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Journal articles on the topic 'Stress suppression'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Beury, Daniel, Phillip Fitzgerald, Minu Srivastava, and Suzanne Ostrand-Rosenberg. "Do stress response genes play a role in maintaining MDSC survival and suppression? (100.17)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 100.17. http://dx.doi.org/10.4049/jimmunol.184.supp.100.17.

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Abstract Myeloid- derived suppressor cells (MDSC) contribute to immune suppression in tumor bearing individuals. Their suppression and survival are increased by inflammation. MDSC production of toxic radicals is the primary mechanism of suppression but the toxic mediators do not affect the MDSC themselves. We are investigating stress response genes that may maintain MDSC survival and facilitate suppression. BALB/c mice were injected with BALB/c derived mammary carcinoma 4T1 or 4T1 constitutively expressing the pro-inflammatory cytokine IL-1β (4T1/IL-1β). Primary tumors were surgically removed after 25 days. At 35 days, spleens were harvested and assayed for the percentage of Gr1+ CD11b+ MDSC. Surgical removal of 4T1 results in a regression of the MDSC population, however MDSC do not regress in mice bearing 4T1/IL-1β tumors, confirming that inflammation increases MDSC survival. Western blots and confocal microscopy of MDSC induced by 4T1 and 4T1/IL-1β tumors localize Nrf2 in the nucleus, demonstrating that Nrf2 is activated in MDSC. Catalase, a protein transcriptionally regulated by Nrf2, when added to a T cell activation assay eliminates MDSC suppressive activity. Addition of catalase to T cells co-cultured with MDSC and peptide causes a synergistic effect, activating T cells to a greater level than peptide alone. Collectively these data suggest that stress genes may play a role in maintaining MDSC survival and suppressive activity.

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2

Pollock, R. E., E. Lotzová, S. D. Stanford, and M. M. Romsdahl. "Effect of surgical stress on murine natural killer cell cytotoxicity." Journal of Immunology 138, no. 1 (January 1, 1987): 171–78. http://dx.doi.org/10.4049/jimmunol.138.1.171.

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Abstract Natural killer cell cytotoxicity (NKCC) against tumors may be important in preventing in vivo solid tumor dissemination. Multiple animal models demonstrate increased rates of tumor dissemination after surgical stress; previously, we have observed that surgical stress impairs murine NKCC. Because of the importance of surgery in the control of solid tumors, it appeared valuable to examine the mechanism underlying surgical stress impairment of NKCC. The results of this study demonstrate that postsurgical suppression of NKCC begins as early as 2 hr after murine hind limb amputation, reaches nadir at 4 days, and does not recover to control level until postoperative day 12. Anesthetic treatment alone does not cause comparable NKCC suppression. The suppression of NKCC accompanied changes in both splenic size and morphology. The immune suppression was observed in multiple compartments including peripheral blood, bone marrow, and spleen. Mixing experiments demonstrated that surgical stress per se generated a suppressor cell population affecting NKCC. The observed suppression apparently required cell-to-cell contact, because supernatants from 4 and 18 hr cultures of suppressor cells did not cause suppression. The observed suppression was prevented by perioperative treatment with the pyrimidinone analog 2-amino-5-bromo-6-phenyl-4-pyrimidinol. These preclinical observations point to the future prospect of NK-specific perioperative immunotherapy that may help prevent possible tumor dissemination from occurring at the time of surgery.

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3

Guigueno, Agnès, Janie Dassa, Pascal Belin, and Paul Louis Boquet. "Oversynthesis of a New Escherichia coliSmall RNA Suppresses Export Toxicity of DsbA′-PhoA Unfoldable Periplasmic Proteins." Journal of Bacteriology 183, no. 4 (February 15, 2001): 1147–58. http://dx.doi.org/10.1128/jb.183.4.1147-1158.2001.

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ABSTRACT In Escherichia coli, the DsbA′-PhoA hybrid proteins carrying an unfoldable DsbA′ fragment can be targeted to the envelope, where they exert their toxicity. Hybrid proteins stick to the periplasmic face of the inner membrane and paralyze the export mechanism, becoming lethal if sufficiently overproduced and if not degraded by the DegP protease (A. Guigueno, P. Belin, and P. L. Boquet, J. Bacteriol. 179:3260–3269, 1997). We isolated a multicopy suppressor that restores viability to a degP strain without modifying the expression level of the toxic fusion. Suppression does not involve activation of the known envelope stress-combative pathways, the Cpx pathway and the ςE regulon. Subclone analysis of the suppressor revealed a 195-bp DNA fragment that is responsible for toxicity suppression. The cloned gene, called uptR, is ≈130 bp long (including the promoter and a transcription termination signal) and is transcribed into a small RNA (92 nucleotides). Using site-directed mutagenesis, we found that UptR RNA does not require translation for toxicity suppression. UptR-mediated action reduces the amount of membrane-bound toxic hybrid protein. UptR RNA is the first example of a small RNA implicated in extracytoplasmic toxicity suppression. It appears to offer a new way of suppressing toxicity, and its possible modes of action are discussed.

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4

Amit, Z., and Z. H. Galina. "Stress-induced analgesia: adaptive pain suppression." Physiological Reviews 66, no. 4 (October 1, 1986): 1091–120. http://dx.doi.org/10.1152/physrev.1986.66.4.1091.

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In this paper we have examined the phenomenon of stress-induced analgesia. We have described the procedures used to measure analgesia and have suggested that the tests can be designed not only to indicate changes in pain threshold but also to allow for the determination of the capacity to execute adaptive behavior. Aside from enabling the analysis of responses, tests that induce reflexive as well as nonreflexive behavior may have the capacity to separate the more complex aspects of pain such as the possible presence of two components of pain, sensory/discriminative and motivational/affective. These components may be of fundamental importance for any attempt to understand the biological significance of SIA. Our examination of the neurotransmitter and neuropeptide systems has revealed that they are affected by the same manipulations that induce SIA. These amines and perhaps peptides play an integral role in learning, motivation, and performance. We conclude that the functional advantage of a reduction of pain during stressful situations is significant because it allows the animal to react in threatening and perhaps critical situations as if there were no pain. Once the pain system is inhibited, other systems modulate and mediate adaptive responses that expedite the survival of the animal.

