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PubMed1994

Transient cold shock induces the heat shock response upon recovery at 37 degrees C in human cells.

We evaluated the effects of a transient cold shock followed by recovery and incubation at 37 degrees C on the regulation of heat shock gene expression in the IMR-90 human diploid fibroblasts and HeLa cells in tissue culture. We showed that preincubation of cells at 4 degrees C induced the synthesis and accumulation of the heat shock proteins (HSPs) upon recovery at 37 degrees C, and the degree of this induction was directly related to the time that the cells spent at 4 degrees C. Assays on the abundance of the hsp 70 transcript, the hsp 70 gene promoter activity, and the trimerization and activation of heat shock factor (HSF) to bind to its consensus heat shock element (HSE) provided evidence that this induction of the heat shock response in cells recovering from a transient cold shock is attributable to a transcriptional event mediated by the activation of HSF. Further, the induction was a response to the temperature upshift from 4 to 37 degrees C as opposed to the 4 degrees C treatment itself; quantitation of the HSE-binding activity of cells incubated at 4 degrees C without recovery and incubation at 37 degrees C gave no evidence of an activated response. Analysis of the effects of protein synthesis inhibitors demonstrated that neither cycloheximide nor puromycin was effective in blocking the induction of HSE-binding activity in cells recovering from a transient cold shock. Experiments on the time course and temperature dependence of this induction of HSE-binding activity showed that the onset, magnitude, and duration of this induction were directly proportional to the severity of the cold stress (measured by time and temperature). We discuss the possible mechanism(s) involved in this induction of the heat shock genes at 37 degrees C by a transient cold shock and the biological implications of this observation.

Base Sequence↗

PubMed1990

DnaK, DnaJ, and GrpE heat shock proteins negatively regulate heat shock gene expression by controlling the synthesis and stability of sigma 32.

The Escherichia coli DnaK heat shock protein has been identified previously as a negative regulator of E. coli heat shock gene expression. We report that two other heat shock proteins, DnaJ and GrpE, are also involved in the negative regulation of heat shock gene expression. Strains carrying defective dnaK, dnaJ, or grpE alleles have enhanced synthesis of heat shock proteins at low temperature and fail to shut off the heat shock response after shift to high temperature. These regulatory defects are due to the loss of normal control over the synthesis and stability of sigma 32, the alternate RNA polymerase sigma-factor required for heat shock gene expression. We conclude that DnaK, DnaJ, and GrpE regulate the concentration of sigma 32. We suggest that the synthesis of heat shock proteins is controlled by a homeostatic mechanism linking the function of heat shock proteins to the concentration of sigma 32.

Alleles↗

PubMed2000

Caveolin internalization by heat shock or hyperosmotic shock.

We investigated the cellular localization of caveolin, a landmark protein of caveolae, by indirect immunofluorescence after heat shock or hyperosmotic shock. Caveolin was internalized to the perinucleus by heat shock (43 degrees C) and relocalized in the plasma membrane after recovery of NIH3T3 cells at 37 degrees C for 4 h. The caveolin internalization was also observed after cells were exposed to hyperosmotic shock. Caveolin disappeared from detergent-insoluble complexes in the heat-shocked cells, but alkaline phosphatase was still there, suggesting that their responses to heat shock are quite different even though both of them were enriched in detergent-insoluble complexes of normal cells. Caveolin was internalized by the actin depolymerizer cytochalasin D, but not by the tubulin depolymerizer nocodazole. In addition, cellular exposure to hydrogen peroxide caused caveolin internalization along with disintegrated microfilaments and intact microtubules. Since cellular exposure to heat shock showed disintegrated microfilaments but intact microtubules, caveolin internalization might be due to depolymerized microfilaments. When cells were exposed to heat shock and allowed to recover for 4 h, actin depolymerization and caveolin internalization were not induced by a second heat shock, suggesting that some heat shock protein(s) might prevent actin depolymerization and caveolin internalization.

