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PubMedDate not supplied

Heat shock proteins in the moderately halophilic bacterium Deleya halophila: protective effect of high salt concentration against thermal shock.

The moderately halophilic eubacterium Deleya halophila grown in medium containing 1 M or 2.5 M NaCl was heat-shocked at various temperatures and the electrophoretic patterns of pulse-labelled proteins were examined. Several polypeptides were induced (heat shock proteins, or hsp) at all temperatures. However, the level of induction of some hsp was dependent on the severity of the thermal shock as well as the salt concentration of the growth medium. Time course studies revealed that synthesis of some of the hsp was transient when cells were grown in 1 M NaCl, while growth at 2.5 M NaCl resulted in the synthesis of most of the hsp at almost maximal level for at least 60 min following temperature shift-up. When cells were returned to normal growth temperature (30 degrees C) after a heat shock treatment (47 degrees C for 5 min), normal protein synthesis resumed faster when cells were grown in 1 M than in 2.5 M NaCl. During the recovery period, several major hsp appeared to be synthesized at near maximal level at both salt concentrations.

Bacterial Proteins↗
PubMed1999

A randomized evaluation of early revascularization to treat shock complicating acute myocardial infarction. The (Swiss) Multicenter Trial of Angioplasty for Shock-(S)MASH.

AIM: To test whether emergency revascularization improves survival in patients with acute myocardial infarction and shock. METHODS AND RESULTS: Patients with acute myocardial infarction and early shock were randomized either to undergo emergency angiography, followed immediately by revascularization when indicated, or to receive initial medical management. In five of the nine participating centres, patients with shock but not randomized were entered in a registry. Only 55 patients could be randomized. Of the 32 patients in the invasive group, 30 (94%) underwent early angiography, 27 (84%) PTCA, and one (4%) CABG. Twenty-two (69%) died within 30 days in the invasive group vs 18/23 (78%) in the medically managed group (ns, RR=0.88, 95% confidence interval 0.6-1.2). Among the registry patients, 24/51 were excluded from randomization solely because of patient or physician preference for the invasive approach: 23 (96%) of them underwent emergency angiography, 21 (88%) PTCA, and 12 (50%) died within 30 days. Among the remaining registry patients (n=27) only nine (33%) underwent early angiography, nine (33%) PTCA and 20 (74%) died. CONCLUSION: We failed to demonstrate that emergency PTCA significantly improves survival in patients with acute myocardial infarction and early cardiogenic shock. Because the study was stopped prematurely, due to an insufficient patient inclusion rate, a clinically meaningful benefit of early reperfusion may have been missed.

Aged↗
PubMed1999

SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK: an international randomized trial of emergency PTCA/CABG-trial design. The SHOCK Trial Study Group.

BACKGROUND: Cardiogenic shock (CS) is the leading cause of death in patients hospitalized with acute myocardial infarction (MI). Nonrandomized studies suggest reduced mortality rate with revascularization. TRIAL DESIGN: The SHOCK trial is a multicenter, randomized, and unblinded study with a Registry for trial-eligible and ineligible nonrandomized patients. The trial is testing the hypothesis that a direct invasive strategy of emergency revascularization for patients with cardiogenic shock complicating acute MI will reduce 30-day all-cause mortality rate by 20 absolute percentage points compared with initial medical stabilization. Eligibility criteria include development of CS within 36 hours of an acute transmural MI as evidenced by ST elevation or new left bundle branch block MI; clinical criteria for CS with hemodynamic confirmation; absence of a mechanical, iatrogenic, or other cause of shock; and enrollment within 12 hours of CS diagnosis. Patients randomly assigned to emergency revascularization immediately undergo coronary angiography, with percutaneous transluminal coronary angioplasty or coronary artery bypass grafting depending on the coronary anatomy. Patients assigned to initial medical stabilization may undergo revascularization >/=54 hours after randomization. END POINTS: The primary end point is all-cause 30-day mortality after randomization. Secondary end points include death at trial termination, changes in left ventricular dimensions and function measured by echocardiography at randomization and 2 weeks later, and changes in quality of life and physical functioning from 2 weeks after discharge to 6 months after MI.