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5

Glaser, Ronald, John Rice, John Sheridan, Richard Fertel, Julie Stout, Carl Speicher, David Pinsky, et al. "Stress-related immune suppression: Health implications." Brain, Behavior, and Immunity 1, no. 1 (March 1987): 7–20. http://dx.doi.org/10.1016/0889-1591(87)90002-x.

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6

Grachev, P., X. F. Li, M. H. Hu, S. Y. Li, R. P. Millar, S. L. Lightman, and K. T. O’Byrne. "Neurokinin B Signaling in the Female Rat: a Novel Link Between Stress and Reproduction." Endocrinology 155, no. 7 (July 1, 2014): 2589–601. http://dx.doi.org/10.1210/en.2013-2038.

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Acute systemic stress disrupts reproductive function by inhibiting pulsatile gonadotropin secretion. The underlying mechanism involves stress-induced suppression of the GnRH pulse generator, the functional unit of which is considered to be the hypothalamic arcuate nucleus kisspeptin/neurokinin B/dynorphin A neurons. Agonists of the neurokinin B (NKB) receptor (NK3R) have been shown to suppress the GnRH pulse generator, in a dynorphin A (Dyn)-dependent fashion, under hypoestrogenic conditions, and Dyn has been well documented to mediate several stress-related central regulatory functions. We hypothesized that the NKB/Dyn signaling cascade is required for stress-induced suppression of the GnRH pulse generator. To investigate this ovariectomized rats, iv administered with Escherichia coli lipopolysaccharide (LPS) following intracerebroventricular pretreatment with NK3R or κ-opioid receptor (Dyn receptor) antagonists, were subjected to frequent blood sampling for hormone analysis. Antagonism of NK3R, but not κ-opioid receptor, blocked the suppressive effect of LPS challenge on LH pulse frequency. Neither antagonist affected LPS-induced corticosterone secretion. Hypothalamic arcuate nucleus NKB neurons project to the paraventricular nucleus, the major hypothalamic source of the stress-related neuropeptides CRH and arginine vasopressin (AVP), which have been implicated in the stress-induced suppression of the hypothalamic-pituitary-gonadal axis. A separate group of ovariectomized rats was, therefore, used to address the potential involvement of central CRH and/or AVP signaling in the suppression of LH pulsatility induced by intracerebroventricular administration of a selective NK3R agonist, senktide. Neither AVP nor CRH receptor antagonists affected the senktide-induced suppression of the LH pulse; however, antagonism of type 2 CRH receptors attenuated the accompanying elevation of corticosterone levels. These data indicate that the suppression of the GnRH pulse generator by acute systemic stress requires hypothalamic NKB/NK3R signaling and that any involvement of CRH therewith is functionally upstream of NKB.

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7

Lin, Yuanshao, Xiaofeng Li, Micol Lupi, James S. Kinsey-Jones, Bei Shao, Strafford L. Lightman, and Kevin T. O'Byrne. "The Role of the Medial and Central Amygdala in Stress-Induced Suppression of Pulsatile LH Secretion in Female Rats." Endocrinology 152, no. 2 (February 1, 2011): 545–55. http://dx.doi.org/10.1210/en.2010-1003.

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Abstract Stress exerts profound inhibitory effects on reproductive function by suppressing the pulsatile release of GnRH and therefore LH. Although the mechanisms by which stressors disrupt the hypothalamic GnRH pulse generator remain to be fully elucidated, numerous studies have implicated the amygdala, especially its medial (MeA) and central nuclei (CeA), as key modulators of the neuroendocrine response to stress. In the present study, we investigated the roles of the MeA and CeA in stress-induced suppression of LH pulses. Ovariectomized rats received bilateral ibotenic acid or sham lesions targeting the MeA or CeA; blood samples (25 μl) were taken via chronically implanted cardiac catheters every 5 min for 6 h for the measurement of LH pulses. After 2 h of baseline sampling, the rats were exposed to either: restraint (1 h), insulin-induced hypoglycemia (IIH) (0.3 U/kg, iv), or lipopolysaccharide (LPS) (25 μg/kg, iv) stress. The restraint but not IIH or LPS stress–induced suppression of LH pulses was markedly attenuated by the MeA lesions. In contrast, CeA lesioning attenuated LPS, but not restraint or IIH stress–induced suppression of LH pulses. Moreover, after restraint stress, the number of Fos-positive neurons and the percentage of glutamic acid decarboxylase67 neurons expressing Fos was significantly greater in the GnRH-rich medial preoptic area (mPOA) of rats with intact, rather than lesioned, MeA. These data indicate that the MeA and CeA play key roles in psychogenic and immunological stress-induced suppression of the GnRH pulse generator, respectively, and the MeA-mediated effect may involve γ-aminobutyric acid ergic signaling within the mPOA.

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8

Tolbert, Dawn, Xiangdong Lu, Chaoying Yin, Mathew Tantama, and Terry Van Dyke. "p19ARF Is Dispensable for Oncogenic Stress-Induced p53-Mediated Apoptosis and Tumor Suppression In Vivo." Molecular and Cellular Biology 22, no. 1 (January 1, 2002): 370–77. http://dx.doi.org/10.1128/mcb.22.1.370-377.2002.

