Journal articles: 'Secretion stress'

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Seo, Jin, Anja Brencic, and Andrew J. Darwin. "Analysis of Secretin-Induced Stress in Pseudomonas aeruginosa Suggests Prevention Rather than Response and Identifies a Novel Protein Involved in Secretin Function." Journal of Bacteriology 191, no. 3 (November 21, 2008): 898–908. http://dx.doi.org/10.1128/jb.01443-08.

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ABSTRACT Secretins are bacterial outer membrane proteins that are important for protein export. However, they can also mislocalize and cause stress to the bacterial cell, which is dealt with by the well-conserved phage shock protein (Psp) system in a highly specific manner. Nevertheless, some bacteria have secretins but no Psp system. A notable example is Pseudomonas aeruginosa, a prolific protein secretor with the potential to produce seven different secretins. We were interested in investigating how P. aeruginosa might deal with the potential for secretin-induced stress without a Psp system. Microarray analysis revealed the absence of any transcriptional response to XcpQ secretin overproduction. However, transposon insertions in either rpoN, truB, PA4068, PA4069, or PA0943 rendered P. aeruginosa hypersensitive to XcpQ production. The PA0943 gene was studied further and found to encode a soluble periplasmic protein important for XcpQ localization to the outer membrane. Consistent with this, a PA0943 null mutation reduced the levels of type 2 secretion-dependent proteins in the culture supernatant. Therefore, this work has identified a novel protein required for normal secretin function in P. aeruginosa. Taken together, all of our data suggest that P. aeruginosa lacks a functional equivalent of the Psp stress response system. Rather, null mutations in genes such as PA0943 may cause increased secretin-induced stress to which P. aeruginosa cannot respond. Providing the PA0943 mutant with the ability to respond, in the form of critical Psp proteins from another species, alleviated its secretin sensitivity.

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Delbende, C., C. Delarue, H. Lefebvre, D. Tranchand Bunel, A. Szafarczyk, E. Mocaër, A. Kamoun, S. Jégou, and H. Vaudry. "Glucocorticoids, Transmitters and Stress." British Journal of Psychiatry 160, S15 (February 1992): 24–35. http://dx.doi.org/10.1192/s0007125000296657.

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Many kinds of stress stimulate the neuroendocrine systems controlling catecholamine and glucocorticoid secretion. Stress-induced stimulation of CRF-containing neurons appears to be mediated by serotonergic, noradrenergic, and possibly other neuronal pathways. Stress can alter various neurobiological and endocrine functions, two essential components of the neuroendocrine responses being release of adrenalin from chromaffin cells of the adrenal medulla and secretion of glucocorticoids from adrenocortical cells. Activation of adrenal steroid secretion is mainly by a reflex activation of hypothalamic neurons, which stimulate ACTH secretion from the anterior pituitary. While the neuropeptide CRF plays a major role in the neuroendocrine response to stress, the neuronal signals which are responsible for the regulation of CRF neurons have not been completely elucidated. A number of other regulatory substances may also participate, alone or with CRF, in the control of ACTH secretion by pituitary corticotrophs, and there is increasing evidence that classical neurotransmitters or neuropeptides may act directly on adrenocortical cells to modulate corticosteroid secretion. We review the neuronal, neuroendocrine, and humoral pathways which participate in the regulation of stress-induced corticosteroid secretion, and present preliminary data on the effect of the tricyclic antidepressant, tianeptine in the response of the HPA axis to stress.

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Cramer, Robert A. "Secretion stress and fungal pathogenesis." Virulence 2, no. 1 (January 2011): 1–3. http://dx.doi.org/10.4161/viru.2.1.13902.

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Aguiar, Tatiana Q., Orquídea Ribeiro, Mikko Arvas, Marilyn G. Wiebe, Merja Penttilä, and Lucília Domingues. "Investigation of protein secretion and secretion stress in Ashbya gossypii." BMC Genomics 15, no. 1 (2014): 1137. http://dx.doi.org/10.1186/1471-2164-15-1137.

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Žarković, Miloš, Elka Stefanova, Jasmina Ćirić, Zorana Penezić, Vladimir Kostić, Mirjana Šumarac-Dumanović, Djuro Macut, Miomira S. Ivović, and Predrag V. Gligorović. "Prolonged psychological stress suppresses cortisol secretion." Clinical Endocrinology 59, no. 6 (November 20, 2003): 811–16. http://dx.doi.org/10.1046/j.1365-2265.2003.01925.x.