Angioplasty, Balloon, Coronary↗
PubMed1984

A heat shock-resistant mutant of Saccharomyces cerevisiae shows constitutive synthesis of two heat shock proteins and altered growth.

A heat shock-resistant mutant of the budding yeast Saccharomyces cerevisiae was isolated at the mutation frequency of 10(-7) from a culture treated with ethyl methane sulfonate. Cells of the mutant are approximately 1,000-fold more resistant to lethal heat shock than those of the parental strain. Tetrad analysis indicates that phenotypes revealed by this mutant segregated together in the ratio 2+:2- from heterozygotes constructed with the wild-type strain of the opposite mating type, and are, therefore, attributed to a single nuclear mutation. The mutated gene in the mutant was herein designated hsr1 (heat shock response). The hsr1 allele is recessive to the HSR1+ allele of the wild-type strain. Exponentially growing cells of hsr1 mutant were found to constitutively synthesize six proteins that are not synthesized or are synthesized at reduced rates in HSR1+ cells unless appropriately induced. These proteins include one hsp/G0-protein (hsp48A), one hsp (hsp48B), and two G0-proteins (p73, p56). Heterozygous diploid (hsr1/HSR1+) cells do not synthesize the proteins constitutively induced in hsr1 cells, which suggests that the product of the HSR1 gene might negatively regulate the synthesis of these proteins. The hsr1 mutation also led to altered growth of the mutant cells. The mutation elongated the duration of G1 period in the cell cycle and affected both growth arrest by sulfur starvation and growth recovery from it. We discuss the problem of which protein(s) among those constitutively expressed in growing cells of the hsr1 mutant is responsible for heat shock resistance and alterations in the growth control.

Crosses, Genetic↗
PubMed1987

Expression of intron-containing C. elegans heat shock genes in mouse cells demonstrates divergence of 3' splice site recognition sequences between nematodes and vertebrates, and an inhibitory effect of heat shock on the mammalian splicing apparatus.

Splicing of a pair of intron-containing heat shock genes from Caenorhabditis elegans has been studied in transfected mouse cells. The hsp16-1 and hsp16-48 genes of C. elegans encode 16,000 Da heat shock polypeptides. Each gene contains a short intron of 52 (hsp16-1) or 55 (hsp16-48) base pairs. When these genes were introduced into mouse cells, they were efficiently induced following heat shock, but splicing of the introns was abnormal. In mouse cells, cleavage of the hsp16 transcripts occurred at the correct 5' splice sites, but the 3' splice sites were located at AG dinucleotides downstream of the correct sites. This aberrant splicing was not solely due to the small size of the C. elegans introns, since a hsp16-1 gene containing an intron enlarged by tandem duplication showed exactly the same splicing pattern. The mouse cells thus seem to be unable to recognize the natural 3' splice sites of the C. elegans transcripts. The efficiency of splicing was greatly reduced under heat shock conditions, and unspliced transcripts accumulated in the nucleus. During a subsequent recovery period at 37 degrees C, these transcripts were spliced and transported to the cytoplasm.

Animals↗
PubMed1995

Expression of DnaK and GroEL homologs in Leuconostoc esenteroides in response to heat shock, cold shock or chemical stress.

The mechanism of adaptation of bacteria to survive at elevated temperature in the human host and the expression of heat-shock proteins in response to stress was examined by labelling with [35S]methionine. An increase in culture temperature from 26 degrees C to 37 degrees C induced expression of certain bacterial proteins (70 and 60 kDa). Heat shock at 40 degrees C, cold shock (10 degrees C), ethanol treatment or arsenite treatment also led to an increased expression of heat shock proteins of 70 and 60 kDa. Actinomycin D completely blocked the induction, indicating that transcription is required for the overexpression of stress proteins in Leuconostoc mesenteroides. N-terminal sequence analysis showed that these proteins were homologous to the highly conserved chaperone proteins DnaK and GroEL of Escherichia coli, respectively.

Arsenites↗
PubMed1986

Heat shock regulatory gene rpoH mRNA level increases after heat shock in Escherichia coli.