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ABSTRACT Recent studies have shown the p19ARF tumor suppressor to be involved in the response to oncogenic stress by regulating the activity of p53. This response is mediated by antagonizing the function of Mdm2, a negative regulator of p53, indicating a pathway for tumor suppression that involves numerous genes altered in human tumors. We previously described a transgenic mouse brain tumor model in which oncogenic stress, provided by cell-specific inactivation of the pRb pathway, triggers a p53-dependent apoptotic response. This response suppresses the growth of developing tumors and thus represents a bona fide in vivo tumor suppressor activity. We further showed that E2F1, a transcription factor known to induce p19ARF expression, was required for the response. Here, we use a genetic approach to test whether p19ARF functions to transduce the signal from E2F1 to p53 in this tumor suppression pathway. Contrary to the currently accepted hypothesis, we show that a deficiency in p19ARF has no impact on p53-mediated apoptosis or tumor suppression in this system. All measures of p53 function, including the level of apoptosis induced by pRb inactivation, the expression of p21 (a p53-responsive gene), and the rate of tumor growth, were comparable in mice with and without a functional p19ARF gene. Thus, although p19ARF is required in some cell types to transmit an oncogenic response signal to p53, it is dispensable for this function in an in vivo epithelial system. These results underscore the complexity of p53 tumor suppression and further indicate the existence of distinct cell-specific pathways that respond to similar stimuli.

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9

Wiest, David L. "Gadd45 stress sensors in suppression of leukemia." Oncotarget 9, no. 76 (September 28, 2018): 34191–92. http://dx.doi.org/10.18632/oncotarget.26154.

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10

Ogawa, Kenji, Masanori Hirai, Takao Katsube, Minoru Murayama, Kanako Hamaguchi, Takeshi Shimakawa, Yoshihiko Naritake, Toshihiko Hosokawa, and Tetsuro Kajiwara. "Suppression of cellular immunity by surgical stress." Surgery 127, no. 3 (March 2000): 329–36. http://dx.doi.org/10.1067/msy.2000.103498.

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11

KAMEI, Hiroyuki, Yukihiro NODA, and Toshitaka NABESHIMA. "The psychological stress model using motor suppression." Folia Pharmacologica Japonica 113, no. 2 (1999): 113–20. http://dx.doi.org/10.1254/fpj.113.113.

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12

White, P. M., C. M. Yee, and C. J. Graver. "Psychological stress impairs P50 suppression in schizotypy." Schizophrenia Research 60, no. 1 (March 2003): 263. http://dx.doi.org/10.1016/s0920-9964(03)80404-8.

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13

Xu, Yuanming, Sindey Johanna Melo Cardenas, Hongjian Jin, Jessica heinrichs voss, Isabella Gau, Juncheng Wei, Elena Montauti, et al. "Hrd1 protects regulatory T cells from ER stress-induced instability and dysfunction." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 47.11. http://dx.doi.org/10.4049/jimmunol.200.supp.47.11.

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Abstract T regulatory cells (Treg)differentiation, maintenance, and function are controlled by the transcription factor FoxP3, which can be destabilized under inflammatory or other pathological conditions. However, the microenvironmental factors that compromise Treg identity and the underlying mechanisms remain unclear. Here, we show that ER stress destabilizes both human and mouse Treg by suppressing FoxP3 expression, suggesting a critical role of the ER stress response in maintaining Treg properties. We found that genetic deletion of Hrd1, an E3 ligase critical in suppressing the ER stress response, leads to elevated expression of ER stress-responsive genes in Treg. Importantly, mice with Treg-specific ablation of Hrd1 displayed massive multi-organ lymphocyte infiltration, body weight loss, and the development of severe small intestine inflammation with aging. At the molecular level, the deletion of Hrd1 led to upregulation of the ER stress response, in particular, the activation of the ER stress sensor IRE1. Impaired FoxP3 expression caused by Hrd1 deletion was largely rescued by an IRE1 kinase inhibitor. Taken together, these findings indicate that Hrd1 is crucial for maintaining the expression and suppressive function of Treg through suppression of the IRE1-mediated ER stress response. The study is significant because it will help to fill fundamental gaps in our knowledge of the role of Hrd1 in T regulatory cells, which will inform the design of future immunotherapies for cancer patients or immune dysregulated diseases.

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14

Matsuwaki, Takashi, Yuko Kayasuga, Keitaro Yamanouchi, and Masugi Nishihara. "Maintenance of Gonadotropin Secretion by Glucocorticoids under Stress Conditions through the Inhibition of Prostaglandin Synthesis in the Brain." Endocrinology 147, no. 3 (March 1, 2006): 1087–93. http://dx.doi.org/10.1210/en.2005-1056.

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We have previously reported that glucocorticoids counteract the suppressive effects of tumor necrosis factor-α on both pulsatile and surge secretion of LH. This suggests that glucocorticoids have a protective effect on reproductive function under infectious stress. In the present study, we examined whether glucocorticoids maintain pulsatile LH secretion under various conditions of acute stress and the possible involvement of prostaglandins (PGs) in glucocorticoid actions. Three different types of stressors, namely infectious (lipopolysaccharide, 0.5 μg/kg), hypoglycemic (2-deoxy-d-glucose, 100 mg/kg), and restraint stress (1 h) were applied to ovariectomized rats. In ovariectomized rats, LH pulses were partially suppressed by restraint, but not by lipopolysaccharide or 2-deoxy-d-glucose. On the other hand, adrenalectomy (ADX) significantly enhanced the suppressive effects of all the stressors applied on LH pulses. Treatment with both corticosterone (25 mg/kg) and indomethacin (10 mg/kg) in ADX rats significantly attenuated the suppressive effects of these stressors on LH pulses. In addition, the immunoreactivity of cyclooxygenase-2, a PG-synthesizing enzyme, in the brain under stress conditions was much enhanced by ADX, and this was counteracted by corticosterone treatment. Similarly, an increase in body temperature under restraint stress was enhanced by ADX and suppressed by corticosterone. These results suggest that suppression of LH pulsatility by stress is mediated by PGs in the brain, and that increased release of endogenous glucocorticoids in response to stress counteracts this suppression by inhibiting PG synthesis, and thereby maintains reproductive function regardless of the nature of the stressor.

