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At least 19 recordsLinked to original sources
PubMed1993

A portion of RNA polymerase II molecules has a component essential for stress responses and stress survival.

Cells respond to stress by altering gene expression, and these adjustments facilitate stress tolerance. Although transcriptional changes are integral to most stress responses, little is known about the mechanisms that permit the transcription apparatus itself to tolerate stress. Here we report that a major role of the RNA polymerase II subunit RPB4 is to permit appropriate transcriptional responses during stress. Yeast cells lacking RPB4 have essentially wild-type growth rates at moderate temperatures (18 to 22 degrees C), but their growth rates are substantially reduced at temperatures outside this range. When subjected to a heat shock, cells lacking RPB4 rapidly lose the ability to transcribe genes and experience a dramatic loss in viability. When cells lacking RPB4 are subjected to the nutrient stress that accompanies entry into stationary phase, they also exhibit a substantial decline in mRNA synthesis and in viability relative to wild-type cells. Interestingly, the portion of RNA polymerase II molecules that contain RPB4 is small in log phase but increases substantially as cells enter stationary phase. We propose that the association of RPB4 with the other RNA polymerase II subunits increases the tolerance of the enzyme to stress.

Blotting, Western↗
PubMed1992

[Consequences of AIDS in the lives of hemophiliacs and their caregiving families in Quebec: stress, response to stress and social support].

The following article focuses on the Québec portion of a national survey on the care needed by hemophiliacs with AIDS or having contracted the HIV virus. The survey was based on an approach that considers social support as a means to face stress. It also examined the needs of dispensers of care and relatives (whether mourning or not) of these persons. Participants revealed having experienced more stress because of an absence of support or simply negative support, than because of the physical deterioration caused by the disease. In addition, the question of confidentiality was often raised. In general, participants said they were satisfied with the support they had received, especially on the part of members of their family.

Acquired Immunodeficiency Syndrome↗
PubMed2025

Genome-wide characterization of ZmCRY genes: unveiling stress response mechanisms and the role of ZmCRYPHR2 in salinity tolerance.

BACKGROUND: Blue light serves as a crucial environmental signal regulating plant growth and development. The cryptochrome (CRY) family represents a key class of blue light receptors involved in these processes, as well as plant growth, development, and defense. However, the functions of CRYs in maize remain largely unexplored. RESULTS: In this study, nine ZmCRY genes were identified and found to be unevenly distributed across five chromosomes. Gene structure and conserved motif analyses revealed that ZmCRYs within the same phylogenetic groups are highly conserved. Synteny analysis indicated a close evolutionary relationship between ZmCRYs and their homologs in Oryza sativa. Promoter analysis identified diverse cis-regulatory elements linked to light response, stress tolerance, and hormone signaling. RT-qPCR analysis showed that ZmCRYs respond to various abiotic and biotic stresses, including high salinity, drought, nitrogen deficiency, Fusarium verticillioides, and Puccinia polysora. Functional studies demonstrated that ZmCRYPHR2, localized in chloroplasts and the cytoplasmic membrane, plays a role in scavenging reactive oxygen and regulating maize salt tolerance. Haplotype 2 of ZmCRYPHR2 was identified as the preferred haplotype in a panel of 269 inbred lines. CONCLUSIONS: These findings provide a comprehensive genomic and functional characterization of the ZmCRY gene family, with ZmCRYPHR2 identified as a pivotal regulator of salt tolerance, offering valuable genetic insights for the development of stress-resilient maize breeding.

Zea mays↗
PubMed1993

The role of chemical-induced stress responses in immunosuppression: a review of quantitative associations and cause-effect relationships between chemical-induced stress responses and immunosuppression.

Although there is an increasing awareness that drugs and chemicals can modulate the immune system by indirect mechanisms, few compounds have been thoroughly evaluated in this regard. Several environmentally relevant chemicals induce stresslike responses, as indicated by elevated glucocorticoid levels. Comparable glucocorticoid levels induced by physical or psychological stressors are consistently associated with suppression of one or more immunological parameters. Thus, it seems likely that stress-related neuroendocrine mechanisms are important in immunosuppression by some environmental chemicals. Distinguishing direct and indirect (stress-related) mechanisms of immunosuppression is generally possible, and this could be done as a routine part of immunotoxicity assessment. Although it is clear that glucocorticoids can contribute to such immunosuppression, it is also clear that several other neuroendocrine mediators associated with stress responses can be immunomodulatory. Thus, correlation between glucocorticoid levels and immunosuppression does not conclusively demonstrate a cause-effect relationship. Demonstrating such relationships has been difficult, but it has been done in a few cases of drug-induced thymic hypoplasia by monitoring several parameters known to be affected by glucocorticoids and by measuring the ability of a glucocorticoid antagonist (RU 486) or adrenalectomy to block changes in these parameters. A similar strategy might be useful for evaluation of the role of glucocorticoids in drug- or chemical-induced suppression of a variety of immune functions, but the effects of RU 486 on neuroendocrine feedback circuits and the possibility of consequent immunological changes must be considered when the data are interpreted. This approach could also be applied to evaluation of the roles in chemical-induced immunosuppression of other neuroendocrine mediators for which antagonists or agents that block the synthesis or release of the mediator are available. However, it is likely that a comprehensive (and perhaps predictive) understanding of the relationship between chemically induced stress responses and immunosuppression will require more detailed and quantitative elucidation of the mechanisms and regulation of neuroendocrine-immune interactions.

