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PubMed1984

Nuclear and nucleolar localization of the 72,000-dalton heat shock protein in heat-shocked mammalian cells.

The intracellular location of the major induced mammalian heat shock (or stress) protein (Mr = 72,000) has been determined by both biochemical and immunological methods. This protein, shown here to be comprised of at least three structurally related isoforms, is produced at high levels within 30 min to 1 h following heat treatment of cells. Biochemical fractionation of cells grown under heat shock showed that following its synthesis a portion of the 72,000-Da protein (and its isoforms) becomes associated with the nucleus while some remains in the cytoplasm. Indirect immunofluorescence studies using antiserum directed against the major isoforms of the 72,000-Da protein were carried out in normal and heat-shocked cells as well as in cells grown under stress by exposure to either an amino acid analogue or to sodium arsenite. Diffuse cytoplasmic and nuclear staining was observed in cells grown at 37 degrees C. In cells grown under heat shock conditions, both the cytoplasmic staining and the nuclear staining were found to increase with the nuclear staining consisting of both granular and patch-like structures, the latter being coincident with phase-dense nucleoli. In the case of cells exposed to amino acid analogues or to sodium arsenite, only cytoplasmic and to a lesser extent nuclear staining was observed, i.e. no localized nucleolar fluorescence was observed. Following return of heat shock-treated cells to normal growth temperatures, both the synthesis of the 72,000-Dalton stress protein and its nucleolar staining were found to diminish.

Animals↗
PubMed1981

[The kidney in shock. A new experimental method for the induction of controlled shock. I].

In this research we identify a new experimental model to study the shock-kidney, since this complication occurs with discreet frequency during high surgery operation. The model that better reproduce the surgical shock-kidney is the controlled hypovolemic shock. We used for this experiment five pigs of weight between 40 and 50 kg and were studied the following data: Ecg, arterial pressure, central venous pressure, diuresis (by incannulation of both ureters), renal arterial flow, levels of the renin in the renal vein. The measurements were made before, during and after the shock. The hypovolemic shock was induced by removing from carotid artery a sufficient quantity of blood to bring the pressure to 45-50 mmHg. This pressure level was kept constant for 120 min and then was reported to normal level by introducing the blood previously removed. During the experiment no kind of drugs were used.

Animals↗
PubMed1993

Transient activation of a distinct serine protein kinase is responsible for 27-kDa heat shock protein phosphorylation in mitogen-stimulated and heat-shocked cells.

We have investigated the phosphorylation of HSP27, a 27-kDa heat shock protein which is involved in cellular thermoresistance and is also an early target of phosphorylation during heat shock and cell stimulation by a variety of growth and differentiation factors. HSP27 is transiently phosphorylated after shifting Chinese hamster cells from their normal temperature of 37 to 44 degrees C. The phosphorylation correlated in time with the transient activation of specific HSP27 protein kinase activities. HSP27 kinase was also induced to maximal levels within 5-15 min following stimulation of quiescent cells with heat shock, serum, thrombin, or basic fibroblast growth factor. Extracts from quiescent cells stimulated by heat shock or serum were analyzed after sequential chromatography on cation exchange and hydroxylapatite columns. In both cases, a single and identical peak of HSP27 kinase activity was obtained, suggesting that the same protein kinase was induced. The HSP27 kinase efficiently phosphorylated recombinant Chinese hamster HSP27 or the synthetic peptide RALNRQLSSGV containing the major in vivo phosphorylation site of rodent HSP27. The kinase was inactive toward the ribosomal S6 protein, the peptide RALSSLRA from S6 protein, or the mutant HSP27 proteins with in vivo phosphorylation sites altered to glycine. The partially purified HSP27 kinase had no kinase C, kinase A, or S6 kinase activities; conversely, HSP27 was not a good substrate for these kinases. HSP27 kinase was rapidly inactivated in the presence of acid phosphatase, suggesting that its activity was regulated by phosphorylation. It is suggested that this heat shock- and serum-induced HSP27 kinase is a novel serine kinase which is linked to a major signal transduction cascade.

Acid Phosphatase↗
PubMed1996

Characterization of a new high-temperature-induced 66-kDa heat-shock protein, antigenically related to heat-shock protein 72.