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Holtmann, Gerald, Reinholde Kriebel, and Manfred V. Singer. "Mental stress and gastric acid secretion." Digestive Diseases and Sciences 35, no. 8 (August 1990): 998–1007. http://dx.doi.org/10.1007/bf01537249.

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Giuliani, Fabrizio, Adam Grieve, and Catherine Rabouille. "Unconventional secretion: a stress on GRASP." Current Opinion in Cell Biology 23, no. 4 (August 2011): 498–504. http://dx.doi.org/10.1016/j.ceb.2011.04.005.

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Freeman, H., K. Shimomura, R. D. Cox, and F. M. Ashcroft. "Nicotinamide nucleotide transhydrogenase: a link between insulin secretion, glucose metabolism and oxidative stress." Biochemical Society Transactions 34, no. 5 (October 1, 2006): 806–10. http://dx.doi.org/10.1042/bst0340806.

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This paper reviews recent studies on the role of Nnt (nicotinamide nucleotide transhydrogenase) in insulin secretion and detoxification of ROS (reactive oxygen species). Glucose-stimulated insulin release from pancreatic β-cells is mediated by increased metabolism. This elevates intracellular [ATP], thereby closing KATP channels (ATP-sensitive potassium channels) and producing membrane depolarization, activation of voltage-gated Ca2+ channels, Ca2+ influx and, consequently, insulin secretion. The C57BL/6J mouse displays glucose intolerance and reduced insulin secretion, which results from a naturally occurring deletion in the Nnt gene. Transgenic expression of the wild-type Nnt gene in C57BL/6J mice rescues the phenotype. Knockdown of Nnt in the insulin-secreting cell line MIN6 with small interfering RNA dramatically reduced Ca2+ influx and insulin secretion. Similarly, mice carrying ENU (N-ethyl-N-nitrosourea)-induced loss-of-function mutations in Nnt were glucose intolerant and secreted less insulin during a glucose tolerance test. Islets isolated from these mice showed impaired insulin secretion in response to glucose, but not to the KATP channel blocker tolbutamide. This is explained by the fact that glucose failed to elevate ATP in Nnt mutant islets. Nnt is a nuclear-encoded mitochondrial protein involved in detoxification of ROS. β-Cells isolated from Nnt mutant mice showed increased ROS production on glucose stimulation. We hypothesize that Nnt mutations enhance glucose-dependent ROS production and thereby impair β-cell mitochondrial metabolism, possibly via activation of uncoupling proteins. This reduces ATP production and lowers KATP channel activity. Consequently, glucose-dependent electrical activity and insulin secretion are impaired.

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Zhang, Irina X., Jianhua Ren, Suryakiran Vadrevu, Malini Raghavan, and Leslie S. Satin. "ER stress increases store-operated Ca2+ entry (SOCE) and augments basal insulin secretion in pancreatic beta cells." Journal of Biological Chemistry 295, no. 17 (March 16, 2020): 5685–700. http://dx.doi.org/10.1074/jbc.ra120.012721.

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Type 2 diabetes mellitus (T2DM) is characterized by impaired glucose-stimulated insulin secretion and increased peripheral insulin resistance. Unremitting endoplasmic reticulum (ER) stress can lead to beta-cell apoptosis and has been linked to type 2 diabetes. Although many studies have attempted to link ER stress and T2DM, the specific effects of ER stress on beta-cell function remain incompletely understood. To determine the interrelationship between ER stress and beta-cell function, here we treated insulin-secreting INS-1(832/13) cells or isolated mouse islets with the ER stress–inducer tunicamycin (TM). TM induced ER stress as expected, as evidenced by activation of the unfolded protein response. Beta cells treated with TM also exhibited concomitant alterations in their electrical activity and cytosolic free Ca2+ oscillations. As ER stress is known to reduce ER Ca2+ levels, we tested the hypothesis that the observed increase in Ca2+ oscillations occurred because of reduced ER Ca2+ levels and, in turn, increased store-operated Ca2+ entry. TM-induced cytosolic Ca2+ and membrane electrical oscillations were acutely inhibited by YM58483, which blocks store-operated Ca2+ channels. Significantly, TM-treated cells secreted increased insulin under conditions normally associated with only minimal release, e.g. 5 mm glucose, and YM58483 blocked this secretion. Taken together, these results support a critical role for ER Ca2+ depletion–activated Ca2+ current in mediating Ca2+-induced insulin secretion in response to ER stress.