Animals↗
PubMed1986

Influence of alexithymic characteristics on physiological and subjective stress responses in normal individuals.

Individual differences in response to stress have been linked to the development of stress-related disorders through the presence of a dissociation between physiological and subjective stress responses. It has been suggested that the presence of alexithymic characteristics may constitute a new source of individual response differences and thereby contribute to the development of a stress-related disorder. However, it is also possible that the presence of alexithymic characteristics is simply a new name for a preexisting construct. The present study examined subjective and physiological stress response patterns in normal individuals with high or low presence of alexithymic characteristics, and the relationship between alexithymia and potentially equivalent constructs. The results revealed that the presence of alexithymic characteristics is independent of repression, trait anxiety, and social desirability. As well, high alexithymics appear to manifest high levels of sympathetic activity, and a dissociation between subjective and physiological stress responses. These results are discussed in terms of the potential contribution of alexithymic characteristics to the development of stress-related disorders.

Adult↗
PubMed1989

Neuroendocrine responses to nicotine and stress: enhancement of peripheral stress responses by the administration of nicotine.

Habitual smokers frequently report that when they are stressed smoking helps them to relax. One potential explanation for the reported stress ameliorating effect of smoking is that cigarette consumption (nicotine self-administration) may decrease the sympathetic autonomic nervous system activity which is associated with the stress response. In the present study, rabbits prepared with chronic vascular cannulae were used to study the effects of nicotine administration on plasma corticosterone, catecholamine (epinephrine, norepinephrine and dopamine) and glucose responses to physical restraint stress. Nicotine (0.025, 0.05 or 0.10 mg nicotine base/kg body weight) was administered for 10 days prior to the "stress test" to allow for the development of habituation/tolerance to its acute toxic effects. Independent administration of nicotine, or the application of the physical restraint stressor, resulted in increases in the plasma concentrations of corticosterone, epinephrine, norepinephrine, and glucose. Nicotine administration during restraint stress enhanced the increase in plasma corticosterone and epinephrine, as compared to the responses induced by either factor alone. The results suggest that the stress ameliorating effect of continued cigarette smoking, as reported by habitual smokers, is not due to a reduction in the activity of the peripheral sympathetic autonomic nervous system.

Animals↗
PubMed1995

The oxidative stress response.

Oxidative stress resulting from toxic effects of reactive oxygen species (ROS) plays an important role in the pathogenesis of a variety of diseases and important biological processes. Toxic effects of these ROS, including the superoxide and hydroxyl radicals, and hydrogen peroxide can cause cellular damage by oxidizing nucleic acids, proteins, and membrane lipids. While the chemical reactions involved in the generation and detoxification of ROS have been studied in great detail, little is known about the cellular and molecular responses to oxidative stress in mammalian cells. This article discusses some of the major aspects of these molecular responses, including alterations in the gene expression of antioxidant enzymes, stress-response genes, and cytokines. The regulatory mechanisms that control this genetic response are highly complex, involving activation of transcription factors and signal transduction pathways. Further characterization of the mechanisms that regulate these molecular responses is essential for understanding the physiologic function of the responses and for the development of new therapeutic modalities to defend and/or adapt to oxidant injury.

Animals↗
PubMed1994

Inhibition of the fetal stress response improves cardiac output and gas exchange after fetal cardiac bypass.