3T3 Cells↗

PubMed1996

Enhanced retrieval of unpleasant memories influenced by shock controllability, shock sequence, and rat strain.

The propensity to recall unpleasant events may be related to depression and posttraumatic stress disorder. This study examined the extent to which the recall of a previously unpleasant event (i.e., passive avoidance training) may be influenced by another aversive event. The other aversive event was tail shock. Since the Wistar Kyoto (WKY) rat strain has been proposed as an animal model of depressive behavior, this study was conducted with WKY and Wistar rats. Parameters manipulated included shock controllability, shock sequence (i.e., tail shock before avoidance training versus tail shock after training), and rat strain. Performance of the passive avoidance (PA) response was greater in WKY rats. Exposure to inescapable tail shock was related to greater PA performance compared to exposure to escapable or no-shock treatments. Tail shock prior to PA training led to a greater recall of the PA response. The magnitude of the PA response was influenced by the rat strain, shock controllability, and shock sequence. The applicability of these data to the memory bias phenomenon in depression is discussed.

Animals↗

PubMedDate not supplied

Psychological reactions and family adjustment in shock versus no shock groups after implantation of internal cardioverter defibrillator.

PURPOSE: The purpose of this study was to compare psychological reactions and family adjustment after sudden cardiac arrest (SCA) and internal cardioverter defibrillator (ICD) implantation in survivors who did and did not experience defibrillatory shocks the first year of recovery. METHODS: Data were collected as part of a longitudinal prospective study that examined patient and family adjustment after SCA. SCA survivors and one family member per patient were interviewed and completed questionnaires three times within the first year (hospital discharge, 6 months, and 12 months) after SCA. SAMPLE: Fifteen SCA survivors (13 men and 2 women) between the ages of 30 and 74 (mean 57 years) and one respective family member, usually the spouse, (mean age 53 years) participated. All SCA survivors had had primary ventricular fibrillation outside the hospital, had automatic defibrillators implanted while hospitalized, and were monitored for 1 year. RESULTS: Participants were divided into shock and no shock groups based on activation of their ICD the first year. The mean number of shocks received in the shock group survivors was 26, with a range of 3 to 100. Anxiety, depression, anger, and stress levels were higher for both survivors and their family members in the group that received defibrillator shocks. Denial was high throughout the entire year in all survivors. Dyadic adjustment and family coping were not found to be significantly different between the no shock and shock groups. A trend toward reduction in family social support and dyadic satisfaction was noted in both groups with time. CONCLUSIONS: Both SCA survivors and their family members experience more psychological distress in the first year after ICD implantation if the defibrillator fires. Families in both shock and no shock groups report lower levels of family support and marital satisfaction the first year after SCA and ICD implantation.

Adaptation, Psychological↗

PubMed1989

Frontal cortex lesions block the opioid and nonopioid hypoalgesia elicited by brief shocks but not the nonopioid hypoalgesia elicited by long shocks.

Previous research (Grau, 1987a, 1987b) suggests that forebrain systems play an essential role in the hypoalgesia observed after brief shock but not long shock. Additional research has shown that pentobarbital anesthesia and decerebration block the hypoalgesia observed after 3 brief (0.75-s) shocks but not the hypoalgesia observed after 3 long (25-s) shocks. This is a study of whether a specific forebrain lesion, a frontal cortex lesion, would have a similar impact on hypoalgesia induced by brief (0.75 s) and long (25-s) shocks. Frontal cortex lesions, like decerebration and pentobarbital anesthesia, eliminated the hypoalgesia observed after brief but not long shocks. Because other research suggests that the stress of surgery may influence whether the hypoalgesia elicited by shock is opioid or nonopioid, the 2nd experiment was to examine whether the sham operation per se alters the form of the hypoalgesia observed after brief shock. It does not; in the sham-treated subjects, brief shock induced the usual transient nonopioid hypoalgesia followed by prolonged opioid hypoalgesia. These data suggest that frontal cortex lesions block nonopioid and opioid hypoalgesia observed after brief shock.