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15

Frosch, Jennifer, Ilia Leontari, and John Anderson. "Combined Effects of Myeloid Cells in the Neuroblastoma Tumor Microenvironment." Cancers 13, no. 7 (April 6, 2021): 1743. http://dx.doi.org/10.3390/cancers13071743.

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Despite multimodal treatment, survival chances for high-risk neuroblastoma patients remain poor. Immunotherapeutic approaches focusing on the activation and/or modification of host immunity for eliminating tumor cells, such as chimeric antigen receptor (CAR) T cells, are currently in development, however clinical trials have failed to reproduce the preclinical results. The tumor microenvironment is emerging as a major contributor to immune suppression and tumor evasion in solid cancers and thus has to be overcome for therapies relying on a functional immune response. Among the cellular components of the neuroblastoma tumor microenvironment, suppressive myeloid cells have been described as key players in inhibition of antitumor immune responses and have been shown to positively correlate with more aggressive disease, resistance to treatments, and overall poor prognosis. This review article summarizes how neuroblastoma-driven inflammation induces suppressive myeloid cells in the tumor microenvironment and how they in turn sustain the tumor niche through suppressor functions, such as nutrient depletion and generation of oxidative stress. Numerous preclinical studies have suggested a range of drug and cellular therapy approaches to overcome myeloid-derived suppression in neuroblastoma that warrant evaluation in future clinical studies.

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Poshyvak, O. B., O. R. Pinyazhko, and L. S. Godlevsky. "Oxidative stress suppression contributes to antiseizure action of axitinib and rapamycin in pentylenetetrazol-induced kindling." Ukrainian Biochemical Journal 93, no. 2 (May 20, 2021): 53–60. http://dx.doi.org/10.15407/ubj93.02.053.

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17

BICKEL, U., A. BLIESTLE, and ST BRETSCHNEIDER. "Escape from dexamethasone suppression by mild physical stress." Acta Endocrinologica 110, no. 1_Suppla (April 1985): S117—S118. http://dx.doi.org/10.1530/acta.0.109s117.

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18

BREEN, K., and F. KARSCH. "New insights regarding glucocorticoids, stress and gonadotropin suppression." Frontiers in Neuroendocrinology 27, no. 2 (July 2006): 233–45. http://dx.doi.org/10.1016/j.yfrne.2006.03.335.

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19

Alfahad, Mohanad, Mahmood H. M. Jasim, Mohannad E. Qazzaz, Fawaz A. Alassaf, and Mohammed N. Abed. "Proton pump inhibitors and peptic ulcer management: Antioxidant mechanisms." Journal of Drug Delivery and Therapeutics 11, no. 4-S (August 15, 2021): 242–46. http://dx.doi.org/10.22270/jddt.v11i4-s.4955.

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Peptic ulcer (P.U.) is the gastrointestinal tract's most frequent disorder affecting mainly the stomach and duodenum. Surgical intervention, ingested materials and microbial infections may trigger inflammation that further predispose to oxidative stress. Proton pump inhibitors (PPIs) are group of compounds established for suppressions of gastric acid secretions profoundly and permanently over a reasonably long period of time. Oxidative stress has been shown to be involved in the pathophysiology of various diseases and disorders, including P.U. Particularly when H. pylori infection accompanies it. In addition to the colonization of this microorganism, gastric mucosa may be subjected to extreme oxidative stress with large levels of inflammatory cell aggregation, which may eventually predispose to the disorder. PPIs exert several effects other than gastric acid suppression that can be used to treat Helicobacter pylori infections, disorders of the respiratory tract, viral infections, and other conditions related to dysfunction of endothelium by activating endogenous antioxidant protection and reducing the release of cytokine. Recent therapeutic protocols have recommended PPIs as gastro-protective compounds not only because of their acid suppression properties, but also because of their potent antioxidant and anti-inflammatory properties. Keywords: Proton Pump Inhibitors, Peptic Ulcer, Oxidative Stress, H. pylori

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20

Tasneef Azam, Tasneef Azam, Fouzia Noreen Fouzia Noreen, Bina S. Siddiqui Bina S Siddiqui, Rahman M. Hafizur Rahman M Hafizur, and Sabira Begum Sabira Begum. "Suppression of β-Cell Apoptosis from H2O2-Induced Oxidative Stress in MIN6 cells using Methyl Gallate." Journal of the chemical society of pakistan 44, no. 1 (2022): 84. http://dx.doi.org/10.52568/000983/jcsp/44.01.2022.

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A major parameter for diabetic relevant diseases and hyperglycemia is the β-cell apoptosis. Anti diabetic drugs used widely these days chiefly target to lower hyperglycemia along with prevention of β-cells from apoptosis. In this study three natural products methyl gallate, syringic acid, and butanedioic acid from Myricaria germanica were analyzed for β-cell protection. Methyl gallate provided significant β-cell protection from H2O2-induced oxidative stress mediated apoptosis in MIN6 cells at 50 μM (95.5% and#177; 16.0 vs 57.6% and#177; 1.1) and at 100 μM (85.5% and#177; 7.0 vs 57.6% and#177; 1.1) concentrations.

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21

Ricker, Emily A., Carl W. Goforth, Amelia S. Barrett, Patricia A. Deuster, and Sarah J. de la Motte. "Female Military Officers Report a Desire for Menstrual Suppression During Military Training." Military Medicine 186, Supplement_1 (January 1, 2021): 775–83. http://dx.doi.org/10.1093/milmed/usaa339.

