Increased thermostability of thermotolerant CHL V79 cells as determined by differential scanning calorimetry

Lepock, James R.; Frey, H.E.; Heynen, Miriam; Nishio, John N.; Waters, Brenda; Ritchie, Ken; Kruuv, J.

doi:10.1002/jcp.1041420324

Cited by 61 publications

(38 citation statements)

References 28 publications

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“…Ablation therapy, which uses microwave or a laser at 80-100 °C, leading to direct cancer cell death by heat denaturation of proteins or necrosis [15] , may also be categorized as hyperthermia in the broad sense. Regional hyperthermia is a less invasive method of thermal therapy.…”

Section: Hyperthermiamentioning

confidence: 99%

Cancer immunity and therapy using hyperthermia with immunotherapy, radiotherapy, chemotherapy, and surgery

Yagawa¹,

Tanigawa²,

Kobayashi³

et al. 2017

JCMT

100

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Hyperthermia is a type of medical modality for cancer treatment using the biological effect of artificially induced heat. Even though the intrinsic effects of elevated body temperature in cancer tissues are poorly understood, increasing the temperature of the body has been recognized as a popular therapeutic method for tumorous lesions as well as infectious diseases since ancient times. Recently accumulated evidence has shown that hyperthermia amplifies immune responses in the body against cancer while decreasing the immune suppression and immune escape of cancer. It also shows that hyperthermia inhibits the repair of damaged cancer cells after chemotherapy or radiotherapy. These perceptions indicate that hyperthermia has potential for cancer therapy in conjunction with immunotherapy, chemotherapy, radiotherapy, and surgery. Paradoxically, the anticancer effect of hyperthermia alone has not yet been adequately exploited because deep heating techniques and devices to aggregate heat effects only in cancer tissues are difficult in practical terms. This review article focuses on the current understanding concerning cancer immunity and involvement of hyperthermia and the innate and adoptive immune system. The potential for combination therapy with hyperthermia and chemotherapy, radiotherapy, and surgery is also discussed. Key words:Hyperthermia, cancer immunity, chemosensitizer, radiosensitizer, combination cancer therapy, hyperthermic intraoperative peritoneal chemotherapy ABSTRACTArticle history:

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Section: Hyperthermiamentioning

confidence: 99%

Cancer immunity and therapy using hyperthermia with immunotherapy, radiotherapy, chemotherapy, and surgery

Yagawa¹,

Tanigawa²,

Kobayashi³

et al. 2017

JCMT

100

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“…Exposing cells to a brief hyperthermic treatment is well-known to block a more severe heat shock applied several hours later from elevating the level of unfolded protein in the cytosol, apparently by increasing the expression of heat shock-inducible protein chaperones (Mizzen and Welch, 1988;Lepock et al, 1990). S180 cells were subjected to either a 15-min thermal preconditioning treatment at 42°C or mock preconditioned at 37°C.…”

Section: Potential Role Of Unfolded Cytosolic Protein In Stressinducementioning

confidence: 99%

Cytosolic Stress Reduces Degradation of Connexin43 Internalized from the Cell Surface and Enhances Gap Junction Formation and Function

VanSlyke

Musil

2005

MBoC

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The protein constituents of gap junctions, connexins, have a rapid basal rate of degradation even after transport to the cell surface. We have used cell surface biotinylation to label gap junction-unassembled plasma membrane pools of connexin43 (Cx43) and show that their degradation is inhibited by mild hyperthermia, oxidative stress, and proteasome inhibitors. Cytosolic stress does not perturb endocytosis of biotinylated Cx43, but instead it seems to interfere with its targeting and/or transport to the lysosome, possibly by increasing the level of unfolded protein in the cytosol. This allows more Cx43 molecules to recycle to the cell surface, where they are assembled into long-lived, functional gap junctions in otherwise gap junction assembly-inefficient cells. Cytosolic stress also slowed degradation of biotinylated Cx43 in gap junction assembly-efficient normal rat kidney fibroblasts, and reduced the rate at which gap junctions disappeared from cell interfaces under conditions that blocked transport of nascent connexin molecules to the plasma membrane. These data demonstrate that degradation from the cell surface can be down-regulated by physiologically relevant forms of stress. For connexins, this may serve to enhance or preserve gap junction-mediated intercellular communication even under conditions in which protein synthesis and/or intracellular transport are compromised.