Animals↗

PubMed1978

Avoidance based on shock intensity reduction with no change in shock probability.

Rats were trained on a free-operant avoidance procedure in which shock intensity was controlled by interresponse time. Shocks were random at a density of about 10 shocks per minute. Shock probability was response independent. As long as interresponse times remained less than the limit in effect, any shocks received were at the lower of two intensities (0.75 mA). Whenever interresponse times exceeded the limit, any shocks received were at the higher intensity (1.6 mA). The initial limit of 15 seconds was decreased in 3-second steps to either 6 or 3 seconds. All animals lever pressed to avoid higher intensity shock. As the interresponse time limit was reduced, the response rate during the lower intensity shock and the proportion of brief interresponse times increased. Substantial warmup effects were evident, particularly at the shorter interresponse-time limits. Shock intensity reduction without change in shock probability was effective in the acquisition and maintenance of avoidance responding, as well as in differentiation of interresponse times. This research suggests limitations on the generality of a safety signal interpretation of avoidance conditioning.

Journal Article↗

PubMed2000

Startle responses to electric shocks: measurement of shock sensitivity and effects of morphine, buspirone and brain lesions.

The present study developed a new protocol to assess shock sensitivity in rats. Male Wistar rats were subjected to footshock stimuli ranging from 0 to 1.6 mA (0.1 s) in a startle apparatus and startle responses elicited by shocks were measured. Acoustic stimuli (95, 105, or 115 dB) were dispersed within the shock series serving as a control measurement of motor performance. Results indicated that the magnitude of shock startle responses significantly increased with the shock intensity in a linear trend. Morphine (8.0 mg/kg) and buspirone (1.0, 2.5, or 5.0 mg/kg), both of which possessing analgesic effects, depressed shock startle but had no such effect on acoustic startle. The effect of morphine was readily reversed by pretreatment of naloxone (1.0 mg/kg). To investigate the neural basis underlying this response, radio-frequency lesions of various structures implicated in processing of nociceptive or aversive information were undertaken. Lesions of the ventroposterior thalamic nucleus, insular cortex, or amygdala decreased startle reactivity to electric shocks but not to acoustic stimuli. Lesions of the anterior cingulate gyrus or medial prefrontal cortex, while altered the reactivity to acoustic stimuli, had no effect on the shock-elicited startle. These results suggested that the amplitude of startle in response to electric shocks provide a quantitative measurement of shock sensitivity within an extended range of stimulus intensities. Performing this response may engage the the central nociceptive pathway.

Animals↗

PubMed2004

Histocompatibility leukocyte antigen-D related expression is specifically altered and predicts mortality in septic shock but not in other causes of shock.

Although the expression of monocyte histocompatibility leukocyte antigen (HLA)-DR has been shown to be decreased during human sepsis, its level of expression in other nonseptic critical conditions is unclear. The aim of this study was to compare the level of HLA-DR expression on circulating monocytes among patients with septic, hemorrhagic, and cardiogenic shocks and severe sepsis without shock. At admission, HLA-DR expression was exclusively decreased in patients with septic shock (n = 30; P < 0.001), whereas the expression was similar between the other studied groups: cardiogenic shock (n = 16), hemorrhagic shock (n = 11), severe sepsis without shock (n = 18), and healthy volunteers (n = 8). HLA-DR expression was not predictive for overall mortality, but at day 1, an HLA-DR expression of less than 14 of mean fluorescence intensity (that corresponds to 40% labeled monocytes) was predictive of mortality exclusively in patients with septic shock (odds ratio, 11.4 and 95% confidence interval, 1.7; 78.4; P < 0.008). Catecholamine infusion, mechanical ventilation, positive blood culture, and number of units of blood or plasma transfused did not correlate with decreased HLA-DR expression. Thus, the decrease in HLA-DR expression is specific to septic shock and is associated, in septic shock patients, with increased mortality risk.