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ABSTRACT Introduction Service women face female-specific challenges that present physiological and logistical burdens and may impact readiness. The stress of training can change menstrual patterns and symptoms, and limited access to hygienic, private facilities can hinder menstrual management. Therefore, suppressing menses with continuous hormonal contraception may be of interest. Materials and Methods The 9-item “Military Women’s Attitudes Toward Menstrual Suppression.” questionnaire was administered to female officers upon entry (baseline) and graduation (post) from a 6-month secondary training course. Respondents rated their attitudes about menstruation and the stress of training, the desire for menstrual suppression, and the logistical burden of menstruation on a 1 (strongly agree) through 5 (strongly disagree) scale. Wilcoxon Signed Rank Tests determined changes in the distribution of responses from baseline to post. Results Female officers (n = 108) completed baseline and post questionnaires (age 25.2 ± 0.3 years). At baseline, the majority disagreed/strongly disagreed that the stress of training “makes periods worse than usual” (n = 77, 71%), “increases menstrual symptoms and bleeding” (n = 77, 71%), or “magnifies premenstrual syndrome” (PMS; n = 69, 64%). Although 50% (n = 54) agreed/strongly agreed that “stopping periods while women are training is a good idea,” 37% (n = 40) disagreed/strongly disagreed. The majority agreed/strongly agreed that menstrual suppression would prevent “the worry about menstrual supplies” (n = 75, 70%) and “the inconvenience of having a period during training” (n = 69, 64%). Many agreed/strongly agreed that it is difficult to deal with periods during training because “there is no privacy” (n = 52, 48%), “the inability to find adequate facilities” (n = 70, 65%), and “the lack of opportunity to use adequate facilities” (n = 52, 48%). Opinions remained largely consistent from baseline to post. Conclusions The desire for menstrual suppression among service women during training is high. Military health care providers should be prepared to counsel service women about strategies to manage menstruation, including the efficacy of continuous hormonal contraception for menstrual suppression. Future studies investigating benefits or risks of continuous hormonal contraception for menstrual suppression in service women should inform the clinical recommendations.

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22

Ávalos, Yenniffer, Jimena Canales, Roberto Bravo-Sagua, Alfredo Criollo, Sergio Lavandero, and Andrew F. G. Quest. "Tumor Suppression and Promotion by Autophagy." BioMed Research International 2014 (2014): 1–15. http://dx.doi.org/10.1155/2014/603980.

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Autophagy is a highly regulated catabolic process that involves lysosomal degradation of proteins and organelles, mostly mitochondria, for the maintenance of cellular homeostasis and reduction of metabolic stress. Problems in the execution of this process are linked to different pathological conditions, such as neurodegeneration, aging, and cancer. Many of the proteins that regulate autophagy are either oncogenes or tumor suppressor proteins. Specifically, tumor suppressor genes that negatively regulate mTOR, such as PTEN, AMPK, LKB1, and TSC1/2 stimulate autophagy while, conversely, oncogenes that activate mTOR, such as class I PI3K, Ras, Rheb, and AKT, inhibit autophagy, suggesting that autophagy is a tumor suppressor mechanism. Consistent with this hypothesis, the inhibition of autophagy promotes oxidative stress, genomic instability, and tumorigenesis. Nevertheless, autophagy also functions as a cytoprotective mechanism under stress conditions, including hypoxia and nutrient starvation, that promotes tumor growth and resistance to chemotherapy in established tumors. Here, in this brief review, we will focus the discussion on this ambiguous role of autophagy in the development and progression of cancer.

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23

Schramek, Daniel, Athanassios Kotsinas, Arabella Meixner, Teiji Wada, Ulrich Elling, J. Andrew Pospisilik, G. Gregory Neely, et al. "The stress kinase MKK7 couples oncogenic stress to p53 stability and tumor suppression." Nature Genetics 43, no. 3 (February 13, 2011): 212–19. http://dx.doi.org/10.1038/ng.767.

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24

Gerits, P., and B. de Brabander. "The effect of stress and psychosocial variables on natural killer cells: a review." Acta Neuropsychiatrica 4, no. 3 (September 1992): 63–68. http://dx.doi.org/10.1017/s0924270800034815.

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SummaryIn this review we discuss the results of studies about the effect of stress, depression, anxiety, social support and various psychosocial treatments on numbers and activity of Natural Killer (NK) cells. In general a suppressive effect is observed among depressive persons and persons who react to stressfull events with feelings of helplessness and anxiety. Lack of social support also seems to engender immunosuppression including NK suppression. Various forms of psychosocial care seem to be able to undo these negative consequences. However, the real clinical relevance of these findings is still a matter of dispute.

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Moraska, Albert, Jay Campisi, Kien T. Nguyen, Steven F. Maier, Linda R. Watkins, and Monika Fleshner. "Elevated IL-1β contributes to antibody suppression produced by stress." Journal of Applied Physiology 93, no. 1 (July 1, 2002): 207–15. http://dx.doi.org/10.1152/japplphysiol.01151.2001.

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Acute stressor exposure can facilitate innate immunity and suppress acquired immunity. The present study further characterized the potentiating effect of stress on innate immunity, interleukin-1β (IL-1β), and demonstrated that stress-induced potentiation of innate immunity may contribute to the stress-induced suppression of acquired immunity. The long-term effect of stress on IL-1β was measured by using an ex vivo approach. Sprague-Dawley rats were challenged with lipopolysaccharide (LPS) in vivo, and the IL-1β response was measured in vitro. Splenocytes, mesenteric lymphocytes, and peritoneal cavity cells had a dose- and time-dependent ex vivo IL-1β response to LPS. Rats that were exposed to inescapable shock (IS, 100 1.6 mA, 5-s tail shocks, 60-s intertrial interval) and challenged with a submaximal dose of LPS 4 days later had elevated IL-1β measured ex vivo. To test whether the acute stress-induced elevation in IL-1β contributes to the long-term suppression in acquired immunity, IL-1β receptors were blocked for 24 h after stress. Serum anti-keyhole limpet hemocyanin (KLH) immunoglobulin (Ig) was measured. In addition, the acute elevation (2 h post-IS) of splenic IL-1β in the absence of antigen was verified. Interleukin-1 receptor antagonist prevented IS-induced suppression in anti-KLH Ig. These data support the hypothesis that stress-induced increases in innate immunity (i.e., IL-1β) may contribute to stress-induced suppression in acquired immunity (i.e., anti-KLH Ig).