Cardiac bypass in late-gestation fetal lambs causes severe placental vasoconstriction, which leads to fetal death from hypoxemia and respiratory acidosis. This response can be blocked by the administration of indomethacin; however, a fatal metabolic acidosis then gradually develops in the fetus. Because the fetus is known to mount an intensive catecholamine response to stress, and because the fetal myocardium is particularly sensitive to increased afterload, we hypothesized that elevated afterload as a result of fetal stress contributes to diminished cardiac output after bypass. Twenty fetal lambs at 80% gestation underwent 30 minutes of normothermic cardiac bypass at flow rates of 200 to 500 ml/kg per minute. All ewes received general anesthesia with ketamine. In 10 fetuses general anesthesia was specifically designed not to inhibit the release of stress-related catechols (ketamine); the remaining 10 fetuses received a "high" (cisterna magna) total spinal anesthetic with tetracaine, to block the fetal stress response. In each anesthetic group, 5 of the 10 lambs received indomethacin. During operation, normal hemodynamics were preserved in the spinal anesthetic group. Cardiac output, placental blood flow, and arterial carbon dioxide tension were all improved relative to results in the ketamine group. When spinal anesthesia and indomethacin are both given, hemodynamics also approach normal after bypass, and gas exchange is further improved. These data suggest that the inhibition of the stress response by spinal anesthesia improves the hemodynamic status of the fetus during operation and, in combination with indomethacin, allows maintenance of near-normal placental function after fetal cardiac bypass. Similar responses may also be possible in human fetuses with use of a high-dose narcotic technique.

Anesthesia, Spinal↗
PubMed1993

Contrasting effects of central alpha-1-adrenoreceptor activation on stress-responsive and stress-nonresponsive subpopulations of corticotropin-releasing hormone neurosecretory cells in the rat.

Stimulation of the rat hypothalamopituitary-adrenal axis during stress involves activation of central alpha 1-adrenergic receptors. The subpopulation of corticotropin-releasing hormone (CRH) neurosecretory cells that contains vasopressin (VP) is selectively activated by several types of stress (immobilization, hypoglycemia, and intracerebroventricular, i.c.v., colchicine), and is located in a catecholamine-rich area of the hypothalamic paraventricular nucleus. Therefore, we tested the hypothesis that the CRH+/VP+ subpopulation is selectively activated by central alpha 1-adrenergic receptors. The alpha 1-agonist methoxamine or vehicle alone was injected i.c.v. after habituation of rats to daily injections of vehicle through a chronic i.c.v. cannula. Activation of the CRH+/VP+ and CRH+/VP- subpopulations was measured by quantifying depletion of neurosecretory vesicles from immunocytochemically identified axons in the external zone of the median eminence. The habituated, vehicle-injected sham control group had normal levels of plasma ACTH and corticosterone, but possessed a significantly higher proportion of VP-containing CRH axons than naive animals. This change is similar to what was observed previously in rats subjected to repeated daily stress. I.c.v. methoxamine caused elevations of plasma ACTH and corticosterone and significant depletions of vesicles from the CRH+/VP+ axons at 1 and 2 h after injection, compared to the sham control group. The CRH+/VP- axons, however, displayed significant accumulations of neurosecretory vesicles at the same times after 300 micrograms methoxamine, compared to the sham control group. After 100 micrograms methoxamine, there was no change in the CRH+/VP- axons, compared to the sham control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed2025

Pre-established ATF4 occupancy and chromatin organization instruct selective transcription activation during integrated stress response.

Cells rapidly and extensively remodel their transcriptome in response to stress to restore homeostasis, but the underlying mechanisms are not fully understood. Here, we characterize the dynamic changes in transcriptome, epigenetics, and 3D genome organization during the integrated stress response (ISR). ISR induction triggers widespread transcriptional changes within 6 h, coinciding with increased binding of ATF4, a key transcriptional effector. Notably, ATF4 binds to hundreds of genes even under non-stress conditions, priming them for stronger activation upon stress. The transcriptional changes at ATF4-bound sites during ISR do not rely on increased H3K27 acetylation, chromatin accessibility, or rewired enhancer-promoter looping. Instead, ATF4-mediated gene activation is linked to the redistribution of CEBPγ from non-ATF4 sites to a subset of ATF4-bound regions, likely by forming an ATF4/CEBPγ heterodimer. CEBPγ preferentially targets the sites pre-occupied by ATF4, as well as genomic regions exhibiting a unique higher-order chromatin structure signature. Thus, the transcriptional responses during ISR are largely pre-wired by intrinsic chromatin properties. These findings provide critical insights into transcriptional remodeling during ISR with broader implications for other stress responses.

Activating Transcription Factor 4↗
PubMed1995

Dose-response effects of intravenous clonidine on stress response during induction of anesthesia in coronary artery bypass graft patients.

