Role of Membrane Components in Thermal Injury of Cells and Development of Thermotolerance

Jóźwiak, Zofia; Leyko, W.

doi:10.1080/09553009214552701

Cited by 17 publications

(11 citation statements)

References 149 publications

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“…This result indicates that heat stress illicits alterations to cancer cell biology features that are both dependent and independent of HSF1. Cellular effects brought about by heat shock can be broad and non-specific, for example, heat shock has been shown to increase ROS levels within cells which in turn can activate a wide range of signalling pathways (Hildebrandt et al 2002;Hsu et al 2011;Jozwiak and Leyko 1992). Consistent with this, heat shock has been shown to activate numerous cell signalling pathways associated with migration and EMT, including c-Src, PI-3-kinase, the MAPK pathway and the EGFR pathway (Wolf et al 2011;Lin et al 1997;Nadeau and Landry 2007;Dubois and Bensaude 1993).…”

Section: Discussionmentioning

confidence: 69%

Heat stress induces epithelial plasticity and cell migration independent of heat shock factor 1

Lang

Nguyen

et al. 2012

Cell Stress and Chaperones

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Current cancer therapies including cytotoxic chemotherapy, radiation and hyperthermic therapy induce acute proteotoxic stress in tumour cells. A major challenge to cancer therapeutic efficacy is the recurrence of therapyresistant tumours and how to overcome their emergence. The current study examines the concept that tumour cell exposure to acute proteotoxic stress results in the acquisition of a more advanced and aggressive cancer cell phenotype. Specifically, we determined whether heat stress resulted in an epithelial-to-mesenchymal transition (EMT) and/or the enhancement of cell migration, components of an advanced and therapeutically resistant cancer phenotype. We identified that heat stress enhanced cell migration in both the lung A549, and breast MDA-MB-468 human adenocarcinoma cell lines, with A549 cells also undergoing a partial EMT. Moreover, in an in vivo model of thermally ablated liver metastases of the mouse colorectal MoCR cell line, immunohistological analysis of classical EMT markers demonstrated a shift to a more mesenchymal phenotype in the surviving tumour fraction, further demonstrating that thermal stress can induce epithelial plasticity. To identify a mechanism by which thermal stress modulates epithelial plasticity, we examined whether the major transcriptional regulator of the heat shock response, heat shock factor 1 (HSF1), was a required component. Knockdown of HSF1 in the A549 model did not prevent the associated morphological changes or enhanced migratory profile of heat stressed cells. Therefore, this study provides evidence that heat stress significantly impacts upon cancer cell epithelial plasticity and the migratory phenotype independent of HSF1. These findings further our understanding of novel biological downstream effects of heat stress and their potential independence from the classical heat shock pathway.

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Section: Discussionmentioning

confidence: 69%

Heat stress induces epithelial plasticity and cell migration independent of heat shock factor 1

Lang

Nguyen

et al. 2012

Cell Stress and Chaperones

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“…It is not clear, however, whether protein denaturation is the primary cause of heat lethality or a consequence of some other initiating event. Lipid membranes are also similarly disrupted by increasing temperature (33,34), and loss of bilayer integrity may contribute to heat toxicity, perhaps through an increase in proton permeability as proposed by Coote et al (14).…”

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confidence: 99%

Cytotoxic and Genotoxic Consequences of Heat Stress Are Dependent on the Presence of Oxygen in Saccharomyces cerevisiae

