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At least 145 records · Page 8Linked to original sources
PubMed1994

Thiol reducing reagents inhibit the heat shock response. Involvement of a redox mechanism in the heat shock signal transduction pathway.

We evaluated the effects of thiol-reducing agents on the heat shock response in human and rodent cells in culture. Using HeLa cells as an example, we demonstrated that dithiothreitol (DTT,2mM) inhibited the heat (42 degrees C) induced increase in the synthesis of heat shock proteins (HSPs), abundance of mRNA of hsp 70, hsp 70 gene promoter activity, and the heat shock factor (HSF) DNA binding activity. This effect of DTT was specific and attributable to its reducing activity; oxidized DTT was ineffective, and other thiol reducing compounds had the same effect as DTT. Time course and dose-response studies showed that DTT significantly inhibited the heat shock induction of heat shock element binding activity with no preincubation and that 0.6 and 1-2 mM DTT gave half-maximal and maximal inhibition, respectively. The effect of DTT was reversible; removal of the DTT-containing medium prior to heat shock rendered the cells fully responsive. Analysis of the effects of DTT on the regulation and function of HSF suggests that DTT blocked an early and important step in the activation process without having a direct effect on the HSF protein. Thus, DTT inhibited the heat-induced trimerization, phosphorylation, and nuclear translocation of HSF and was also effective against a number of other reagents that are known to activate HSF. On the other hand, DTT did not block the response induced by heat shock at 45 degrees C, and in vitro addition of DTT failed to modulate the DNA binding activity of activated HSF present in cell extracts, suggesting that the HSF protein itself is unlikely to be a direct target of action of DTT. These results, together with the observation that activation of HSF DNA binding activity was attenuated under an anoxic condition and that hydrogen peroxide mimicked the effects of heat shock, suggest the involvement of a redox mechanism as an early and important step in the heat shock signal transduction pathway.

Cell Nucleus↗
PubMed1997

Heat shock protein 27 stimulates recovery of RNA and protein synthesis following a heat shock.

Constitutive expression of human hsp27 resulted in a 100-fold increase in survival to a single lethal heat shock in CHO cells without effecting the development of thermotolerance. A possible mechanism for the thermoprotective function of hsp27 may be increased recovery of protein synthesis and RNA synthesis following a heat shock. A lethal heat shock (44 degrees C, 30 min) results in a 90% reduction in the rate of protein synthesis in non-tolerant cells. Control transfected cells recovered protein synthesis to a pre-heat shock rate 10 h after the heat shock; while cell lines that constitutively express human hsp27 recovered 6 h after the heat shock. Thermotolerant cells had a 50% reduction in protein synthesis, which recovered within 7 h following the heat shock. The same lethal heat shock (44 degrees C, 30 min) reduced RNA synthesis by 60% in the transfected cell lines, with the controls recovering in 7 h; while the hsp27 expressing cell lines recovered within 5 h. Thermotolerant cells had a 40% reduction in RNA synthesis and were able to recover within 4 h. The enhanced ability of hsp27 to facilitate recovery of protein synthesis and RNA synthesis following a heat shock may provide the cell with a survival advantage.

Animals↗
PubMed2002

Heat shock inhibits activation of NF-kappaB in the absence of heat shock factor-1.

The heat shock response is known to inhibit NF-kappaB activation and NF-kappaB-dependent gene expression. Herein we determined if cells lacking heat shock factor-1 (HSF-1), the major transcription factor regulating heat shock protein gene expression, have an altered ability to modulate NF-kappaB activation. Embryonic fibroblasts from HSF-1-null mutant mice (HSF-1-/- cells) had a drastically reduced ability to express heat shock protein-70 in response to heat shock, compared to embryonic fibroblasts from wild-type mice (HSF+/+ cells). There was no difference, however, in the ability of heat shock to inhibit TNFalpha-mediated NF-kappaB activation, IkappaBalpha degradation, IkappaB kinase activation, and macrophage chemotactic protein-1 expression in the HSF-1-/- cells compared to the HSF-1+/+ cells. These data demonstrate that heat shock inhibits activation of the NF-kappaB/IkappaBalpha pathway and NF-kappaB-dependent gene expression in the absence of an intact heat shock response.

