Low concentration of GA activates a preconditioning response in HepG2 cells during oxidative stress—roles of Hsp90 and vimentin

Kang, Hong-yun; Zou, Fei

doi:10.1007/s12192-008-0092-7

Cited by 5 publications

(4 citation statements)

References 49 publications

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“…Consistent with our finding, an in vitro study using HepG2 cells revealed that pre-treatment with low concentrations of H 2 O 2 (50 µM) induced increased levels of vimentin, and reduced the cleavage of vimentin following exposure to oxidative stress (26). It has been reported that the cleavage of vimentin by caspases results in the disruption of its filamentous structure, which may promote apoptosis by facilitating nuclear condensation and subsequent fragmentation and amplifying the cell death signal (26). Thus, fewer EPCs may undergo apoptosis induced by oxidative stress through the upregulation of vimentin.…”

Section: Discussionsupporting

confidence: 91%

Proteomic analysis of endothelial progenitor cells exposed to oxidative stress

Liu

Wei

Chen

et al. 2013

International Journal of Molecular Medicine

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Endothelial progenitor cells (EPCs) repair vascular damage and participate in neovascularization. Accumulating evidence has demonstrated that EPCs have therapeutic potential in reactive oxygen species (ROS)-mediated vascular diseases. In this study, to investigate the effects of oxidative stress on EPCs, EPCs were treated with H2O2 at different final concentrations for 3 h. MTT assay, scratch-wound assay and Matrigel invasion assay revealed that cell proliferation, migration and tubule formation and function, respectively, were impaired under H2O2 stress in a concentration-dependent manner. To determine protein response to H2O2 stress, two-dimensional differential in-gel electrophoresis (2D-DIGE) combined with matrix-assisted laser desorption-ionization time-of-flight (MALDI-TOF/TOF) mass spectrometry were performed. The results revealed that triosephosphate isomerase and ADP-sugar pyrophosphatase were downregulated, while peroxiredoxin-2, thioredoxin-dependent peroxide reductase, mitochondrial (Prx‑3), peroxiredoxin-6, EGF-containing fibulin-like extracellular matrix protein 1, vimentin and Rab GDP dissociation inhibitor α were upregulated in the H2O2-treated EPCs. To further confirm the results from mass spectrometry, the expression pattern of Prx-3 in response to H2O2 stress was examined by western blot analysis. The data presented in this study provide novel insight into the defensive mechanisms of EPCs and the pathways of oxidative damage in an oxidative environment.

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Section: Discussionsupporting

confidence: 91%

Proteomic analysis of endothelial progenitor cells exposed to oxidative stress

Liu

Wei

Chen

et al. 2013

International Journal of Molecular Medicine

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“…It is also responsible for subcellular localization of other organelles, especially nucleus and mitochondria [ 4 , 5 ]. One of the important functions of vimentin is to help the cells adapt to various kinds of stresses including heat [ 6 , 7 , 8 ], oxidative and electrophilic addition [ 9 ]. It is considered a marker of epithelial mesenchymal transition (EMT) and is highly expressed during cancer metastasis [ 10 , 11 ].…”

