules activated the apoptosis-like process in the parasite. All the signals observed were indicative of the death process that the parasites were undergoing. Conclusions The present results highlight the potential use of phenalenone derivatives against Leishmania species and further studies should be undertaken to establish them as novel leishmanicidal therapeutic agents.

scholarly journals Geranylgeranyl Acetone Prevents Glutamate-induced Cell Death in HT-22 Cells by Increasing Mitochondrial Membrane Potential

2020 ◽  
Author(s):  
Eriko Sugano ◽  
Yuka Endo ◽  
Akihisa Sugai ◽  
Yuki Kikuchi ◽  
Kitako Tabata ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Oxygen Species ◽  
Mouse Hippocampus ◽  
Calcium Buffering ◽  
Shock Proteins

Geranylgeranyl acetone (GGA) protects against various types of cell damages by upregulating heat shock proteins. We investigated whether GGA protect neuronal cells from cell death induced by oxidative stress. Glutamate exposure was lethal to HT-22 cells which comprise a neuronal line derived from mouse hippocampus. This configuration is often used as a model for hippocampus neurodegeneration in vitro. In the present study, GGA protected HT-22 cells from glutamate-induced oxidative stress. GGA pretreatment did not induce Hsps. Moreover, reactive oxygen species increased to the same extent in both GGA-pretreated and untreated cells exposed to glutamate. In contrast, glutamate exposure and GGA pretreatment increased mitochondrial membrane potential. However, increases in intracellular Ca2+ concentration were inhibited by GGA pretreatment. In addition, the increase of phosphorylated ERKs by the glutamate exposure was inhibited by GGA pretreatment. These findings suggest that GGA protects HT-22 cells from glutamate-provoked cell death without Hsp induction and that the mitochondrial calcium buffering capacity plays an important role in this protective effect.

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