Adult↗

PubMed1987

Study on glucocorticoid receptors during intestinal ischemia shock and septic shock.

Glucocorticoid receptors (GCRs) were studied by the radioligand binding assay in peripheral leukocytes obtained from dogs during intestinal ischemia shock and obtained from patients with septic shock. Sixteen healthy adult mongrel dogs were divided into two groups at random. The model of intestinal ischemia shock was made by occluding both superior mesenteric artery and vein in the occlusion group. Leukocytic GCRs and plasma cortisol were measured just at the time when mean arterial pressure (MAP) was 13.3 kPa (100 mmHg), 6.6 kPa (50 mmHg), and 3.3 kPa (25 mmHg). Clinically leukocytic GCRs were measured in ten patients in septic shock during hypotensive period and in ten normal volunteers used as control subjects. The results showed that in the occlusion group of animals, the levels of GCRs decreased progressively after shock; there was a significant positive correlation between the extent of reduction of MAP and that of GCRs. Leukocytes from the occlusion group contained significantly lower levels of GCRs than those from controls. The results of clinical observation confirmed the reduction of GCR levels in patients with septic shock. This paper reports for the first time the finding of secondary disorder of GCRs during septic shock, advances a new hypothesis concerning the pathophysiology of shock at the receptor level, and offers the experimental evidence for early use of massive doses of glucocorticoid (GC) in dealing with septic shock.

Adolescent↗

PubMed1996

Translational control during recovery from heat shock in the absence of heat shock proteins.

Heat shock results in a reduction in translational efficiency and an increase in mRNA stability in plants that is proportional to the severity of the stress. To determine whether the absence of heat shock proteins may affect the observed changes during translation or mRNA turnover, the effect that inhibiting transcription during a heat shock has on the subsequent translation of a reporter mRNA was examined. The presence of actinomycin D repressed heat shock protein synthesis in response to the application of a heat shock by more than 80%. The translational efficiency of the reporter mRNA was subject to a greater degree of repression following a heat shock when transcription was inhibited than it was in heat-shocked cells in which transcription was not inhibited. In contrast, inhibiting transcription during a heat shock did not prevent the heat-mediated increase in mRNA stability. These data suggest that ongoing transcription is needed during a heat shock to support a basal level of translational activity in the subsequent recovery from the stress but does not appear to be required for the heat-mediated increase in mRNA stability.

Animals↗

PubMed1997

Improvement of survival from hemorrhagic shock by enterectomy in rats: finding to implicate the role of the gut for irreversibility of hemorrhagic shock.