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Mitchell, J. C., X. F. Li, L. Breen, J. C. Thalabard, and K. T. O’Byrne. "The Role of the Locus Coeruleus in Corticotropin-Releasing Hormone and Stress-Induced Suppression of Pulsatile Luteinizing Hormone Secretion in the Female Rat." Endocrinology 146, no. 1 (January 1, 2005): 323–31. http://dx.doi.org/10.1210/en.2004-1053.

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Despite a wealth of evidence for CRH mediating stress-induced suppression of the hypothalamic GnRH pulse generator, and hence reproductive dysfunction, the site and mechanism of action remains elusive. The locus coeruleus (LC), a prominent noradrenergic brain stem nucleus, is innervated by CRH neurons, mediates several behavioral stress responses, and is implicated in the control of pulsatile LH secretion. The aim of this study was to test the hypothesis that LC CRH has a critical role in mediating stress-induced suppression of pulsatile LH secretion in the rat. Ovariectomized rats with 17β-estradiol or oil-filled sc capsules were implanted with bilateral LC and iv cannulae. Central administration of CRH (10 ng to 1 μg) resulted in a dose-dependent suppression of LH pulses, which was reversed by a CRH receptor antagonist (α-helical CRF9–41, 1 μg). The induction of c-fos expression in glutamic acid decarboxylase67 immunostained neurons in the preoptic area suggests activation of the secretion of γ-aminobutyric acid in response to intracoerulear administration of CRH; 17β-estradiol further increased the percentage of glutamic acid decarboxylase67-positive neurons that expressed fos and augmented suppression of LH pulses. Furthermore, intracoerulear administration of α-helical CRF9–41 completely blocked restraint stress-induced suppression of LH pulses, without affecting the inhibitory response to hypoglycemia. These results suggest that CRH innervation of the LC may play a pivotal, but differential, role in the normal physiological response of stress-induced suppression of the GnRH pulse generator and hence the reproductive system.

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27

Merrell, R. C., M. Maeda, G. Basadonna, F. Marincola, and L. Cobb. "Suppression, Stress, and Accommodation of Transplanted Islets of Langerhans." Diabetes 34, no. 7 (July 1, 1985): 667–70. http://dx.doi.org/10.2337/diab.34.7.667.

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28

Muhie, S., R. Hammamieh, C. Cummings, D. Yang, and M. Jett. "Transcriptome characterization of immune suppression from battlefield-like stress." Genes & Immunity 14, no. 1 (October 25, 2012): 19–34. http://dx.doi.org/10.1038/gene.2012.49.

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29

Shipherd, Jillian C., and J. Gayle Beck. "The role of thought suppression in posttraumatic stress disorder." Behavior Therapy 36, no. 3 (2005): 277–87. http://dx.doi.org/10.1016/s0005-7894(05)80076-0.

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30

Thipyapong, Piyada, Jeffrey Melkonian, David W. Wolfe, and John C. Steffens. "Suppression of polyphenol oxidases increases stress tolerance in tomato." Plant Science 167, no. 4 (October 2004): 693–703. http://dx.doi.org/10.1016/j.plantsci.2004.04.008.

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31

Duva, J. M., B. R. Olson, and H. N. G. Wadley. "Functionally graded materials for yield suppression at stress concentrators." Composites Engineering 4, no. 1 (January 1994): 107–14. http://dx.doi.org/10.1016/0961-9526(94)90012-4.

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32

Chen, Hua-Li, Yan Liu, Wei Jiang, Xiao-xiao Wang, Guo-lin Yuan, Yi-lin Zhao, and Chao Yu. "Secretoneurin suppresses cardiac hypertrophy through suppression of oxidant stress." European Journal of Pharmacology 822 (March 2018): 13–24. http://dx.doi.org/10.1016/j.ejphar.2018.01.008.

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33

Ceulemans, Dominique L. S., Herman G. M. Westenberg, and Herman M. van Praag. "The effect of stress on the dexamethasone suppression test." Psychiatry Research 14, no. 3 (March 1985): 189–95. http://dx.doi.org/10.1016/0165-1781(85)90013-7.

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34

Frecska, Ede, Hedvig Lukács, Mihály Arató, László Mód, Antal Alföldi, and István Magyar. "Dexamethasone suppression test and coping behavior in psychosocial stress." Psychiatry Research 23, no. 2 (February 1988): 137–45. http://dx.doi.org/10.1016/0165-1781(88)90003-0.

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35

Kaufer, D., A. Friedman, S. Seidman, and H. Soreq. "Acute stress induces long-lasting suppression of cholinergic neurotransmission." Neuroscience Letters 237 (November 1997): S27. http://dx.doi.org/10.1016/s0304-3940(97)90110-5.

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36

Al-attar, Rasha, and Kenneth B. Storey. "RAGE against the stress: Mitochondrial suppression in hypometabolic hearts." Gene 761 (November 2020): 145039. http://dx.doi.org/10.1016/j.gene.2020.145039.