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Turakulov, Ya Kh, R. B. Burikhanov, P. P. Patkhitdinov, and A. I. Myslitsksya. "Immobilization stress effect on thyroid hormone secretion." Problems of Endocrinology 39, no. 5 (October 14, 1993): 47–48. http://dx.doi.org/10.14341/probl11990.

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Analysis of blood flowing from the rat thyroid has shown that an acute immobilization stress enhanced thyroid hormone secretion with an increase of the T3/T4-100 index. The most marked response to stress was observed after repeated 2 min immobilization with a 3 min interval: Such increase of secretion was arrested by injection of prasosin, an -adrenoblocker. Propylthiouracil injected an hour before the experiment reduced T4 thyroid conversion index. These results permit a conclusion that short-term repeated immobilization enhanced thyroid hormone secretion via -adrenergic system stimulation, this being paralleled by increased production of hormonally more active T3.

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Kar, Louis D. "FOREBRAIN PATHWAYS MEDIATING STRESS-INDUCED RENIN SECRETION." Clinical and Experimental Pharmacology and Physiology 23, no. 2 (February 1996): 166–70. http://dx.doi.org/10.1111/j.1440-1681.1996.tb02591.x.

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Copper, Rachel L., and Robert L. Goldenberg. "Catecholamine Secretion in Fetal Adaptation to Stress." Journal of Obstetric, Gynecologic & Neonatal Nursing 19, no. 3 (May 1990): 223–26. http://dx.doi.org/10.1111/j.1552-6909.1990.tb01640.x.

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Oberbeck, R., R. J. Benschop, R. Jacobs, W. Hosch, J. U. Jetschmann, T. H. Schürmeyer, R. E. Schmidt, and Manfred Schedlowski. "Endocrine mechanisms of stress-induced DHEA-secretion." Journal of Endocrinological Investigation 21, no. 3 (March 1998): 148–53. http://dx.doi.org/10.1007/bf03347293.

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Van de Kar, Louis D., and Martha L. Blair. "Forebrain Pathways Mediating Stress-Induced Hormone Secretion." Frontiers in Neuroendocrinology 20, no. 1 (January 1999): 1–48. http://dx.doi.org/10.1006/frne.1998.0172.

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Mani, Bharath K., Sherri Osborne-Lawrence, Nathan Metzger, and Jeffrey M. Zigman. "Lowering oxidative stress in ghrelin cells stimulates ghrelin secretion." American Journal of Physiology-Endocrinology and Metabolism 319, no. 2 (August 1, 2020): E330—E337. http://dx.doi.org/10.1152/ajpendo.00119.2020.

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Ghrelin is a predominantly stomach-derived peptide hormone with many actions including regulation of food intake, body weight, and blood glucose. Plasma ghrelin levels are robustly regulated by feeding status, with its levels increasing upon caloric restriction and decreasing after food intake. At least some of this regulation might be due to direct responsiveness of ghrelin cells to changes in circulating nutrients, including glucose. Indeed, oral and parental glucose administration to humans and mice lower plasma ghrelin. Also, dissociated mouse gastric mucosal cell preparations, which contain ghrelin cells, decrease ghrelin secretion when cultured in high ambient glucose. Here, we used primary cultures of mouse gastric mucosal cells in combination with an array of pharmacological tools to examine the potential role of changed intracellular oxidative stress in glucose-restricted ghrelin secretion. The antioxidants resveratrol, SRT1720, and curcumin all markedly increased ghrelin secretion. Furthermore, three different selective activators of Nuclear factor erythroid-derived-2-like 2 (Nrf2), a master regulator of the antioxidative cellular response to oxidative stress, increased ghrelin secretion. These antioxidant compounds blocked the inhibitory effects of glucose on ghrelin secretion. Therefore, we conclude that lowering oxidative stress within ghrelin cells stimulates ghrelin secretion and blocks the direct effects of glucose on ghrelin cells to inhibit ghrelin secretion.

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Wirtz, Petra H., Roland von Känel, Changiz Mohiyeddini, Luljeta Emini, Katharina Ruedisueli, Sara Groessbauer, and Ulrike Ehlert. "Low Social Support and Poor Emotional Regulation Are Associated with Increased Stress Hormone Reactivity to Mental Stress in Systemic Hypertension." Journal of Clinical Endocrinology & Metabolism 91, no. 10 (October 1, 2006): 3857–65. http://dx.doi.org/10.1210/jc.2005-2586.

