INDUCTION OF HEAT SHOCK PROTEIN 70 BY ZINC-bis-(DLHYDROGENASPARTATE) REDUCES CYTOKINE LIBERATION, APOPTOSIS, AND MORTALITY RATE IN A RAT MODEL OF LD100 ENDOTOXEMIA

Klosterhalfen, B.; Hauptmann, Steffen; Offner, Felix-albert; Amo-Takyi, B.; Töns, C.; Winkeltau, G.; Affify, Mamdouh; Küpper, Werner; Kirkpatrick, Charles James; Mittermayer, Christian

doi:10.1097/00024382-199704000-00003

Cited by 49 publications

(44 citation statements)

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“…Most heavy metals are toxic, but some, such, as zinc, are safe to use. Zinc is used to treat the common cold, rhinitis, pneumonia, and dermatitis (10)(11)(12)(13)(14) and zinc has been shown to protect in pig and rat models of endotoxemia (15,16). We here show that addition of zinc to the drinking water of mice protected them against TNF-induced lethal shock, metabolic disturbances, and bowel toxicity.…”

Section: Introductionmentioning

confidence: 60%

“…In rat and pig models of endotoxemia, protection by zinc and induction of HSP70 have been described, although no causal relationship between both activities were shown (15,16). In previous experiments, we found that treatment of mice for 7 days with ZnSO 4 in the drinking water increases the expression of f2,700 genes, of which the inducible hsp70.1 gene is a major and recurrent one.…”

Section: Discussionmentioning

confidence: 86%

“…One group (n = 8) received daily s.c. injections of PBS for 10 days (days [11][12][13][14][15][16][17][18][19][20]. The second group (n = 8) received daily WBHS for 10 days (days [11][12][13][14][15][16][17][18][19][20].…”

Section: Cancer Researchmentioning

confidence: 99%

“…The third group (n = 8) was treated with 25 mmol/L ZnSO 4 in the drinking water starting from day 3 to day 19. The other three groups (n = 10) were treated as the three first groups but received daily s.c. injections of 10 Ag TNF in combination with 5,000 IU IFNg for 10 consecutive days (days [11][12][13][14][15][16][17][18][19][20]. TNF/IFNg was given 12 h after WBHS.…”

Section: Cancer Researchmentioning

confidence: 99%

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Protection of Zinc against Tumor Necrosis Factor–Induced Lethal Inflammation Depends on Heat Shock Protein 70 and Allows Safe Antitumor Therapy

Molle¹,

Roy²,

Bogaert³

et al. 2007

Cancer Research

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Tumor necrosis factor (TNF)-induced inflammation prevents its broad application as an antitumor agent. We here report that addition of ZnSO 4 to the drinking water of mice induces expression of heat shock protein 70 (HSP70) in several organs, notably the gastrointestinal track. Zinc conferred doseresponsive protection against TNF-induced hypothermia, systemic induction of interleukin-6 and NO x , as well as against TNF-induced bowel cell death and death of the organism. The protective effect of zinc was completely absent in mice deficient in the major HSP70-inducible gene, hsp70.1, whereas transgenic mice constitutively expressing the human HSP70.A gene, under control of a B-actin promoter, was also protected against TNF, indicating that an increase in HSP70 is necessary and sufficient to confer protection. The therapeutic potential of the protection induced by ZnSO 4 was clearly shown in a TNF/IFN;-based antitumor therapy using three different tumor models. In hsp70.1 wild-type mice, but not in hsp70.1-deficient mice, zinc very significantly protected against lethality but left the antitumor effect intact. We conclude that zinc protects against TNF in a HSP70-dependent way and that protection by zinc could be helpful in developing a safer anticancer therapy with TNF/IFN;. [Cancer Res 2007;67(15):7301-7]

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Section: Introductionmentioning

confidence: 60%

Section: Discussionmentioning

confidence: 86%

Section: Cancer Researchmentioning

confidence: 99%

Section: Cancer Researchmentioning

confidence: 99%

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Protection of Zinc against Tumor Necrosis Factor–Induced Lethal Inflammation Depends on Heat Shock Protein 70 and Allows Safe Antitumor Therapy