The Escherichia coli rpoH gene product sigma 32 is essential for the increase in heat shock gene transcription found after exposure of the bacteria to a sudden temperature increase. It is not known how the concentration of active sigma 32 is modulated. We showed that rpoH transcript levels increased after heat shock and that the magnitude of the increase in the level of mRNA was correlated with the magnitude of the temperature shift. The increase in the level of rpoH mRNA was still found in rpoH mutants so the mechanism of induction differed from that of the set of previously identified heat shock genes. The increased concentration of rpoH mRNA should result in a higher level of sigma 32, which is likely to be important for increasing heat shock gene transcription.

Bacterial Proteins↗
PubMed1998

Heat shock element architecture is an important determinant in the temperature and transactivation domain requirements for heat shock transcription factor.

The baker's yeast Saccharomyces cerevisiae possesses a single gene encoding heat shock transcription factor (HSF), which is required for the activation of genes that participate in stress protection as well as normal growth and viability. Yeast HSF (yHSF) contains two distinct transcriptional activation regions located at the amino and carboxyl termini. Activation of the yeast metallothionein gene, CUP1, depends on a nonconsensus heat shock element (HSE), occurs at higher temperatures than other heat shock-responsive genes, and is highly dependent on the carboxyl-terminal transactivation domain (CTA) of yHSF. The results described here show that the noncanonical (or gapped) spacing of GAA units in the CUP1 HSE (HSE1) functions to limit the magnitude of CUP1 transcriptional activation in response to heat and oxidative stress. The spacing in HSE1 modulates the dependence for transcriptional activation by both stresses on the yHSF CTA. Furthermore, a previously uncharacterized HSE in the CUP1 promoter, HSE2, modulates the magnitude of the transcriptional activation of CUP1, via HSE1, in response to stress. In vitro DNase I footprinting experiments suggest that the occupation of HSE2 by yHSF strongly influences the manner in which yHSF occupies HSE1. Limited proteolysis assays show that HSF adopts a distinct protease-sensitive conformation when bound to the CUP1 HSE1, providing evidence that the HSE influences DNA-bound HSF conformation. Together, these results suggest that CUP1 regulation is distinct from that of other classic heat shock genes through the interaction of yHSF with two nonconsensus HSEs. Consistent with this view, we have identified other gene targets of yHSF containing HSEs with sequence and spacing features similar to those of CUP1 HSE1 and show a correlation between the spacing of the GAA units and the relative dependence on the yHSF CTA.

Base Sequence↗
PubMed1986

Cellular localization of Drosophila 83-kilodalton heat shock protein in normal, heat-shocked, and recovering cultured cells with a specific antibody.

To gain insight on the possible functions of heat shock proteins (hsp's) in Drosophila, we have purified the 83-kilodalton hsp (hsp 83) from cultured cells and studied its intracellular localization by immunofluorescence in normal, heat-shocked, and recovering cells. The specificity of the antibody was assessed by one- and two-dimensional gel immunoblotting and by partial proteolytic digestion. The anti-hsp 83 antibody does not show any significant cross-reactivity with hsp's of different avian or mammalian cell lines, but cross-reacts with hsp's of similar molecular masses in other dipteran insects. The partial proteolytic peptide maps of Drosophila hsp 83 differ from those of mouse hsp 89 and chicken hsp 84. Immunoblotting of Drosophila Kc cells heat shocked at different temperatures indicates a maximal expression of hsp 83 at 33 degrees C. By immunofluorescence, hsp 83 is shown to have a strictly cytoplasmic localization. In unstressed cells, it is distributed in the entire cytoplasm with a slight enrichment in the perinuclear region. After heat shock, it seems to concentrate at the cell periphery close to the plasma membrane and it gradually redistributes to the whole cytoplasm during cellular recovery at normal temperatures.

Animals↗
PubMed1995

A fas antigen receptor mutation allows development of toxic shock syndrome toxin-1-induced lethal shock in V beta 8.2 T-cell receptor transgenic mice.

