METHYLPREDNISOLONE-INDUCED EXPRESSION OF MITOCHONDRIAL HEAT SHOCK PROTEIN 60 PROTECTS MITOCHONDRIAL MEMBRANE POTENTIAL IN THE HYPOXIC RAT LIVER

Shock ◽  
2004 ◽  
Vol 22 (3) ◽  
pp. 234-239 ◽  
Author(s):  
Satoru Motoyama ◽  
Satoshi Saito ◽  
Hideaki Itoh ◽  
Yoshihiro Minamiya ◽  
Kiyotomi Maruyama ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Mitochondrial Membrane Potential ◽  
Rat Liver ◽  
Mitochondrial Membrane ◽  
Heat Shock Protein 60 ◽  
Induced Expression ◽  
Mitochondrial Heat Shock Protein

scholarly journals Overexpression of Mitochondrial Hsp70/Hsp75 Protects Astrocytes against Ischemic Injury in vitro

2007 ◽  
Vol 28 (5) ◽  
pp. 1009-1016 ◽  
Author(s):  
Ludmila A Voloboueva ◽  
Melissa Duan ◽  
YiBing Ouyang ◽  
John F Emery ◽  
Christian Stoy ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Mitochondrial Membrane Potential ◽  
Heat Shock Protein 70 ◽  
Mitochondrial Membrane ◽  
Ischemic Injury ◽  
Glucose Deprivation ◽  
Hsp70 Family

Mitochondrial heat shock protein 70 (mtHsp70/Hsp75/Grp75/mortalin/TRAP-1/PBP74) is an essential mitochondrial chaperone and a member of the heat shock protein 70 (HSP70) family. Although many studies have shown the protective properties of overexpression of the cytosolic inducible member of the HSP70 family, Hsp72, few studies have investigated the protective potential of Hsp75 against ischemic injury. Mitochondria are one of the primary targets of ischemic injury in astrocytes. In this study, we analyzed the effects of Hsp75 overexpression on cellular levels of reactive oxygen species (ROS), mitochondrial membrane potential, ATP levels, and viability during the ischemia-like conditions of oxygen-glucose deprivation (OGD) or glucose deprivation (GD) in primary astrocytic cultures. We show that Hsp75 overexpression decreases ROS production and preserves mitochondrial membrane potential during GD, and preserves ATP levels and cell viability during OGD. These findings indicate that Hsp75 can provide protection against ischemia-like in vitro injury and suggest that it should be further studied as a potential candidate for protection against ischemic injury.

scholarly journals Effect of 50-Hz Sinusoidal Magnetic Field on the Production of Superoxide Anion and the Expression of Heat-shock Protein 70 in RAW264 Cells

2017 ◽  
Vol 9 (2) ◽  
pp. 23 ◽  
Author(s):  
Marootpong Pooam ◽  
Maresuke Nakayama ◽  
Chihiro Nishigaki ◽  
Hidetake Miyata
Keyword(s):  
Oxidative Stress ◽  
Magnetic Field ◽  
Membrane Potential ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Hsp70 Protein ◽  
Enhanced Production ◽  
Sinusoidal Magnetic Field

There is a growing concern if the power-line frequency (50/60 Hz) magnetic field (termed in this paper ELF-MF) increases cancer risks. Since one of the major causes of cancer is cellular oxidative stress, whether the ELF-MF increases the oxidative stress is a central problem in the studies on the biological effect of the ELF-MF. Here, we have investigated the effect of 50-Hz sinusoidal magnetic field on the production of O2-, the expression of heat shock protein (HSP) 70 and the mitochondrial membrane potential in cell line macrophage RAW264 cells. Macrophages were exposed to or not exposed to 0.1-mT or 0.5-mT, 50-Hz sinusoidal magnetic field and were subjected to (1) assay for O2- (2) analysis of the expression of HSP70, and (3) measurement of the mitochondrial membrane potential with a fluorescent indicator. The 50-Hz magnetic field enhanced production of O2- and the expression of HSP70, both of which are consistent with previous studies. The exposure to 50-Hz magnetic field decreased mitochondrial membrane potential indicating the diminished activity of mitochondria. The uncoupler of mitochondrial function, carbonyl cyanide p-trifluoromethoxyphenylhydrazone diminished the membrane potential, as expected. On the other hand, it increased the production of O2-. The results collectively suggest that the 50-Hz magnetic field diminished the mitochondrial membrane potential, which led to the increase in the production of O2- and the expression of HSP70 protein.

scholarly journals The Life Span Determinant p66Shc Localizes to Mitochondria Where It Associates with Mitochondrial Heat Shock Protein 70 and Regulates Trans-membrane Potential

2004 ◽  
Vol 279 (24) ◽  
pp. 25689-25695 ◽  
Author(s):  
Francesca Orsini ◽  
Enrica Migliaccio ◽  
Maurizio Moroni ◽  
Cristina Contursi ◽  
Veronica A. Raker ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Life Span ◽  
Heat Shock Protein 70 ◽  
Mitochondrial Heat Shock Protein

Tet-Regulated Expression of Mutant Neutrophil Elastase in HL-60 Cells: A Cellular Model of Severe Congenital Neutropenia.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 1452-1452
Author(s):  
Andrew A.G. Aprikyan ◽  
Nara A. Markosyan
Keyword(s):  
Cell Cycle ◽  
Membrane Potential ◽  
Cell Cycle Arrest ◽  
Mitochondrial Membrane Potential ◽  
Neutrophil Elastase ◽  
Mitochondrial Membrane ◽  
Apoptotic Cell ◽  
Induced Expression ◽  
Maturation Arrest ◽  
Cycle Arrest