M-14 human melanoma cells, following severe hyperthermic exposures, synthesized a heat-shock protein of 66 kDa (hsp 66), in addition to the major "classic" heat-shock proteins. This hsp 66 was not expressed following mild hyperthermic exposures sufficient to trigger the synthesis of the other heat-shock proteins. The induction of hsp 66 was observed also in Li human glioma cells treated at 45 degrees C for 20 min. By contrast, hsp 66 was not induced in seven other human cell lines (both melanoma and nonmelanoma) when they were subjected to the same hyperthermic treatment. Immunological recognition experiments showed that hsp 66 cross-reacted with the inducible hsp 72, but not with the constitutive hsp 73. The possibility that hsp 66 is a breakdown product of hsp 72 was ruled out by the fact that Poly(A)+ RNA extracted from cells treated at 45 degrees C for 20 min was able to direct the synthesis of hsp 66 (together with hsp 72) in a message-dependent rabbit reticulocyte lysate, as well as in microinjected Xenopus oocytes. By contrast, only the hsp 72 was expressed using Poly(A)+ RNA extracted from cells heated at 42 degrees C for 1 h. Affinity chromatography experiments on ATP-agarose showed that hsp 66 did not bind ATP in vitro. hsp 66 was localized both in the cytoplasm (cytosol, mitochondria, and microsome fraction) and in the nuclei of cells recovered from a severe heat shock: this intracellular distribution closely corresponded to that of hsp 72. The nuclear-associated hsp 66 was found to be tightly bound to nuclear structures and could not be extracted by incubation in ATP-containing buffer.

Animals↗
PubMed2003

Bimoclomol, a heat shock protein co-inducer, acts by the prolonged activation of heat shock factor-1.

The novel hydroxylamine derivative, bimoclomol, has been shown previously to act as a co-inducer of several heat shock proteins (Hsp-s), enhancing the amount of these proteins produced following a heat shock compared to heat shock alone. Here we show that the co-inducing effect of bimoclomol on Hsp expression is mediated via the prolonged activation of the heat shock transcription factor (HSF-1). Bimoclomol effects are abolished in cells from mice lacking HSF-1. Moreover, bimoclomol binds to HSF-1 and induces a prolonged binding of HSF-1 to the respective DNA elements. Since HSF-1 does not bind to DNA in the absence of stress, the bimoclomol-induced extension of HSF-1/DNA interaction may contribute to the chaperone co-induction of bimoclomol observed previously. These findings indicate that bimoclomol may be of value in targeting HSF-1 so as to induce up-regulation of protective Hsp-s in a non-stressful manner and for therapeutic benefit.

Animals↗
PubMed1998

Concomitant alterations in distribution of 70 kDa heat shock proteins, cytoskeleton and organelles in heat shocked 9L cells.

Maintenance of cell architecture and positioning of organelles are major functions of the cytoskeleton. On the other hand, induction of heat shock proteins (HSPs) and reorganization of the cytoskeleton are the most significant changes in heat-shocked mammalian cells. We examine the alterations in HSP70 and its constitutively expressed cognate, HSC70, as well as the cytoskeleton and organelles in 9L rat brain tumor cells upon heat shock. We employed fluorescence microscopy and scanning electron microscopy to follow these changes. Levels of HSP70s were quantified by Western blotting. Accumulation of HSC70 was more transient and the protein translocated to and subsequently exited from the nucleus more rapidly than HSP70. Changes in actin microfilaments include the nuclear localization of actin fraction and disappearance of cytoplasmic microfilament bundles, while the cortical actin microfilaments were almost unaffected. Furthermore, microtubules retracted slightly from the cell periphery but remained largely unchanged. In contrast, the intermediate filaments collapsed into the perinuclear region. The mitochondria converted from filamentous into granular forms and clustered in a region overlapping with the collapsed intermediate filaments. All of the above alterations are reversible and largely reverted after 8 h of recovery. The effect on Golgi organization was very transient and the apparatus assumed a normal appearance within 4 h after the heat treatment. The ER, on the other hand, was totally unaffected by the heat treatment. These observations help correlate the sequential events following a stress like heat shock and suggest possible physiological functions of these essential constituents of a cell under stress.

Animals↗
PubMed2002

The Escherichia coli small heat-shock proteins IbpA and IbpB prevent the aggregation of endogenous proteins denatured in vivo during extreme heat shock.