Recombinant toxic shock syndrome toxin-1 (rTSST-1) administered to MRL-lpr/lpr TCR V beta 8.2 transgenic mice at doses of 0.1 microgram/mouse resulted in 100% mortality. This was an unexpected finding since TSST-1 does not activate V beta 8.2 T cells. In contrast, control mice heterozygous at the lpr locus and also for the transgene (MRL-lpr/+; V beta 8.2/0) survived doses of superantigen 100 times higher. The transgenic mice which succumbed to rTSST-1 challenge exhibited histopathology of the liver consistent with toxic shock (generalized inflammation and hepatocellular necrosis) as well as substantially elevated serum TNF-alpha, IL-2, and IL-6 cytokine levels. Splenic T cells derived from transgenic mice stimulated with rTSST-1 in vitro did not undergo detectable proliferation as measured in a standard mitogen assay. However, PCR amplification of cDNA prepared from the V beta 8.2 splenocytes revealed the presence of minor populations of TSST-1-reactive V beta elements (i.e. V beta 3 and V beta 15). Furthermore, an expansion of the V beta 3 and V beta 15 T-cell families was detected by PCR assay of spleen cell cultures stimulated with rTSST-1. These results suggested that the exquisite sensitivity of the MRL-lpr/lpr V beta 8.2 transgenic animals to rTSST-1 was not dependent exclusively on T-cell proliferation but was augmented by the influence of a defective fas antigen receptor expressed in homozygous lpr mice. To test this hypothesis more directly, we compared the sensitivity of MRL-lpr/lpr mice (not carrying the V beta 8.2 transgene) to MRL-+/+ mice. The MRL-lpr/lpr fas antigen-defective mice were substantially more susceptible to rTSST-1 challenge. Mice carrying the lpr mutation on another genetic background (C57BL/6.C3H-lpr/lpr) were also more sensitive to rTSST-1 challenge than were C57BL/6.C3H-+/+ mice. Although induction of toxic shock is clearly associated with T-cell proliferation, defects in fas antigen receptor or ligand may also contribute substantively to superantigen-mediated lethal shock by still undefined mechanisms.

Adenine↗
PubMed2005

Heat shock protein 70, heat shock protein 32, and vascular endothelial growth factor production and their effects on lipopolysaccharide-induced apoptosis in porcine aortic endothelial cells.

Lipopolysaccharide (LPS) is a highly proactive molecule that causes in vivo a systemic inflammatory response syndrome and activates in vitro the inflammatory pathway in different cellular types, including endothelial cells (EC). Because the proinflammatory status could lead to EC injury and apoptosis, the expression of proinflammatory genes must be finely regulated through the induction of protective genes. This study aimed at determining whether an LPS exposure is effective in inducing apoptosis in primary cultures of porcine aortic endothelial cells and in stimulating heat shock protein (Hsp)70 and Hsp32 production as well as vascular endothelial growth factor (VEGF) secretion. Cells between third and eighth passage were exposed to 10 microg/mL LPS for 1, 7, 15, and 24 hours (time-course experiments) or to 1, 10, and 100 microg/mL LPS for 7 and 15 hours (dose-response experiments). Apoptosis was not affected by 1 microg/mL LPS but significantly increased in a dose-dependent manner with the highest LPS doses. Furthermore, apoptosis rate increased only till 15 hours of LPS exposure. LPS stimulated VEGF secretion in a dose-dependent manner; its effect became significant after 7 hours and reached a plateau after 15 hours. Both Hsp70 and Hsp32 expressions were induced by LPS in a dose-dependent manner after 7 hours. Subsequent studies were addressed to evaluate the protective role of Hsp32, Hsp70, and VEGF. Hemin, an Hsp32 inducer (5, 20, 50 microM), and recombinant VEGF (100 and 200 ng/mL), were added to the culture 2 hours before LPS (10 microg/mL for 24 hours); to induce Hsp70 expression, cells were heat shocked (42 degrees C for 1 hour) 15 hours before LPS (10 microg/mL for 24 hours). Hemin exposure upregulated Hsp32 expression in a dose-dependent manner and protected cells against LPS-induced apoptosis. Heat shock (HS) stimulated Hsp70 expression but failed to reduce LPS-induced apoptosis; VEGF addition did not protect cells against LPS-induced apoptosis at any dose tested. Nevertheless, when treatments were associated, a reduction of LPS-induced apoptosis was always observed; the reduction was maximal when all the treatments (HS + Hemin + VEGF) were associated. In conclusion, this study demonstrates that LPS is effective in evoking "the heat shock response" with an increase of nonspecific protective molecules (namely Hsp70 and Hsp32) and of VEGF, a specific EC growth factor. The protective role of Hsp32 was also demonstrated. Further investigations are required to clarify the synergic effect of Hsp32, Hsp70, and VEGF, thus elucidating the possible interaction between these molecules.