Molle¹,

Roy²,

Bogaert³

et al. 2007

Cancer Research

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“…Many data indicated that activation of HS response could inhibit the production of cytokines in response to proinflammatory stimulation (9,25,27,28). Furthermore, the increased level of TNF-␣ recorded in HSF-1-deficient mice, in parallel with their higher susceptibility to endotoxin challenge compared with wild-type (WT) animals, suggested a link between HSF-1 and inhibition of this cytokine expression (45).…”

mentioning

confidence: 99%

Evidence for a role of heat shock factor 1 in inhibition of NF-κB pathway during heat shock response-mediated lung protection

Wirth

Bureau

Mélotte³

et al. 2004

American Journal of Physiology-Lung Cellular and Molecular Phys

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Wirth, Delphine, Fabrice Bureau, Dorothée Melotte, Elisabeth Christians, and Pascal Gustin. Evidence for a role of heat shock factor 1 in inhibition of NF-B pathway during heat shock responsemediated lung protection. Am J Physiol Lung Cell Mol Physiol 287: L953-L961, 2004. First published June 25, 2004 doi:10.1152/ ajplung.00184.2003.-Heat shock transcription factor (HSF)-1 is recognized as a central component of the heat shock response, which protects against various harmful conditions. However, the mechanisms underlying the protection and the role of HSF-1 in these mechanisms have not yet been clearly elucidated. Using HSF-1 knockout mice (Hsf1 Ϫ/Ϫ ), we examined whether heat shock responsemediated lung protection involved an inhibition of the proinflammatory pathway via an interaction between HSF-1 and NF-B, in response to cadmium insult. The HSF-1-dependent protective effect against intranasal instillation of cadmium (10 and 100 g/mouse) was demonstrated by the higher protein content (1.2-and 1.4-fold), macrophage (1.6-and 1.9-fold), and neutrophil (2.6-and 1.8-fold) number in bronchoalveolar fluids, higher lung wet-to-dry weight ratio, and more severe lung damage evaluated by histopathology in Hsf1 Ϫ/Ϫ compared with wild-type animals. These responses were associated with higher granulocyte/macrophage colony-stimulating factor (GM-CSF; 1.7-fold) but not TNF-␣ concentrations in bronchoalveolar fluids of Hsf1 Ϫ/Ϫ mice compared with those of wild-type animals, indicating that HSF-1 behaved as a repressor of specific cytokine production in our model. To further investigate the mechanism of GM-CSF repression, we analyzed the NF-B activity and IB stability. The DNA binding NF-B activity, in particular p50 homodimer activity, was higher in Hsf1 Ϫ/Ϫ mice than in wild-type mice after cadmium exposure. These results provide a first line of evidence that mechanisms of lung protection depending on HSF-1 involve specific cytokine repression via inhibition of NF-B activation in vivo. knockout mice; cadmium; heat shock proteins; granulocyte/macrophage colony-stimulating factor; nuclear factor-B

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Heat preconditioning prevents oxidative stress-induced damage in the intestine and lung following surgical manipulation

Thomas

Pulimood

Balasubramanian

2003

British Journal of Surgery

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INDUCTION OF HEAT SHOCK PROTEIN 70 BY ZINC-bis-(DLHYDROGENASPARTATE) REDUCES CYTOKINE LIBERATION, APOPTOSIS, AND MORTALITY RATE IN A RAT MODEL OF LD100 ENDOTOXEMIA

Cited by 49 publications

References 0 publications

Protection of Zinc against Tumor Necrosis Factor–Induced Lethal Inflammation Depends on Heat Shock Protein 70 and Allows Safe Antitumor Therapy

Protection of Zinc against Tumor Necrosis Factor–Induced Lethal Inflammation Depends on Heat Shock Protein 70 and Allows Safe Antitumor Therapy

Evidence for a role of heat shock factor 1 in inhibition of NF-κB pathway during heat shock response-mediated lung protection

Heat preconditioning prevents oxidative stress-induced damage in the intestine and lung following surgical manipulation

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