The roles of the Escherichia coli IbpA and IbpB chaperones in protection of heat-denatured proteins against irreversible aggregation in vivo were investigated. Overproduction of IbpA and IbpB resulted in stabilization of the denatured and reversibly aggregated proteins (the S fraction), which could be isolated from E. coli cells by sucrose gradient centrifugation. This finding is in agreement with the present model of the small heat-shock proteins' function, based mainly on in vitro studies. Deletion of the ibpAB operon resulted in almost twofold increase in protein aggregation and in inactivation of an enzyme (fructose-1,6-biphosphate aldolase) in cells incubated at 50 degrees C for 4 h, decreased efficiency of the removal of protein aggregates formed during prolonged incubation at 50 degrees C and affected cell viability at this temperature. IbpA/B proteins were not needed for removal of protein aggregates or for the enzyme protection/renaturation in cells heat shocked at 50 degrees C for 15 min. These results show that the IbpA/B proteins are required upon an extreme, long-term heat shock. Overproduction of IbpA but not IbpB caused an increase of the level of beta-lactamase precursor, which was localized in the S fraction, together with the IbpA protein, which suggests that the unfolded precursor binds to IbpA but not to IbpB. Although in the wild-type cells both E. coli small heat-shock proteins are known to localize in the S fraction, only 2% of total IbpB co-localized with the aggregated proteins in the absence of IbpA, while in the absence of IbpB, the majority of IbpA was present in the aggregates fraction.

Escherichia coli↗
PubMed1998

Altered expression of constitutive type and inducible type heat shock proteins in response of D-galactosamine-sensitized mice to lipopolysaccharide as an experimental endotoxic shock model.

The expression of heat shock proteins (HSPs) as stress-induced proteins was studied in mice injected with D-galactosamine (D-GalN) and lipopolysaccharide (LPS) as an experimental endotoxic shock model. The expression of constitutive type heat shock protein 70 (HSC70) was significantly reduced in livers of mice injected with D-galactosamine and lipopolysaccharide, while its expression was unaffected in livers of mice injected with D-galactosamine or lipopolysaccharide alone. The expression of other constitutive type heat shock proteins, namely HSP60, HSP32 and HSP25 was also reduced in mice injected with D-galactosamine and lipopolysaccharide. On the other hand, inducible type HSP70 was detected in livers from mice injected with D-galactosamine and lipopolysaccharide, but not in livers from mice injected with D-galactosamine or lipopolysaccharide alone. Simultaneous injection of anti-tumor necrosis factor (TNF)-alpha antibody prevented the liver from reduced expression of constitutive type HSC70, and lead to marked expression of inducible type HSP70 in the liver. Reduced expression of constitutive type HSC70 was also found when D-galactosamine and recombinant TNF-alpha was injected. Therefore, TNF-alpha was suggested to play a critical role on altered expression of constitutive HSC70 and inducible type HSP70 in response of D-galactosamine-sensitized mice to lipopolysaccharide.

Animals↗
PubMed2004

Male Drosophila melanogaster flies exposed to hypergravity at young age are protected against a non-lethal heat shock at middle age but not against behavioral impairments due to this shock.

Previous studies have shown that exposing flies to hypergravity (3 or 5 g) for two weeks at young age slightly increases longevity of male flies and survival time at 37 degrees C of both sexes, and delays an age-linked behavioral change. The present experiments tested whether hypergravity could also protect flies from a non-lethal 37 degrees C heat shock applied at young, middle or old age (2, 4 or 6 weeks of age). Various durations of exposure at 37 degrees C had similar deleterious effects on climbing activity, spontaneous locomotor activity and learning in flies that lived or not in hypergravity at young age. Therefore, hypergravity does not protect the behavior of flies from a deleterious non-lethal heat shock. Hypergravity increased longevity of virgin males and decreased that of mated ones; it also increased longevity of virgins at 25 degrees C, the usual rearing temperature, but not at 30 degrees C. Thus, the positive effect of hypergravity on longevity is observed only if flies are not subjected to living conditions decreasing longevity, like mating and high temperature. Finally, 4 weeks-old males that lived in hypergravity at young age lived slightly longer (+ 15%) after a non-lethal heat shock (60 or 90 min at 37 degrees C) than flies that always lived at 1 g, but this positive effect of hypergravity was not observed in females or in older males. Therefore, all these results show that hypergravity exposure can help male middle-aged flies recovering from a heat shock, but does not protect them from behavioral impairments linked to this shock: a mild stress occurring at young age can partially protect from a moderate stress at middle age.

Aging↗
PubMed1981

Clozapine effects on responding maintained under shock presentation and shock termination schedules.

Clozapine, a novel antipsychotic, was studied in different squirrel monkeys responding under a 3-min fixed-interval schedule of stimulus-shock termination and a multiple 5-min fixed-interval schedule of shock presentation, 5-min fixed-interval schedule of stimulus-shock termination. Some doses (0.1-1.0 mg/kg IM) of clozapine increased responding under each fixed-interval schedule, whereas higher doses (3.0 and 5.6 mg/kg IM) usually decreased responding under each schedule. Lower response rates maintained under the stimulus-shock termination schedule were increased relatively more by clozapine than were higher rates of responding maintained under the fixed-interval schedule of shock-presentation. The present results illustrate that the effects of clozapine on schedule-controlled behaviors of squirrel monkeys differ from those of other antipsychotics.