OBJECTIVE: This study used a Wiggers shock model to investigate the effect of the removal of the intestines on the outcome of hemorrhagic shock. METHODS: Rats were subjected to laparotomy for the removal of the entire small and large intestines (experimental group) or a sham operation (control group) before bloodshedding. During the period of shock, animals were maintained at 30-35 mm Hg arterial pressure for 2 hours. After reinfusion of the shed blood, rats were observed for over 3 hours for survival. The average volumes (mean +/- SEM) of shed blood were 6.84 +/- 0.23 mL (experimental group) and 6.49 +/- 0.39 mL (control group), with no significant difference between the two (p > 0.05). RESULTS: This protocol resulted in a 42% mortality (11 of 26) in the control group and 0% mortality (0 of 25) in the experimental group (p < 0.005, chi2). Moreover, in the survivors, the mean arterial pressure was significantly lower in the control (65.7 +/- 4.3 mm Hg) than in the experimental group (78.2 +/- 3.5 mm Hg) at the end of the experiment (p < 0.05). Comparing volume status, neither serial hematocrit values nor body weight changes through the experiment had a significant difference between the two groups (p's > 0.05). Serial quantitation of blood levels of tumor necrosis factor-alpha (TNF-alpha) revealed that systemic TNF-alpha concentrations peaked at 4 hours after shock in both groups. TNF-alpha levels were not reduced by enterectomy. Instead, the peak concentrations were significantly higher in the enterectomized (387.5 +/- 36.5 pg/mL, n = 13) than in the sham-enterectomized group (175.7 +/- 35.9 pg/mL, n = 12,p < 0.001). Limulus assay, used to detect endotoxins in the blood at 2 hours after restoration of blood volume, showed no endotoxemia in any specimen from either group. Four hours after hemorrhagic shock, blood levels of platelet-activating factor, quantitated by the radioimmunoassay method, were 2.88 +/- 0.18 ng/mL (experimental group, n = 8) and 2.32 +/- 0.32 ng/mL (control group, n = 6). The difference between these two means was not significant (p > 0.05). Measurement of hepatic adenosine triphosphate (ATP) by the luminometric method showed that hepatic ATP contents were significantly reduced in both groups after shock (p's < 0.05). However, a higher magnitude of hepatic ATP depletion occurred in the control group; significantly lower amounts of ATP in the liver tissues of the sham-enterectomized group (367 +/- 95 nmol/g, n = 7) than in that of the enterectomized group (870 +/- 100 nmol/g, n = 13) were observed at 5 hours after shock (p < 0.05). CONCLUSIONS: These experimental findings show that, in the absence of the intestines, hemorrhagic shock is associated with both an improved outcome and higher hepatic ATP levels in rats, suggesting the importance of intestinal participation in the process leading to hepatic ATP depletion as well as irreversibility in shock.

Adenosine Triphosphate↗

PubMed2003

Characterization of two classes of pancreatic shock factors: functional differences exhibited by hydrophilic and hydrophobic shock factors.

Pancreatic tissue homogenate induces a powerful pathophysiologic response sufficient to produce lethal shock in a rat. However, limited progress has been made in the biochemical characterization of these pancreas-derived active factors or their mechanisms of action. It has been shown that the pancreas is a major source of these shock-inducing factors and that they are generated by pancreatic proteinases. Porcine pancreas was homogenized and the filtered homogenate was subjected to organic extraction both before and after incubation for 2.5 h at 37 degrees C. The aqueous and lipid extracts of pancreatic homogenates were collected and analyzed for their ability to activate human neutrophils and to induce lethal shock in the rat. Neutrophil activation, a presumed hallmark of shock, was determined by chemiluminescence and myeloperoxidase (MPO) release. Only the intact homogenate and lipid extracts stimulated the neutrophils, and the aqueous extracts proved to be inactive. Neutrophils exhibited enhanced cellular activation when exposed to substimulatory levels of either formyl-methionyl-leucyl-phenylalanine (FMLP) or platelet-activating factor (PAF) followed by substimulatory levels of the lipid extracts, but not by the aqueous extracts. Both the lipid and aqueous extracts induced dramatic decreases in heart rate and blood pressure when injected in the rat, often resulting in lethal shock. In all cases, incubation of the homogenates at 37 degrees C enhanced the potency of the extracts. Our results demonstrated that the pancreas-derived homogenate and lipid factors were capable of inducing both neutrophil activation and shock. These results support the hypothesis that shock is produced via neutrophils that have been activated by inflammatory components. However, the shock-inducing factors in the aqueous extracts (i.e., hydrophilic fraction of the homogenate) apparently function via a pathway independent of neutrophil activation. This is the first evidence that there are both hydrophobic and hydrophilic factors generated in tissue homogenates capable of inducing shock, and that these different chemical classes of factors appear to function via separate mechanisms.

Animals↗

PubMed1994

Weak acid preservatives block the heat shock response and heat-shock-element-directed lacZ expression of low pH Saccharomyces cerevisiae cultures, an inhibitory action partially relieved by respiratory deficiency.