Animals↗
PubMed2006

Recovery of conditioned fear by a single postextinction shock: effect of similarity of shock contexts and of time following extinction.

Subjects in six experimental groups (n = 16 each) received one-trial passive avoidance (PA) training in which shock was delivered upon movement from a white wooden floor compartment to a black grid compartment. Then fear was extinguished (30 min) in the black compartment. After either 24 or 168 h, all the groups were treated in a room distinctively different from the training room. At each interval, one group received a shock in an apparatus similar to the conditioning box, another received a shock in a dissimilar apparatus, and another was placed in a neutral box. A PA test trial in the training apparatus indicated reinstatement of extinguished fear in all the groups given a postextinction shock except the 24-h dissimilar group. Control groups revealed that the extinction treatment was effective and that spontaneous recovery was not evident. The results were explained in terms of classical conditioning, stimulus generalization, and the broadening (flattening) of stimulus generalization gradients with time.

Animals↗
PubMed2003

Prospective evaluation of early abciximab and primary percutaneous intervention for patients with ST elevation myocardial infarction complicated by cardiogenic shock: results of the REO-SHOCK trial.

OBJECTIVE: Patients with acute myocardial infarction complicated by cardiogenic shock have a high mortality despite the use of early reperfusion therapies with thrombolysis or percutaneous coronary intervention (PCI). Therefore, there is still need to evaluate therapy strategies in these patients. DESIGN: The REO-SHOCK trial was a prospective, non-randomized study, aimed at evaluation of a routine strategy of early abciximab and PCI in a high-risk group of acute ST elevation myocardial infarction (STEMI) patients with cardiogenic shock. RESULTS: Patients (n = 40) planned for coronary angioplasty or stenting received abciximab (0.25 mg/kg bolus followed by 0.125 mg/kg/minute over 12 hours), heparin and aspirin. The intervention was successful in 92.5% of the patients and achieved Thrombolysis In Myocardial Infarction (TIMI) grade 3 patency in 32 patients (80%). The primary endpoint, total mortality after 30 days, was observed in 42.5% (17/40), and was significantly different between patients aged > 75 years and patients aged 75 years (91% versus 24%, respectively; p < 0.001). Major bleeding occurred in 2 patients (5%), but stroke occurred in none. CONCLUSION: A strategy of abciximab with primary PCI in high-risk patients with cardiogenic shock is safe, associated with a high procedural success rate and seems to improve outcomes in patients < 75 years old.

Abciximab↗
PubMed2003

Effects of hypertonic saline, HAES and dimethylsulphoxide on free oxygen radicals in haemorrhagic shock oxygen radicals in haemorrhagic shock.

BACKGROUND: The aim of this study was to investigate the effects of antioxidant and resuscitation fluids which were used during haemorrhagic shock on tissue ischemia. METHODS: Forty New Zealand type rabbits were divided into four groups as C (control), I (hypertonic saline), H (HAES) and D (Dimethylsulphoxide-DMSO). Haemorrhagic shock was induced by bleeding from carotid artery. Thirty minutes after shock, Group C was not resuscitated while Group I was resuscitated with Hypertonic saline 7.2, Group H with 10 % HAES and Group D with HAES 10 % and DMSO. Thiobarbituric acid reactive substances (TBARS) and lactate levels in blood, liver and small bowel samples were measured. RESULTS: There were no significant differences among the groups tissue and plasma TBARS and lactate levels. CONCLUSION: Resuscitation fluids and addition of antioxidants to the resuscitation fluids do not have any superiorities over each other to prevent tissue ischemic insult in haemorrhagic shock.

Animals↗
PubMed1994

Differentiation of mouse embryonal carcinoma cells PCC4 by heat shock and the kinetics of induction of heat shock proteins.