Davidson

Schiestl

2001

J Bacteriol

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Lethal heat stress generates oxidative stress in Saccharomyces cerevisiae, and anaerobic cells are several orders of magnitude more resistant than aerobic cells to a 50°C heat shock. Here we characterize the oxidative effects of this heat stress. The thermoprotective effect in anaerobic cells was not due to expression of HSP104 or any other heat shock gene, raising the possibility that the toxicity of lethal heat shock is due mainly to oxidative stress. Aerobic but not anaerobic heat stress caused elevated frequencies of forward mutations and interchromosomal DNA recombination. Oxidative DNA repair glycosylase-deficient strains under aerobic conditions showed a powerful induction of forward mutation frequencies compared to wild-type cells, which was completely abolished under anaerobiosis. We also investigated potential causes for this oxygen-dependent heat shock-induced genetic instability. Levels of sulfhydryl groups, dominated mainly by the high levels of the antioxidant glutathione (reduced form) and levels of vitamin E, decreased after aerobic heat stress but not after anaerobic heat stress. Aerobic heat stress also led to an increase in mitochondrial membrane disruption of several hundredfold, which was 100-fold reduced under anaerobic conditions.All organisms have an optimal temperature range for growth. When the temperature rises above this optimal temperature, cellular growth ceases and toxicity ensues. For baker's yeast, Saccharomyces cerevisiae, this optimum is within the range of 25 to 35°C. Above 45°C, yeast cells are severely stressed and progressively die so that after 5 min at 50°C, more than 99% of growing nonadapted aerobic yeast cells have died. In the range of 35 to 37°C yeast cells are moderately stressed but continue to grow, developing a protective tolerance to higher lethal heat exposures. In these sublethal heat shock conditions, the cell responds by synthesizing a discrete subset of stress proteins via heat shock-dependent transcription pathways (heat shock, stress response, and yAP-1 elements) and concomitantly attains the increased capacity to resist higher lethal temperatures (38,39,46). Among the heat shock proteins in baker's yeast, only HSP104 has been conclusively associated with adaptive thermotolerance (37,44,45,48). HSP70 is involved in adaptive thermotolerance only in the absence of HSP104 (49).Furthermore, general inhibition of gene expression during heating does not block the acquisition of thermotolerance (5). In addition, the acquisition of thermotolerance is independent of mitotic cell cycle arrest and of the majority of the full spectrum of heat shock proteins (6). For instance o-phenanthroline, a cell cycle inhibitor, causes thermotolerance without induction of the characteristic pattern of heat shock proteins (6). Heat shock proteins are, however, thought to play a role during recovery from stressful conditions (33, 35). For example, Hsp104p is a multifunctional protein having known roles in solubilization of aggregated proteins following heat stress and maintenance o...

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“…Identification of non-toxic, reversibly acting cell sensitizers may facilitate cancer tissue ablation and help introduce therapeutic or diagnostic substances into the cells and tissues. The discovery of cell sensitizers for light significantly increased the effectiveness of phototherapy [39,40] and temperature sensitizers are likely to improve thermotherapy in oncology [41,42]. One can expect that the results presented here will stimulate further search for cell sensitizers and help open new avenues for the application of RE and IRE in biotechnology and medicine.…”

Section: Discussionmentioning

confidence: 98%

Decreasing the thresholds for electroporation by sensitizing cells with local cationic anesthetics and substances that decrease the surface negative electric charge

Grys

Madeja

Korohoda

2014

Cellular and Molecular Biology Letters

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12 664 61 42Abbreviations used: 9-AAA -9-aminoacridine; dcEF -direct current electric field; EthBr 2 -ethidium bromide; FBS -fetal bovine serum; FDA -fluorescein diacetate; HSF -human skin fibroblasts; IRE -irreversible electroporation; PBS -phosphate buffered saline with or without calcium and magnesium ions; RE -reversible electroporation Research article DECREASING THE THRESHOLDS FOR ELECTROPORATION BY SENSITIZING CELLS WITH LOCAL CATIONIC ANESTHETICS AND SUBSTANCES THAT DECREASE THE SURFACE NEGATIVE ELECTRIC CHARGEMACIEJ GRYS, ZBIGNIEW MADEJA* and WŁODZIMIERZ KOROHODA* Department of Cell Biology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Gronostajowa 7, 30-387, Kraków, Poland Abstract: The recently described method of cell electroporation by flow of cell suspension through localized direct current electric fields (dcEFs) was applied to identify non-toxic substances that could sensitize cells to external electric fields. We found that local cationic anesthetics such as procaine, lidocaine and tetracaine greatly facilitated the electroporation of AT2 rat prostate carcinoma cells and human skin fibroblasts (HSF). This manifested as a 50% reduction in the strength of the electric field required to induce cell death by irreversible electroporation or to introduce fluorescent dyes such as calcein, carboxyfluorescein or Lucifer yellow into the cells. A similar decrease in the electric field thresholds for irreversible and reversible cell electroporation was observed when the cells were exposed to the electric field in the presence of the non-toxic cationic dyes 9-aminoacridine (9-AAA) or toluidine blue. Identifying non-toxic, reversibly acting cell sensitizers may facilitate cancer tissue ablation and help introduce therapeutic or diagnostic substances into the cells and tissues.

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Role of Membrane Components in Thermal Injury of Cells and Development of Thermotolerance

Cited by 17 publications

References 149 publications

Heat stress induces epithelial plasticity and cell migration independent of heat shock factor 1

Heat stress induces epithelial plasticity and cell migration independent of heat shock factor 1

Cytotoxic and Genotoxic Consequences of Heat Stress Are Dependent on the Presence of Oxygen in Saccharomyces cerevisiae

Decreasing the thresholds for electroporation by sensitizing cells with local cationic anesthetics and substances that decrease the surface negative electric charge

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