This study was designed to evaluate the dose-response effects of different doses of clonidine on the stress response to laryngoscopy and endotracheal intubation. In a randomized, double-blind study, 48 coronary artery bypass grafting (CABG) patients received 0, 2, 4, or 6 micrograms/kg clonidine as an intravenous (IV) infusion during a 15-min period 30 min prior to induction of anesthesia with etomidate (0.3 mg/kg), fentanyl (5-7 micrograms/kg), and pancuronium (0.1 mg/kg). Sedation was assessed prior to induction of anesthesia. Cardiovascular variables and catecholamine plasma levels were measured at predefined intervals. Additional bolus doses of etomidate and fentanyl for suppression of stress-induced reactions were administered if predefined limits of heart rate and blood pressure were exceeded. Clonidine 4 and 6 micrograms/kg significantly attenuated hemodynamic and adrenergic reactions to stress, reduced pharmacologic interventions, and increased sedation. However, clonidine 6 micrograms/kg was not more effective than 4 micrograms/kg, and clonidine 2 micrograms/kg was equally effective as placebo. We conclude that clonidine 4 micrograms/kg IV is the appropriate dose to attenuate the stress response to laryngoscopy in CABG patients. Side effects limiting the use of IV clonidine were not observed.

Blood Pressure↗
PubMed2026

Twenty-Five Years of the Environmental Stress Response and the Enduring Power of Yeast in Stress Biology.

All organisms must be able to sense and respond to adverse environments, especially those that threaten cellular integrity. The age of genomics clarified the breadth and specificity of cellular stress responses, including in free-living microbes directly exposed to a changing environment. The environmental stress response (ESR) in Saccharomyces cerevisiae was among the first responses defined at the transcriptome-wide level as a common program triggered by diverse types of stress. Since its original publication over 25 years ago, many studies have explored the role, regulation, and evolution of the ESR and underlying principles of stress defense. This perspective reviews the history of the ESR, recent insights and perspectives into its purpose and regulation, and remaining questions in stress biology primed for the power of yeast experimentation.

Saccharomyces cerevisiae↗
PubMed1987

Oxytocin stress responses are dependent upon emotionality.

Comparison of posterior pituitary responses to stress in rat strains with contrasting emotionality has revealed an inverse relationship between oxytocin (OT) responses and emotional reactivity. The plasma OT and arginine-vasopressin (AVP) responses to stress were determined in two psychogenetically selected strains of rat, Roman high avoidance (RHA) and Roman low avoidance (RLA), RLA's being more emotionally reactive than RHA's. Following 1 min immobilisation stress, plasma levels of OT were significantly higher in RHA's compared to RLA's. This finding correlates with the previous demonstration of a sex difference in the OT stress response, females having a higher response than males. Plasma levels of AVP were not significantly modified by immobilization in either strain of rat. However, control levels of AVP were markedly raised in both male and female RHA's.

Arginine Vasopressin↗
PubMed1994

Role of the AMP-activated protein kinase in the cellular stress response.

BACKGROUND: AMP-activated protein kinase is the central component of a protein kinase cascade that phosphorylates and inactivates key regulatory enzymes of several biosynthetic pathways. Elevation of cellular AMP levels activates this kinase, both by allosteric activation, which causes more than 5-fold activation, and by phosphorylation by an upstream kinase kinase, leading to more than 20-fold activation; the result is a greater than 100-fold activation overall. As AMP is usually elevated when cellular ATP is depleted, we have assessed the possibility that the AMP-activated kinase is involved in the cellular response to stress, which is known to lead to ATP depletion. RESULTS: We report that AMP is elevated, and ATP depleted, when isolated rat hepatocytes are subjected to treatments that activate the cellular stress response, namely heat shock or treatment with arsenite. Several events are correlated with these changes in nucleotide levels: first, a large activation of the AMP-activated protein kinase, which can be reversed by treatment with a protein phosphatase; second, phosphorylation and inactivation of one of the known substrates of the AMP-activated kinase, HMG-CoA reductase; and third, inhibition of two of the biosynthetic pathways known to be affected by the AMP-activated kinase, namely sterol and fatty-acid synthesis. CONCLUSIONS: Our results suggest that a major function of the AMP-activated protein kinase is to act protectively, switching off biosynthetic pathways when the cell is subjected to stress that causes ATP depletion, the key signal being a rise in AMP level. By this mechanism, ATP is preserved for processes that may be more essential in the short term, such as the maintenance of ion gradients. This function of the kinase represents a novel role for protein phosphorylation.

AMP-Activated Protein Kinases↗
PubMed1992

Independent regulation of prostaglandin production and the stress response in human fibroblasts.