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37

Merrell, R. C., M. Maeda, G. Basadonna, F. Marincola, and L. Cobb. "Suppression, stress, and accommodation of transplanted islets of Langerhans." Diabetes 34, no. 7 (July 1, 1985): 667–70. http://dx.doi.org/10.2337/diabetes.34.7.667.

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38

Mellsop, G. W., J. D. Hutton, and J. W. Delahunt. "Dexamethasone suppression test as a simple measure of stress?" BMJ 290, no. 6484 (June 15, 1985): 1804–6. http://dx.doi.org/10.1136/bmj.290.6484.1804.

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39

Keshavan, M. S., and M. Farrell. "Dexamethasone suppression test as a simple measure of stress?" BMJ 291, no. 6488 (July 13, 1985): 143. http://dx.doi.org/10.1136/bmj.291.6488.143-a.

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40

Boyd, O. "Dexamethasone suppression test as a simple measure of stress?" BMJ 291, no. 6490 (July 27, 1985): 280. http://dx.doi.org/10.1136/bmj.291.6490.280.

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41

Lancaster, R. "Dexamethasone suppression test as a simple measure of stress?" BMJ 291, no. 6490 (July 27, 1985): 280. http://dx.doi.org/10.1136/bmj.291.6490.280-a.

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42

Nixon, Reginald D. V., and Julie Rackebrandt. "Cognitive Load Undermines Thought Suppression in Acute Stress Disorder." Behavior Therapy 47, no. 3 (May 2016): 388–403. http://dx.doi.org/10.1016/j.beth.2016.02.010.

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43

Gianaros, Peter J., Ikechukwu C. Onyewuenyi, Lei K. Sheu, Israel C. Christie, and Hugo D. Critchley. "Brain systems for baroreflex suppression during stress in humans." Human Brain Mapping 33, no. 7 (May 12, 2011): 1700–1716. http://dx.doi.org/10.1002/hbm.21315.

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44

Lance, Valentine A., and Ruth M. Elsey. "Stress-induced suppression of testosterone secretion in male alligators." Journal of Experimental Zoology 239, no. 2 (August 1986): 241–46. http://dx.doi.org/10.1002/jez.1402390211.

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45

Tobin, John P. "Post traumatic stress disorder and the adrenal gland." Irish Journal of Psychological Medicine 18, no. 1 (March 2001): 27–29. http://dx.doi.org/10.1017/s0790966700006194.

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AbstractLow serum and urinary Cortisol has been a consistent finding in post traumatic stress disorder (PTSD). Glucocorticoid receptor numbers are increased. PTSD patients have a significantly lower adrenocorticotropic hormone (ACTH) in response to corticotrophin releasing hormone (CRH) when compared to a control group of normal volunteers. The dexamethasone suppression test exhibits an exaggerated suppression response of Cortisol to dexamethasone, when the dose utilised is lower than that utilised to test patients with depression. Increased urine levels of noradrenaline and dopamine has been noted in patients with PTSD. This is believed to be related to the hyperarousal state of PTSD.

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46

Greeson, Jeffrey M., Haley Zarrin, Moria J. Smoski, Jeffrey G. Brantley, Thomas R. Lynch, Daniel M. Webber, Martica H. Hall, Edward C. Suarez, and Ruth Q. Wolever. "Mindfulness Meditation Targets Transdiagnostic Symptoms Implicated in Stress-Related Disorders: Understanding Relationships between Changes in Mindfulness, Sleep Quality, and Physical Symptoms." Evidence-Based Complementary and Alternative Medicine 2018 (2018): 1–10. http://dx.doi.org/10.1155/2018/4505191.

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Mindfulness-Based Stress Reduction (MBSR) is an 8-week meditation program known to improve anxiety, depression, and psychological well-being. Other health-related effects, such as sleep quality, are less well established, as are the psychological processes associated with therapeutic change. This prospective, observational study (n=213) aimed to determine whether perseverative cognition, indicated by rumination and intrusive thoughts, and emotion regulation, measured by avoidance, thought suppression, emotion suppression, and cognitive reappraisal, partly accounted for the hypothesized relationship between changes in mindfulness and two health-related outcomes: sleep quality and stress-related physical symptoms. As expected, increased mindfulness following the MBSR program was directly correlated with decreased sleep disturbance (r=-0.21, p=0.004) and decreased stress-related physical symptoms (r=-0.38, p<0.001). Partial correlations revealed that pre-post changes in rumination, unwanted intrusive thoughts, thought suppression, experiential avoidance, emotion suppression, and cognitive reappraisal each uniquely accounted for up to 32% of the correlation between the change in mindfulness and change in sleep disturbance and up to 30% of the correlation between the change in mindfulness and change in stress-related physical symptoms. Results suggest that the stress-reducing effects of MBSR are due, in part, to improvements in perseverative cognition and emotion regulation, two “transdiagnostic” mental processes that cut across stress-related disorders.

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47

Eskla, Kattri-Liis, Hans Vellama, Liisi Tarve, Hillar Eichelmann, Toomas Jagomäe, Rando Porosk, Vello Oja, et al. "Hypothermia Alleviates Reductive Stress, a Root Cause of Ischemia Reperfusion Injury." International Journal of Molecular Sciences 23, no. 17 (September 3, 2022): 10108. http://dx.doi.org/10.3390/ijms231710108.