Inhibition of microbial growth by weak acid preservatives increases with medium acidification, since these agents enter cells in the undissociated state. Many of the effects of these acids are due to the cytoplasmic acidification they cause as they dissociate in the higher pH environment of the cytosol. Sorbic and benzoic acids, two widely used preservatives, were found to exert pronounced effects on the heat shock response and thermotolerance of Saccharomyces cerevisiae. These effects were strongly influenced by the pH of the culture medium. In low pH cultures sorbate inhibited the induction of thermotolerance by sublethal heat shock, causing strong induction of respiratory-deficient petites among the survivors of heat treatment. However, when the culture pH was above 5.5 sorbate acted as a powerful chemical inducer of thermotolerance in the absence of any sublethal heat treatment. Sorbate and benzoate also inhibited heat induction of the major heat shock proteins in low pH yeast cultures. This appears to result from lack of induction of the heat shock element (HSE) promoter sequence since sorbate prevented heat induction of a HSE-lacZ fusion at low pH. The uncoupler carbonyl cyanide m-chlorophenylhydrazone (CCCP) and the plasma-membrane-ATPase inhibitor diethylstilboestrol were identified as additional inhibitors of heat induction of heat shock proteins. Numerous chemicals induce the heat shock response in the absence of heat stress, but sorbate, benzoate, CCCP and diethylstilboestrol are the first compounds shown to act as selective inhibitors of heat-induced protein expression in yeast. In the presence of sorbate concentrations which, at low pH, totally inhibit both the heat shock response and growth of cells competent in respiration, respiratory-deficient petites still retain a limited capacity for growth and for heat induction of heat shock proteins. This restoration of a response to heat shock in acidified sorbate-treated cultures of petites might contribute to their higher capacity for growth in the presence of sorbate.

Adaptation, Physiological↗

PubMed1992

The plasma membrane of yeast acquires a novel heat-shock protein (hsp30) and displays a decline in proton-pumping ATPase levels in response to both heat shock and the entry to stationary phase.

Recent studies have revealed that the action of the proton-translocating ATPase of the plasma membrane of yeast is an important determinant of several stress tolerances and affects the capacity of cells to synthesise heat shock proteins in response to heat shock [Panaretou, B. & Piper, P. W. (1990) J. Gen. Microbiol. 136, 1763-1770; Coote, P. J., Cole, M. B. & Jones, M. V. (1991) J. Gen. Microbiol. 137, 1701-1708]. This study investigated the changes to the protein composition of the Saccharomyces cerevisiae plasma membrane that result from a heat shock to dividing cultures and the entry to stationary growth caused by carbon source limitation. Plasma membranes were prepared from exponential, heat-shocked and stationary yeast cultures. The proteins of these membrane preparations were then analysed by polyacrylamide gel electrophoresis and immunoblot measurement of ATPase levels. The protein composition of plasma membranes displayed two prominent changes in response to both heat shock and the entry to stationary phase: (a) a reduction in the level of the plasma membrane ATPase; and (b) the acquisition of a previously uncharacterised 30 kDa heat-shock protein (hsp30). The ATPase decline with heat shock probably exerts an important influence over the ability of the cell to maintain ATPase activity, and therefore intracellular pH, during extended periods of stress. Through in vivo pulse-labelling of plasma membrane proteins synthesised before and during heat shock, followed by subcellular fractionation, it was shown that hsp30 is the only protein induced by the yeast heat-shock response that substantially copurifies with plasma membranes. It might therefore exert a stress-protective function specifically at this membrane.

Cell Membrane↗

PubMed1995

Cordycepin blocks recovery of non-heat-shock mRNA translation following heat shock in Drosophila.