The stress, or heat shock response of eukaryotic cells is characterized by dramatic changes in the metabolism of responding cells, most notably the increased synthesis of a group of proteins known as heat shock proteins. In this study, we examined the relationship of prostaglandin synthesis/release to the stress response. Stress protein synthesis was induced with sodium arsenite, and prostaglandin E2 and prostacyclin (measured as 6-keto PGF1 alpha) levels were determined by enzyme immunoassay. The stress response was monitored by the incorporation of [35S]methionine and separation of protein by one-dimensional sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Prostaglandin synthesis and the stress response were both induced by sodium arsenite. However, aspirin, a cyclooxygenase inhibitor, inhibited arsenite-induced prostaglandin synthesis but did not inhibit stress protein synthesis. Conversely, the calcium ionophore A23187 also stimulated prostaglandin synthesis, but did not induce the stress response. The results of this study indicate that sodium arsenite, a stress response inducer, stimulates prostaglandin production, but this appears to be a correlative rather than causative occurrence in the stress response. Determination of the cytotoxicity of arsenite indicated a high correlation of stimulation of prostaglandin release with cytotoxicity.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

The integrity of the ventral noradrenergic bundle (VNAB) is not necessary for a normal neuroendocrine stress response.

The paraventricular nucleus of the hypothalamus (PVN) receives a dense noradrenergic innervation originating in the caudal brainstem and conveyed by the ventral noradrenergic bundle (VNAB). To evaluate the importance of this pathway, rats were bilaterally injected with 6-hydroxydopamine (6-OHDA) into the VNAB, posterior to the locus coeruleus to avoid the lesion of the dorsal noradrenergic system. These lesions reduced noradrenaline (NA) levels in the PVN by 60% without any significant change of NA levels in the cortex or of dopamine or serotonin in any part of the brain, indicating the specificity of the lesion. After one or three weeks, the neuroendocrine responses to stress were monitored. The secretion of adrenocorticotropic hormone (ACTH), corticosterone and prolactin were studied under basal conditions and after exposure to a novel environment. The activity of the sympathetic nervous system (SNS) was studied in catheterized rats. Plasma catecholamines were measured in basal conditions, and in response to gentle handling or exposure to footshocks. Apart from a transient increase of the adrenocortical axis activity which disappeared 3 weeks after surgery, the lesion did not change either basal levels of the hormones measured or their response to stress, indicating that the noradrenergic input to the PVN conveyed by the VNAB is not necessary for a normal neuroendocrine stress response to occur.

Adrenergic Fibers↗
PubMed2026

Genome-wide mapping of stress-responsive lncRNA, uc.104, reveals the chromatin-mediated regulation of stress and plasticity-related genes in the hippocampus of chronic restraint rats.

Chronic stress significantly impacts hippocampal function through transcriptional and epigenetic mechanisms. While the roles of lncRNAs in stress-related transcriptional and epigenetic regulation have recently been recognized, their genome-wide functions controlling the transcriptional network remain largely unclear. Evidence indicates that the lncRNA uc.104 is involved in stress responses; however, its genome-wide chromatin interactions and gene regulatory effects are yet to be explored. To examine this, we combined chromatin isolation by RNA purification sequencing (ChIRP-seq) and RNA sequencing (RNA-seq) in the hippocampus from handled control and chronic restraint stress (CRS) rats. ChIRP-seq identified 6,664 uc.104 binding peaks under CRS, including 6,517 enriched and 149 reduced. Many peaks were mapped to intronic and promoter-proximal regions of protein-coding genes. Integration of ChIRP-seq with RNA-seq data revealed 1,839 differentially expressed genes associated with uc.104 binding sites, with 106 high-confidence overlaps. Several genes (Gabra3, Htr7, Irs1, Gpr37, Clu, Hspa1b, Ppp3r2, Nfasc, Pcdhac2, and Cysltr2) identified as regulatory targets of uc.104, have been directly implicated in stress responses, synaptic plasticity, and neuroinflammation. Gene ontology and Synapse GO (SynGO) analyses revealed significant enrichment for processes involving dendritic spine formation, synapse organization, and pre- and postsynaptic signaling. Protein-protein interaction analysis identified hub genes, including EGFR, CDC42, IGF1R, CTNNB1, CALM1, CALM3, POLR2A, MDM2, TBP, and CSNK1E, several of which have been linked to stress-responsive pathways. Together, our findings reveal that uc.104 binding to chromatin near stress- and synapse-related genes may act as a regulator of stress-responsive transcriptional networks in the hippocampus. By linking uc.104 occupancy to stress and synaptic responsive genes, this study highlights uc.104 as a potential mediator of stress-induced hippocampal malfunctions.

Animals↗