Animals↗
PubMed1985

Effects of threat of shock and control over shock on finger pulse volume, pulse rate and systolic blood pressure.

Previous research has evaluated finger pulse volume (FPV) as a psychophysiological measure and found it to reflect anxiety, orienting, effort and anger. Controllable versus uncontrollable threats have been found to have different effects on cardiovascular parameters, including pulse rate (PR) and systolic blood pressure (SBP). To date, no studies have compared the effects of such coping efforts on FPV with their effects on PR and SBP. The present study examined the response of PR, SBP and FPV to conditions of controllable shock, uncontrollable shock and no shock. As expected, SBP and PR measures were elevated in the controllable as compared to uncontrollable shock conditions, replicating previous work on cardiovascular responses to coping demands. In contrast, FPV was sensitive to the threat of shock, but did not differ as a function of the coping demands of the task. The findings were discussed in terms of the interpretation of FPV as a psychophysiological measure.

Adolescent↗
PubMed1988

Biological effects of shock waves: kidney damage by shock waves in dogs--dose dependence.

The effect of shock waves on normal canine kidneys was examined in three groups of dogs whose right kidneys were exposed to 500, 1500, or 3000 shock waves. Autopsy was performed 24-30 h later. The kidneys were enlarged with haemorrhages in the outer and inner renal capsule and intraparenchymally. Macroscopically intraparenchymal haemorrhages were restricted to the high pressure field of the shock wave and consisted of haematomas up to 18 mm diameter (most frequently 6 mm or less) and diffuse haemorrhages. Histologically, haemorrhages were shown to originate from interlobular and arcuate veins. Venous thrombosis, tubular dilatation, and diffuse interstitial haemorrhage occurred in the same area. The number of haematomas was larger, and diffuse haemorrhages were more extended after the application of 1500 and 3000 than after 500 shock waves. No difference was seen between 1500 and 3000 shock waves.

Animals↗
PubMed1990

Biological effects of shock waves: cell disruption, viability, and proliferation of L1210 cells exposed to shock waves in vitro.

L1210 cells were exposed in suspension to shock waves generated with a Dornier XL1 lithotripter. After 1000 discharges at 25 kV, the number of nondisrupted cells was 15% and the number of trypan blue excluding cells was 7% as compared to 100% in sham treated controls; the shock-wave effect was more prominent at higher voltages and less prominent at higher discharge numbers when compared at similar electrical input energies. Overall proliferation of cells which were trypan blue negative after exposure exceeded 70% of the proliferation of sham treated controls, except after 1000 shocks at 25 kV, where proliferation was reduced to 42%. The latter reduction in proliferation was found to be due to a reduced growth for 24 h after exposure, with a return to normal proliferation during the following days. Limiting dilution analysis revealed that the reduced growth was mainly due to a transitory increase of the doubling time and not to a reduction of the number of proliferating cells. Cell disruption by shock waves was completely inhibited by exposing the cells at an elevated pressure of 101 atmospheres, pointing to the possible involvement of cavitation in the shock wave effect.

Animals↗
PubMed1998

Effects of threat of shock, shock electrode placement and darkness on startle.

Fear can be elicited by physically-presented explicit threat stimuli or by more static contextual stimuli that are not an immediate source of danger. Research in both humans and animals suggest that fear produced by these two types of stimuli represents separate processes mediated by different brain structures. The present study used the startle reflex methodology to examine affective responses elicited by an explicit threat cue signalling a period of shock anticipation and by two types of contextual stimuli; darkness and attaching the shock electrodes. As expected, shock anticipation potentiated startle (fear-potentiated startle). Startle was also facilitated by darkness and by the placement of shock electrodes. Further, darkness increased fear-potentiated startle to an explicit threat cue, but did not affect the facilitation of startle produced by attaching the shock electrodes. It is suggested that affective responses to contextual stimuli should be considered when investigating both normal and pathological fear.

Adult↗
PubMed1991

Reduction in defibrillator shocks with an implantable device combining antitachycardia pacing and shock therapy.