Heat shock to embryonal carcinoma cells PCC4 at 45 degrees C for 30 min resulted in the differentiation of cells although heat shock response was induced on exposure to 42 degrees C for 60 min. Differentiated cells were large and well spread with reduced nuclear/cytoplasmic ratios as compared to undifferentiated cells. Change in cell morphology was associated with the disappearance and appearance of stage specific embryonic antigens 1 and 3 respectively. We also found a change in intracellular pH in PCC4 cells within 30 min of heat shock as measured by the change in fluorescence intensity of a probe incorporated into cells during heat shock.

Animals↗
PubMed1994

Stabilization of protein synthesis in thermotolerant cells during heat shock. Association of heat shock protein-72 with ribosomal subunits of polysomes.

Thermotolerance is defined as the capacity of cells, following a cycle of stress and recovery, to survive a second stress which would otherwise be lethal. Whereas this is a well-documented phenomenon, the mechanisms underlying this protective event remain to be elucidated. Protection of protein synthesis appears to be one of the components in the induction of thermotolerance termed "translational thermotolerance." In the present study we show that translational thermotolerance is not the result of an increase in the concentration of cellular transcripts or the stabilization of preexisting messages, nor the preservation of the rate of amino acid uptake, synthesis of aminoacyl-tRNA, or protection from degradation of newly synthesized polypeptides. These results suggest that translational thermotolerance is the consequence of stabilization of translational initiation and/or polypeptide chain elongation during heat shock. We found that heat shock protein (hsp)-72, the major inducible form of the hsp-70 family of heat shock proteins, is associated with ribosomal subunits in polysomes of thermotolerant cells during heat shock. We hypothesize that such interaction is responsible for rescuing translational initiation and/or polypeptide chain elongation in thermotolerant cells during a subsequent stress. It is possible that hsp-72 on the ribosome is "waiting" for the nascent polypeptide to emerge from the ribosome. Such interaction may maintain the growing polypeptide in solution during stress, allowing elongation to continue, and maintaining a constant rate of translation during the stress.

Adaptation, Biological↗
PubMed1993

[Current concepts in the pathogenesis and treatment of abortion and septic shock. II. The physiopathological bases and outlook in the management of septic shock].

The septic shock has a low frequency in the gynecologic-obstetric patients, nevertheless several obstetric conditions like: septic abortion, chorioamnionitis or puerperal infections can be complicated with this syndrome. The infections cause near 20% of the maternal deaths. Because the high morbidity and mortality of the patients with septic shock is necessary to have an actual knowledge of its pathogenesis and treatment. Any person can be infected but only few of them will develop a septic shock, the response of the host to the microorganisms is the critical point for the develop of this syndrome. Many studies had showed the importance of the bacterial endotoxin and the tumoral necrosis factor as mediators of septic shock. The treatment include: control of the infectious process, restoration of tissue perfusion pressure, restoration of blood volume, use of inotropic agents and general support measures. The role of monoclonal antibodies against endotoxin in the management of Gram-negative sepsis is still ignored, but there are several studies that support its use.

Abortion, Septic↗
PubMed2000

During ischemia-reperfusion in rat kidneys, heat shock response is not regulated by expressional changes of heat shock factor 1.

Ischemia-reperfusion injury is known to induce the inducible form of the 70 kDa heat shock protein HSP70i (or HSP72) mainly via rapid activation of heat shock transcription factor 1 (HSF1). However, little is known about the regulation of the HSF1 gene. We therefore studied the time course of HSF1 mRNA transcription and its relation to the expression pattern of the HSP70i mRNA in the renal cortex, this being the most vulnerable and functionally most important part of the kidney, after different periods of unilateral renal ischemia (10-180 min) and reperfusion (up to 60 min) in male Wistar rats (10 weeks old). Immediately after ischemia there was a significant induction of HSP70i genes. While HSP70i expression constantly increased (up to 4-fold) during reperfusion, even to a higher extent with prolongation of ischemia, HSF1 mRNA remained constitutively expressed under all conditions. Thus, we conclude that during ischemia-reperfusion in rat kidneys, the heat shock response is regulated by other means than expressional changes of HSF1.

Animals↗