Abstract Severe congenital neutropenia (SCN) is an inheritable hematopoietic disorder characterized by extremely low level of circulating neutrophils, ineffective intramedulary hematopoiesis with “maturation arrest” at the promyelocytic stage of differentiation, recurrent severe infections, and evolution to acute myelogenous leukemia (AML). Accelerated apoptosis of bone marrow-derived myeloid progenitor cells and cell cycle arrest of CD34+ cells was reported in SCN patients. We also reported that heterozygous mutations in the neutrophil elastase (NE) gene have been identified in approximately 80% of SCN patients. Transient expression of mutant but not normal NE triggered accelerated apoptotic cell death of human promyelocytic HL-60 cells supporting the causative role of mutant NE in pathogenesis of SCN. Here we present cellular model of SCN based on newly established tet-off HL-60 human promyelocytic cell line with inducible doxycycline-regulated expression of mutant NE with 8-amino acid deletion identified in a patient evolved to develop AML. Induced expression of mutant elastase in tet-off HL-60 cells treated with DMSO led to a block of differentiation or “maturation arrest” at the promyelocytic stage of differentiation with a significantly reduced proportion of differentiated cells (approximately 20% vs 70% in control) and higher proportion (~40%) of primitive undifferentiated cells compared with control DMSO-treated HL-60 cells expressing only normal NE (~10%). Flow cytometry analysis of annexin V-labeled cells repeatedly revealed approximately 2-fold higher rate of apoptosis in tet-off HL-60 cells with induced expression of mutant NE compared with control cells. FACS analysis of DAPI-labeled tet-off HL-60 cells with induced expression of mutant NE revealed abnormal cell cycle progression with gradual accumulation and apparent arrest of cells in G1-phase of the cell cycle similar to that reported for SCN patients. Interestingly, the apoptotic cell shrinking and swelling as determined by flow cytometry was observed in all phases of the cell cycle suggesting that accelerated apoptosis rather than cell cycle arrest is the primary abnormality caused by expression of mutant NE, and the abnormal cell cycle progression is a consequence of this impaired cell survival. Further analysis revealed a dramatic reduction in mitochondrial membrane potential of tet-off HL-60 cells expressing mutant NE compared with control cells. The reduced mitochondrial membrane potential as determined by FACS was observed as early as 24 hours of induction of mutant NE expression and before the accelerated apoptosis or cell cycle arrest was detected. Western blot analysis demonstrated that caspase-3 was not activated in the cells even after 3 days of mutant NE induction. Further analysis of apoptosis regulators revealed a down-regulation of Bcl-2 expression and up-regulation of Bax in cells with induced expression of mutant elastase. These data suggest that mutant elastase-mediated “maturation arrest” of human promyelocytic cells in patients with SCN and SCN/AML is associated with reduced expression of anti-apoptotic Bcl-2 and upregulation of pro-apoptotic Bax proteins that trigger a dramatic reduction in mitochondrial membrane potential and subsequent caspase-independent apoptosis and cell cycle arrest. Current studies focused on elucidating and characterizing specific molecular interactions mediating the pro-apoptotic effect of mutant neutrophil elastase in SCN.

Molecular characterization of the mitochondrial heat shock protein 60 gene from Trypanosoma brucei

1995 ◽  
Vol 74 (1) ◽  
pp. 119-123 ◽  
Author(s):  
Frédéric Bringaud ◽  
Sophie Peyruchaud ◽  
Dominique Baltz ◽  
Chrystiane Giroud ◽  
Larry Simpson ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Molecular Characterization ◽  
Trypanosoma Brucei ◽  
Heat Shock Protein 60 ◽  
Mitochondrial Heat Shock Protein

scholarly journals T-2307 Causes Collapse of Mitochondrial Membrane Potential in Yeast

2012 ◽  
Vol 56 (11) ◽  
pp. 5892-5897 ◽  
Author(s):  
Tatsuya Shibata ◽  
Toshinari Takahashi ◽  
Eio Yamada ◽  
Akiko Kimura ◽  
Hiroshi Nishikawa ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Rat Liver ◽  
Mitochondrial Function ◽  
Mitochondrial Membrane ◽  
Liver Mitochondria ◽  
Yeast Cells ◽  
Rat Liver Mitochondria ◽  
Content Type ◽  
Glycerol Medium

ABSTRACTT-2307, an arylamidine compound, has been previously reported to have broad-spectrumin vitroandin vivoantifungal activities against clinically significant pathogens, includingCandidaspecies,Cryptococcus neoformans, andAspergillusspecies, and is now undergoing clinical trials. Here we investigated the mechanism of action of T-2307 using yeast cells and mitochondria isolated from yeast and rat liver. Nonfermentative growth ofCandida albicansandSaccharomyces cerevisiaein glycerol medium, in which yeasts relied on mitochondrial respiratory function, was inhibited at 0.001 to 0.002 μg/ml (0.002 to 0.004 μM) of T-2307. However, fermentative growth in dextrose medium was not inhibited by T-2307. Microscopic examination using Mitotracker fluorescent dye, a cell-permeant mitochondrion-specific probe, demonstrated that T-2307 impaired the mitochondrial function ofC. albicansandS. cerevisiaeat concentrations near the MIC in glycerol medium. T-2307 collapsed the mitochondrial membrane potential in mitochondria isolated fromS. cerevisiaeat 20 μM. On the other hand, in isolated rat liver mitochondria, T-2307 did not have any effect on the mitochondrial membrane potential at 10 mM. Moreover, T-2307 had little inhibitory and stimulatory effect on mitochondrial respiration in rat liver mitochondria. In conclusion, T-2307 selectively disrupted yeast mitochondrial function, and it was also demonstrated that the fungal mitochondrion is an attractive antifungal target.

Sign in / Sign up

Export Citation Format

Share Document