Implantable defibrillators reduce the risk of sudden death in patients with malignant ventricular arrhythmias, but significant restriction in quality of life can occur as a result of frequent device activation. To determine if a device that provides both antitachycardia pacing and shock therapy can safely reduce the frequency of shocks after implantation, 46 consecutive patients undergoing initial implantation of a defibrillator were studied. In all patients, the implanted device provided antitachycardia pacing and shock therapy. Detected tachycardia characteristics and the results of therapy were stored in the device's memory. There were 42 men and 4 women, aged 26 to 71 years (mean 58.7 +/- 13.5). Left ventricular ejection fraction ranged from 13% to 67% (mean 32.2 +/- 13.4%) and 31 patients had experienced one or more episodes of cardiac arrest. Induced arrhythmias included sustained monomorphic ventricular tachycardia in 38 patients, nonsustained polymorphic ventricular tachycardia in 2 and ventricular fibrillation in 4. Over a total follow-up period of 255 patient-months (range 1 to 13, mean 6.1), 25 patients experienced spontaneous arrhythmic events. In 22 patients, 909 episodes of tachycardia were treated by antitachycardia pacing, which was successful on 840 occasions (92.4%). Acceleration of ventricular tachycardia by pacing therapy was estimated to have occurred 39 times. Syncope occurred once during pacing-induced acceleration of ventricular tachycardia. Forty-four episodes of tachycardia in seven patients were treated directly by shocks because of short tachycardia cycle length; 88% of all detected tachycardias were treated without the need for shocks. Four patients died from cardiorespiratory failure and one patient died suddenly without any detected tachyarrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1999

Cold-shock response and cold-shock proteins.

Both prokaryotes and eukaryotes exhibit a cold-shock response upon an abrupt temperature downshift. Cold-shock proteins are synthesized to overcome the deleterious effects of cold shock. CspA, the major cold-shock protein of Escherichia coli, has recently been studied with respect to its structure, function and regulation at the level of transcription, translation and mRNA stability. Homologues of CspA are present in a number of bacteria. Widespread distribution, ancient origin, involvement in the protein translational machinery of the cell and the existence of multiple families in many organisms suggest that these proteins are indispensable for survival during cold-shock acclimation and that they are probably also important for growth under optimal conditions.

Adaptation, Biological↗
PubMed2002

Optimization of transthoracic ventricular defibrillation-biphasic and triphasic shocks, waveform rounding, and synchronized shock delivery.

The aim of this study is to optimize the truncated exponential waveform for transthoracic ventricular defibrillation. Discharge of a capacitor gives a fast-rising waveform with a spike; rounding of the waveform slows the rate of rise and removes the spike. Defibrillation thresholds for electrically induced VF were determined for rounded and conventional biphasic and triphasic waveforms (apex-anterior paddles; 130 microF capacitor; 3-10 ms phase duration), and for the Lown waveform in 29 anesthetized pigs. Rounding of the leading edge of the biphasic waveform reduced the threshold voltage and current for defibrillation at 3 + 3 ms and 6 + 6 ms phase duration, relative to the conventional unrounded biphasic or the Lown waveforms. The threshold delivered energy was lower for rounded truncated exponential biphasic shocks at 3 + 3 ms (55.3 +/- 2.5 J) than at 6 + 6 ms (67.6 +/- 2.9 J; reduction 15.9 +/- 3.8%; P <.001; n = 29) phase duration. Triphasic shocks (total duration 6-12 ms) showed no advantages over biphasic shocks in this model. The rounded waveform (6 + 6 ms phase duration) had a reduced delivered energy at threshold (9%) with transthoracic shock delivery synchronized to peak (71.1 +/- 4.2 J) or trough (71.5 +/- 4.9 J) of the high amplitude body surface electrocardiogram signal in ventricular fibrillation, compared with unsynchronized shocks (78.7 +/- 4.7 J; P <.05). In this study a biphasic, rounded waveform of total duration 6 or 12 ms, was optimal for the correction of electrically-induced ventricular fibrillation. Synchronization to the peak or trough of the high amplitude electrocardiogram signal gave a further reduction in the energy to defibrillate.

Animals↗
PubMed1990

Evidence for a heat shock transcription factor-independent mechanism for heat shock induction of transcription in Saccharomyces cerevisiae.

Transcription of the DNA damage-responsive gene, DDRA2, of Saccharomyces cerevisiae is activated by heat shock treatment as well as by mutagen/carcinogen exposure. Deletion analysis of upstream noncoding sequence indicated that sequences between approximately -190 and -140 base pairs were necessary for heat shock and DNA damage regulation of transcription. Fusion of this region to a CYC1-lacZ reporter gene demonstrated that the sequence between -202 and -165 base pairs was sufficient for basal level and heat shock-induced expression. This DNA sequence was unable to bind heat shock transcription factor as judged by binding competition experiments in vitro. These results indicate that yeast possesses a second, heat shock transcription factor-independent mechanism for activating transcription in response to thermal stress.

Amino Acid Sequence↗