Treatment of cells with cordycepin (3-deoxyadenosine), an inhibitor of cytoplasmic adenylation, blocks the restoration of normal translation following heat shock. Cordycepin also reduces heat-shock protein 70 (Hsp70) protein synthesis greater than 10-fold, while having little to no effect on mRNA accumulation. Parallel analysis of the poly(A)-binding protein detects no change in its abundance during heat shock or subsequent recovery. These results suggest that normal, non-heat-shock mRNA translational repression during heat shock may be caused by deadenylation, and that readenylation is required for restoration of activity. However, three independent analyses of the adenylation status of mRNAs during heat shock and recovery indicate that no significant changes in polyadenylation occur. (a) The total poly(A) content decreases by only about 10% during heat shock; (b) the size of the poly(A) tract decreases only marginally, from an average length of 75-90 nucleotides in non-heated cells to 45-60 nucleotides during heat shock; (c) virtually all mRNAs bind to oligo d(T)-cellulose, whether extracted from normal-temperature, heat-shock or recovered cells. Our results are most consistent with a model where the process of readenylation, rather than the specific poly(A) tail length, influences translational activation during recovery, paralleling a proposed model for the activation of translation during Xenopus oocyte maturation.

Animals↗

PubMed1996

The role of the 5'-end untranslated region of the mRNA for CspA, the major cold-shock protein of Escherichia coli, in cold-shock adaptation.

During cellular adaptation to low temperature, Escherichia coli transiently synthesizes the major cold-shock protein CspA. It was found that adaptation to cold shock is blocked when the 143-base sequence of the 5' untranslated region (5' UTR) of the cspA mRNA is overproduced. The overproduction of this UTR at 15 degrees C caused the synthesis of not only CspA but also other cold-shock proteins such as CspB and CsdA to be no longer transient but rather prolonged. In addition, inhibition of both the synthesis of cellular proteins other than cold-shock proteins and cell growth was observed. Interestingly, when CspA was also overproduced together with the 5' UTR, normal cold-shock adaptive response was resumed without a prolonged lag period of cell growth. This indicates that the 5' UTR of the cspA mRNA and its gene product CspA play a critical role in the regulation of the expression of cold-shock genes and cold-shock adaptation. An 11-base common sequence (cold box) was found in the 5' UTRs of cspA, cspB, and csdA mRNAs. Indeed, the 25-base sequence within the 5' UTR of the cspA mRNA containing the cold-box sequence was able to prolong CspA production at 15 degrees C. We propose that a putative repressor binds to the cold-box sequence of the cold-shock mRNAs during the adaptive process and this binding in turn blocks the transcription of the cold-shock genes or destabilizes their mRNAs. CspA appears to promote either directly or indirectly the repressor function.

Adaptation, Physiological↗

PubMed1986

Induction of heat shock gene expression without heat shock by hepatocarcinogens and during hepatic regeneration in rat liver.

We investigated the expression of the rat hepatic heat-shock protein (hsp) genes under the influence of hepatocarcinogens and during hepatic regeneration. This was undertaken because of the inducibility of the heat-shock response in rat liver and because heat-shock genes can be expressed with or without heat shock in various cell states in a developmentally regulated manner. We found that acute administration of hepatocarcinogens to rats induced an increased hsp gene transcription in a time- and dose-dependent manner. Chronic exposure of rats to complete hepatocarcinogens induced increased levels of mainly Mr 83,000 heat-shock protein gene transcription and, to a lesser extent, Mr 70,000 heat-shock protein. However, the tumor promoter phenobarbital did not induce increased hsp gene expression. Increased levels of both Mr 83,000 heat-shock protein and Mr 70,000 heat-shock protein gene transcription were found during hepatic regeneration. Thus, increased hsp gene transcription, which correlated with increased heat-shock protein synthesis, was observed under the acute and chronic influence of hepatocarcinogens and during normal hepatic proliferation. These results are similar to those observed for c-H-ras and c-myc expression in rat liver, and they suggest that a coordinate expression of these three genes may occur in hepatic regeneration and in the early stages of experimental chemical hepatocarcinogenesis.

2-Acetylaminofluorene↗