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“…Differential scanning calorimetry (DSC) is a thermal-analysis technique that has become a powerful tool for detecting and quantifying thermotropic transitions of various materials (10,13). The DSC method is usually used to characterize isolated biopolymers and macromolecular assemblies but has also been applied successfully to characterize more complex systems such as mammalian cells (24,25,27), bacterial vegetative cells (2,9,26,30,31,37,46), and bacterial spores (32)(33)(34)37). DSC can be used to determine the enthalpy of a thermally induced transition by measuring the differential heat flow required to maintain a sample and an inert reference at the same temperature.…”

mentioning

confidence: 99%

“…These perturbations can be sensed by DSC and recorded as a characteristic pattern of positive transitions (endotherms) and negative transitions (exotherms) representing various cellular components. DSC profiles are analogous to low-resolution gel electrophoresis profiles, except that the separation of DSC peaks is determined by thermostability rather than by mass or charge (25).…”

mentioning

confidence: 99%

Heat killing of bacterial spores analyzed by differential scanning calorimetry

et al. 1992

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Thermograms of the exosporium-lacking dormant spores of Bacillus megaterium ATCC 33729, obtained by differential scanning calorimetry, showed three major irreversible endothermic transitions with peaks at 56, 100, and 114°C and a major irreversible exothermic transition with a peak at 119°C. The 114°C transition was identified with coat proteins, and the 56°C transition was identified with heat inactivation. Thermograms of the germinated spores and vegetative cells were much alike, including an endothermic transition attributable to DNA. The ascending part of the main endothermic 100°C transition in the dormant-spore thermograms corresponded to a first-order reaction and was correlated with spore death; i.e., >99.9%o of the spores were killed when the transition peak was reached. The maximum death rate of the dormant spores during calorimetry, calculated from separately measured D and z values, occurred at temperatures above the 73°C onset of thermal denaturation and was equivalent to the maximum inactivation rate calculated for the critical target. Most of the spore killing occurred before the release of most of the dipicolinic acid and other intraprotoplast materials. The exothermic 119°C transition was a consequence of the endothermic 100°C transition and probably represented the aggregation of intraprotoplast spore components. Taken together with prior evidence, the results suggest that a crucial protein is the rate-limiting primary target in the heat killing of dormant bacterial spores.How do bacterial spores resist heat, and, conversely, how are they killed when their thermal-defense mechanisms are overcome? Answering these two questions is fundamentally important to practical solutions of food spoilage, food poisoning, and infectious disease in which spores are causative. Furthermore, much of microbiological practice depends on heat sterilization, which is predicated on killing all spores in the material.The question of heat resistance mechanisms now seems mainly answered as follows: bacterial spores are able to resist heat because their protoplasts have become dehydrated to a water content that is low enough to immobilize and therefore to protect the vital macromolecules (e.g., proteins, RNA, and DNA) from denaturation and the supramolecular assemblies (e.g., membranes and ribosomes) from disruption. Although dehydration is the only property necessary and sufficient in itself to impart heat resistance, it is enhanced by mineralization (especially by calcification) and thermal adaptation. The physiological processes by which the spore attains the resistant state are less well understood, but the retention of resistance clearly is a function of an intact peptidoglycan cortex encasing the protoplast. The experimental evidence supporting these assertions has been reviewed by Gerhardt and Marquis (19).The question of heat killing mechanisms, however, remains mainly unanswered. In an effort to obtain experimental evidence about these mechanisms, we undertook the study of a selected spore morphotype, Bacillus m...

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Increased thermostability of thermotolerant CHL V79 cells as determined by differential scanning calorimetry

Cited by 61 publications

References 28 publications

Cancer immunity and therapy using hyperthermia with immunotherapy, radiotherapy, chemotherapy, and surgery

Cancer immunity and therapy using hyperthermia with immunotherapy, radiotherapy, chemotherapy, and surgery

Cytosolic Stress Reduces Degradation of Connexin43 Internalized from the Cell Surface and Enhances Gap Junction Formation and Function

Heat killing of bacterial spores analyzed by differential scanning calorimetry

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