Section: Introductionmentioning

confidence: 99%

Impact of N-Terminal Tags on De Novo Vimentin Intermediate Filament Assembly

Usman

Aldehlawi²,

Nguyen

et al. 2022

IJMS

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Vimentin, a type III intermediate filament protein, is found in most cells along with microfilaments and microtubules. It has been shown that the head domain folds back to associate with the rod domain and this association is essential for filament assembly. The N-terminally tagged vimentin has been widely used to label the cytoskeleton in live cell imaging. Although there is previous evidence that EGFP tagged vimentin fails to form filaments but is able to integrate into a pre-existing network, no study has systematically investigated or established a molecular basis for this observation. To determine whether a tag would affect de novo filament assembly, we used vimentin fused at the N-terminus with two different sized tags, AcGFP (239 residues, 27 kDa) and 3 × FLAG (22 residues; 2.4 kDa) to assemble into filaments in two vimentin-deficient epithelial cells, MCF-7 and A431. We showed that regardless of tag size, N-terminally tagged vimentin aggregated into globules with a significant proportion co-aligning with β-catenin at cell–cell junctions. However, the tagged vimentin aggregates could form filaments upon adding untagged vimentin at a ratio of 1:1 or when introduced into cells containing pre-existing filaments. The resultant filament network containing a mixture of tagged and untagged vimentin was less stable compared to that formed by only untagged vimentin. The data suggest that placing a tag at the N-terminus may create steric hinderance in case of a large tag (AcGFP) or electrostatic repulsion in case of highly charged tag (3 × FLAG) perhaps inducing a conformational change, which deleteriously affects the association between head and rod domains. Taken together our results shows that a free N-terminus is essential for filament assembly as N-terminally tagged vimentin is not only incapable of forming filaments, but it also destabilises when integrated into a pre-existing network.

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“…The occurrence, development, and treatment of cancer may also be related to cyclin B1. Deregulated expression of cyclin B1 may lead to a disrupted control of cell growth and a malignant phenotype (Egloff et al 2006 ; Chen et al 2009 ). Abundance of cyclin B1 (Porter et al 2000 ) and increased expression of cyclin B1 (Gomez et al 2007 ) are parallel to better prognosis.…”

Section: Discussionmentioning

confidence: 99%

“…Cyclin B1 is a client protein of Hsp90 and also a key protein in the control of cell cycle transition from G2 to M phase (Ortiz et al 2002 ). Deregulated expression of cyclin B1 may induce a disrupted control of cell growth and a malignant phenotype (Egloff et al 2006 ; Chen et al 2009 ). Hence, the mechanism of the level change of cyclin B1 affected by hypoxia and 17-DMAG treatment in HCC cells was further explored in this paper.…”

Section: Introductionmentioning

confidence: 99%

Hypoxia attenuates Hsp90 inhibitor 17-DMAG-induced cyclin B1 accumulation in hepatocellular carcinoma cells

Zhang

Huang

et al. 2016

Cell Stress and Chaperones

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Hypoxia stress plays a pivotal role in tumor formation, proliferation, and invasion. Conventional chemotherapy is less effective in the hypoxia microenvironment of solid tumor. Heat shock protein 90 (Hsp90) is an important molecular chaperone in cancer cells and has been a pharmaceutical target for decades. However, Hsp90 inhibitors demonstrate limited effect on solid tumor and the mechanism underlying is not clear. To determine whether hypoxia impairs the therapeutic effect of Hsp90 N-terminal inhibitor, 17-demethoxygeldanamycin hydrochloride (17-DMAG), in live cancer cells, we measured cell proliferation and cell cycle distribution. Cell proliferation assay indicates that hypoxia obviously promotes the proliferation of HepG2 and Huh7 cells after 24, 48, and 72 h and impairs 17-DMAG-induced G2/M arrest in liver cancer cells. As a client protein of Hsp90, cyclin B1 is critical for the transition from G2 to M phase and is related to the prognosis of the patients. We further checked the cyclin B1 messenger RNA (mRNA) level, protein level, ubiquitination of cyclin B1, nuclear translocation, and degradation of cyclin B1 affected by hypoxia after 17-DMAG treatment. The results demonstrate that hypoxia decreases the transcription of cyclin B1 and accelerates the ubiquitination, nuclear translocation, and degradation of cyclin B1. Taken together, our results suggest that hypoxia attenuates cyclin B1 accumulation induced by 17-DMAG and, hence, alleviates 17-DMAG-induced G2/M arrest.

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Low concentration of GA activates a preconditioning response in HepG2 cells during oxidative stress—roles of Hsp90 and vimentin

Abstract: Oxidative stress can be a significant cause of cell death and apoptosis.

Cited by 5 publications

References 49 publications

Proteomic analysis of endothelial progenitor cells exposed to oxidative stress

Proteomic analysis of endothelial progenitor cells exposed to oxidative stress

Impact of N-Terminal Tags on De Novo Vimentin Intermediate Filament Assembly

Hypoxia attenuates Hsp90 inhibitor 17-DMAG-induced cyclin B1 accumulation in hepatocellular carcinoma cells

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