Animals↗
PubMed1996

Metallothionein and HSP-72 are induced in the liver by hemorrhagic shock and resuscitation but not by shock alone.

BACKGROUND: Previous reports have indicated that HSP-72 and metallothionein mRNA undergo induction in the liver after resuscitated hemorrhagic shock. In this study we investigated whether unresuscitated shock triggers induction and whether protein induction also occurs. METHODS: Rats were subjected to resuscitated and unresuscitated shock protocols of varying severity; livers were isolated and processed for Northern, Western, and immunohistochemical analysis. Cadmium binding assay was used to measure metallothionein protein. RESULTS: Unresuscitated shock led to no induction of HSP-72 or metallothionein. Severe resuscitated shock led to prompt induction of HSP-72 mRNA and protein in hepatocytes, up to 20-fold over sham group; metallothionein mRNA induction appeared later than HSP-72 and did not lead to elevated protein levels. Mild resuscitated shock had little effect. CONCLUSIONS: These findings indicate resuscitated severe shock, not shock alone, leads to induction of HSP-72 and metallothionein in the liver. Metallothionein expression lags behind HSP-72 expression.

Animals↗
PubMed1995

Relationship between the induction of heat shock proteins and the decrease in glucocorticoid receptor during heat shock response in human osteosarcoma cells.

Previously, it has been found that glucocorticoid receptor (GR) binding activity decreased rapidly during heat shock response in HOS-8603, a human osteosarcoma cell line. In this study, The relationship between the induction of heat shock proteins (HSPs) and the decrease in GR was further studied in the same cell line. It was found that even though quercetin could specifically inhibit the expression of hsp90 alpha and hsp70 mRNA, it could not prevent GR from the decrease in response to the heat shock treatment. This represents the first reported evidence that the induction of HSPs and the decrease in GR during heat shock response were 2 independent biological events. The results of the present study further showed that although the heat shock treatment alone had no effects on alkaline phosphatase (AKP) activity, it could completely block the induction of AKP activity in HOS-8603 cells by dexamethasone (Dex), a synthetic glucocorticoid. These results demonstrate that the heat shock-induced alteration in GR was accompanied by a decrease in GR functional activity. Furthermore, when the induction of HSPs was inhibited by the treatment of cells with quercetin, the stimulatory effects of Dex on AKP activity could still be inhibited completely by the heat shock treatment. The results of this part, on the basis of GR functional activity, further demonstrate that quercetin could not inhibit the heat shock-induced decrease in GR even though it could inhibit the induction of HSPs. To clarify further the effects of quercetin alone on GR binding activity in HOS-8603 cells, the regulation of GR by quercetin was also studied. It was found for the first time that quercetin could down-regulate GR in a time-dependent manner significantly, and that the down-regulation of GR by quercetin in HOS-8603 cells paralelled with a decrease in glucocorticoid-mediated functional responses, suggesting that the down-regulation of GR by quercetin is of biological significance.

Alkaline Phosphatase↗
PubMed1993

Transthoracic defibrillation: effect of dual-pathway sequential pulse shocks and single-pathway biphasic pulse shocks in a canine model.

To determine whether dual-pathway sequential shocks and single-pathway biphasic shocks improved the efficacy of transthoracic defibrillation, we delivered single or sequential truncated waveform shocks of variable duration, voltage, and direction (polarity) to three groups of closed-chest dogs. Dual-pathway sequential shocks were assessed in group 1 (eight animals), biphasic shocks with a single pathway were compared in 11 dogs (group 2), and the effect of varying the duration of the biphasic shocks was assessed in group 3 (four animals). There was no improvement in success rates of the intervention shocks compared with a standard single "control" shock at any energy level. In this experimental model unidirectional or biphasic sequential shocks given over single or dual pathways were not superior to standard single-pulse transthoracic defibrillation.