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Ischemia reperfusion injury is common in transplantation. Previous studies have shown that cooling can protect against hypoxic injury. To date, the protective effects of hypothermia have been largely associated with metabolic suppression. Since kidney transplantation is one of the most common organ transplant surgeries, we used human-derived renal proximal tubular cells (HKC8 cell line) as a model of normal renal cells. We performed a temperature titration curve from 37 °C to 22 °C and evaluated cellular respiration and molecular mechanisms that can counteract the build-up of reducing equivalents in hypoxic conditions. We show that the protective effects of hypothermia are likely to stem both from metabolic suppression (inhibitory component) and augmentation of stress tolerance (activating component), with the highest overlap between activating and suppressing mechanisms emerging in the window of mild hypothermia (32 °C). Hypothermia decreased hypoxia-induced rise in the extracellular lactate:pyruvate ratio, increased ATP/ADP ratio and mitochondrial content, normalized lipid content, and improved the recovery of respiration after anoxia. Importantly, it was observed that in contrast to mild hypothermia, moderate and deep hypothermia interfere with HIF1 (hypoxia inducible factor 1)-dependent HRE (hypoxia response element) induction in hypoxia. This work also demonstrates that hypothermia alleviates reductive stress, a conceptually novel and largely overlooked phenomenon at the root of ischemia reperfusion injury.

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48

Chiu, Yen-Hsin, Yu-Ling Hung, Hsin-Ping Wang, Wei-Lun Wei, Qian-Wen Shang, Thanh Ha Pham, Chien-Kang Huang, Zhao-Jun Pan, and Shih-Shun Lin. "Investigation of P1/HC-Pro-Mediated ABA/Calcium Signaling Responses via Gene Silencing through High- and Low-Throughput RNA-seq Approaches." Viruses 13, no. 12 (November 23, 2021): 2349. http://dx.doi.org/10.3390/v13122349.

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The P1/HC-Pro viral suppressor of potyvirus suppresses posttranscriptional gene silencing (PTGS). The fusion protein of P1/HC-Pro can be cleaved into P1 and HC-Pro through the P1 self-cleavage activity, and P1 is necessary and sufficient to enhance PTGS suppression of HC-Pro. To address the modulation of gene regulatory relationships induced by turnip mosaic virus (TuMV) P1/HC-Pro (P1/HC-ProTu), a comparative transcriptome analysis of three types of transgenic plants (P1Tu, HC-ProTu, and P1/HC-ProTu) were conducted using both high-throughput (HTP) and low-throughput (LTP) RNA-Seq strategies. The results showed that P1/HC-ProTu disturbed the endogenous abscisic acid (ABA) accumulation and genes in the signaling pathway. Additionally, the integrated responses of stress-related genes, in particular to drought stress, cold stress, senescence, and stomatal dynamics, altered the expressions by the ABA/calcium signaling. Crosstalk among the ABA, jasmonic acid, and salicylic acid pathways might simultaneously modulate the stress responses triggered by P1/HC-ProTu. Furthermore, the LTP network analysis revealed crucial genes in common with those identified by the HTP network in this study, demonstrating the effectiveness of the miniaturization of the HTP profile. Overall, our findings indicate that P1/HC-ProTu-mediated suppression in RNA silencing altered the ABA/calcium signaling and a wide range of stress responses.

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49

Blouin, Jane, Eric Spindler, Edgardo Perez, Arthur Blouin, Steven Hotz, and Joanne Hakkaku. "The Role of Stress in Interpreting the Dexamethasone Suppression Test." Canadian Journal of Psychiatry 37, no. 10 (December 1992): 724–27. http://dx.doi.org/10.1177/070674379203701009.

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Stress has been implicated as a major confounding factor in the interpretation of Dexamethasone Suppression Test (DST) results. This study was designed to examine the effects of stress on DST results. Fifty patients with high levels of acute, chronic, and environmental stress participated in the study. Each patient was given a comprehensive psychiatric and psychological assessment, a routine administration of dexamethasone, and blood tests of cortisol values. The results indicate that the three measures of stress do not appear to affect levels of cortisol suppression, however, all three measures of stress predicted depression. As expected, DST cortisol levels were related to depression. Results are discussed in terms of their implications for understanding the associations among stress, depression and DST results.

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50

Scaglioni, Pier P., Thomas M. Yung, Lu F. Cai, Hediye Erdjument-Bromage, Andrew J. Kaufman, Bhuvanesh Singh, Julie Teruya-Feldstein, Paul Tempst, and Pier Paolo Pandolfi. "A CK2-Dependent Mechanism for PML Degradation upon Cellular and Oncogenic Stress." Blood 108, no. 11 (November 16, 2006): 1426. http://dx.doi.org/10.1182/blood.v108.11.1426.1426.

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Abstract The PML tumor suppressor controls key pathways for growth suppression, induction of apoptosis and cellular senescence. PML loss occurs frequently in hematopoietic and solid tumors through unknown post-translational mechanisms. PML loss often correlates with tumor progression. Casein kinase 2 (CK2) is a stress activated serine/threonine protein kinase that is oncogenic and frequently over-expressed in human tumor of multiple histological origins including non Hodgkin’s lymphomas, acute leukemias and multiple myeloma. In addition, CK2 over-expression due to gene amplification has been reported to be a powerful adverse prognostic factor in non-small cell lung cancer. We recently reported that PML undergoes ubiquitin/proteasome mediated degradation in immortalized and tumor derived cell lines (Cell. 2006, 126:269). PML degradation depends on direct CK2 phosphorylation of Ser517 in the PML C-terminal degron. PML mutants that are resistant to CK2 phosphorylation display increased tumor suppressive functions in assays measuring apoptosis, replicative senescence and in xenograft models. Now, we report the identification and characterization of novel cellular and oncogenic stress signaling pathways that control the CK2/PML degradation pathway. This analysis allowed us to determine the signaling cascades upstream of CK2. In addition, we found an inverse correlation between CK2 kinase activity and PML protein levels in cancer-derived cell lines and primary specimens. Significantly, CK2 pharmacological inhibition enhances PML tumor suppressive property in vivo and in vitro. These data identify a key post-translational mechanism that controls PML protein levels and provide therapeutic means toward PML restoration through CK2 inhibition. The implications of these new findings during the physiologic response to cellular stress and in the pathogenesis of hemopoietic malignancies will be discussed at the meeting.

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