Analysis of Variance↗
PubMed1990

Biological effects of shock waves: cavitation by shock waves in piglet liver.

Shock waves are known to generate cavitation in vitro. In vivo, extracorporeal shock waves may cause haemorrhages in tissues. Two types of changes were detected by conventional, real-time B-scan ultrasound when shock waves were administered to 5 piglet livers in vivo: transient changes consisting of bright signals in intrahepatic branches of the portal vein and tributaries of the hepatic vein, presumed to originate from gas bubbles, and stationary changes consisting of brightening of the area along the long axis of the high pressure field, presumed to indicate an increased number of gas-filled bubbles in this area. Transient changes appeared from the start of shock wave administration; bright signals were seen in liver vessels for several hundred microseconds before they were flushed away with the blood flow. Stationary changes appeared later, increased in intensity over several hundred shock waves and persisted for minutes after cessation of shock wave administration. Both types of signals were interpreted as direct evidence that lithotripter shock waves generated cavitation in vivo. Similar signals were received in the partly degassed water of the lithotripter tub. At autopsy of the piglets, focal intralobular haemorrhages and thrombi of portal veins were detected in the shock wave path. The occurrence of cavitation and tissue damage in the same gross area suggests that cavitation might be involved in the generation of tissue damage by shock waves.

Animals↗
PubMed1998

Extracorporeal shock waves act by shock wave-gas bubble interaction.

The effect of extracorporeal shock waves on hemoglobin release from red blood cells was recently found to be minimized under minute static excess pressure. It was proposed that this can be explained by shock wave-gas bubble interaction. We substantiated this further by two experiments by applying shock waves to suspended human RBC in a lithotripter at a lower frequency (1 pulse every 5 s) and by administering just a single or 2 strong shock waves at 30 kV. Compared to the usual application rate of 1 discharge per s, the lower frequency reduced the hemoglobin release under minimal static excess pressure in the range from 0-100 kPa. A single strong shock wave released a small amount of hemoglobin at ambient pressure and a similar amount at 200 kPa excess pressure. Two strong shock waves increased the hemoglobin release considerably at ambient pressure when there was a 1- or a 10-s pause between them. Under 200 kPa excess pressure, the hemoglobin release was minimal. A similar low hemoglobin release was also found with 1 shock at ambient and the other at excess pressure. The results are interpreted as clear evidence of shock wave-gas bubble interaction as a dominant mechanism of shock wave action.

Erythrocytes↗
PubMed1984

Shock-induced analgesia on the formalin test: effects of shock severity, naloxone, hypophysectomy, and associative variables.

Rats were exposed to three shocks, spaced 20 s apart, at two different levels of severity, low (.75 s, 1 mA) and high (3 s, 4 mA). Both shock levels produced a similar suppression of the recuperative behavior elicited by an injection of formalin into a rat's hind paw. Naloxone fully reversed the analgesia produced by the low-severity shock but only partially reversed the analgesia produced by the high-severity shock (Experiment 1). Hypophysectomy did not alter the level of analgesia (Experiment 2). When the rats were tested in a chamber different from the one they were shocked in, both analgesias were totally reversed (Experiment 3). However, imposing a delay between shock and analgesia testing did not reduce analgesia (Experiment 4). These results suggest that analgesia is not directly elicited by the shock but by apparatus stimuli associated with shock. Further support for this position was obtained when it was found that a Pavlovian extinction procedure could completely eliminate analgesia (Experiment 5). In all of the experiments, the freezing response, one of the rat's species-specific defense reactions, was monitored simultaneously with recuperative behavior. A parallel was found between analgesia and this defensive response, a result suggesting that an animal's endogenous analgesic systems may be activated along with the animal's defensive motivational system. The results point to the critical nature of associative variables in the control of endogenous analgesic systems. They also suggest that shock severity is a determinant of analgesia's sensitivity to naloxone.

Animals↗