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Abstract Context: There is strong evidence for a physiological hyperreactivity to stress in systemic hypertension, but data on associated or potentially moderating psychological factors are scarce. Objective: The objective of the study was to identify psychological correlates of physiological stress reactivity in systemic hypertension. Design: This was a cross-sectional, quasiexperimentally controlled study. Study participants underwent an acute standardized psychosocial stress task combining public speaking and mental arithmetic in front of an audience. Setting: The study was conducted in the population in the state of Zurich, Switzerland. Subjects: Subjects included 22 hypertensive and 26 normotensive men (mean ± sem 44 ± 2 yr). Main Outcome Measures: We assessed the psychological measures social support, emotional regulation, and cognitive appraisal of the stressful situation. Moreover, we measured salivary cortisol and plasma epinephrine and norepinephrine before and after stress and several times up to 60 min thereafter as well as blood pressure and heart rate. Results: We found poorer hedonistic emotional regulation (HER) and lower perceived social support in hypertensives, compared with normotensives (P < 0.01). Compared with normotensives, hypertensives showed higher cortisol, epinephrine, and norepinephrine secretions after stress (P < 0.038) as well as higher systolic and diastolic blood pressure (P < 0.001). Cortisol reactivity and norepinephrine secretion were highest in hypertensive men with low HER (P < 0.05). In contrast, hypertensives with high HER did not significantly differ from normotensives in both cortisol and norepinephrine secretion after stress. Epinephrine secretion was highest in hypertensives with low social support but was not different between hypertensives with high social support and normotensives. Conclusions: The findings suggest that both low social support and low HER are associated with elevated stress hormone reactivity in systemic hypertension.

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Belay, Tesfaye, Alexis Ray, and Kaitlyn Cook. "Cytokine production profiles of immune cells of stressed beta2-adrenergic receptor knockout mouse model during Chlamydia muridarumgenital infection." Journal of Immunology 210, no. 1_Supplement (May 1, 2023): 81.10. http://dx.doi.org/10.4049/jimmunol.210.supp.81.10.

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Abstract Chlamydia genital infection by Chlamydia trachomatisis the most common bacterial sexually transmitted disease worldwide. The relationships between stress and chlamydia genital infection remain unknown. Beta2-adrenergic receptor(β2-AR), the major receptor of the stress hormone norepinephrine (NE), is known to impair the function of immune cells. Stress was induced by immersing mice in cold water for five minutes daily for 21 days before infection. This study determined profiles of immune cells of stressed β2-AR KO and stressed WT C57BL/6J after 48 h of Chlamydia muridarumgenital infection. Splenic T cells and differentiated bone marrow-derived macrophages and dendric cells (DCs) were purified by negative selection and stimulated by seeding T cells on anti-CD3/CD28 antibodies coated wells and by treating macrophages and DCs with LPS. After 48 h proliferation, cytokine levels in culture supernatants of the cells were determined using ELISA. Results show increased IFN-γ and IL-1β secretions but deceased IL-4 secretion by CD4+ T cells of β2-AR KO compared to WT (p<0.05). The secretion of IL-13, IL-5, and IL-10 but not IL-23 in CD4 T cells of stressed β2-AR KO mice was two-fold lower than that of stressed WT. TNF-α and IL-1β secretions in macrophages and DCs or IL-12 secretion in DCs was high in stressed β2-AR KO compared to WT (p<0.05). Overall, this study provides insights into the β2-AR signaling pathway’s role in suppressing the secretion of protective cytokines suggesting that inhibiting β2-AR signaling pathway may restore the function of immune cells during chlamydia genital infection. However, further study is warranted. This work was funded by NIH grant # 1R15AI124156-01 awarded to Bluefield State University

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Carew, Nolan, Ashley Nelson, Zhitao Liang, Sage Smith, and Christine Milcarek. "Linking Endoplasmic Reticular Stress and Alternative Splicing." International Journal of Molecular Sciences 19, no. 12 (December 7, 2018): 3919. http://dx.doi.org/10.3390/ijms19123919.

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RNA splicing patterns in antibody-secreting cells are shaped by endoplasmic reticulum stress, ELL2 (eleven-nineteen lysine-rich leukemia gene 2) induction, and changes in the levels of snRNAs. Endoplasmic reticulum stress induces the unfolded protein response comprising a highly conserved set of genes crucial for cell survival; among these is Ire1, whose auto-phosphorylation drives it to acquire a regulated mRNA decay activity. The mRNA-modifying function of phosphorylated Ire1 non-canonically splices Xbp1 mRNA and yet degrades other cellular mRNAs with related motifs. Naïve splenic B cells will activate Ire1 phosphorylation early on after lipopolysaccharide (LPS) stimulation, within 18 h; large-scale changes in mRNA content and splicing patterns result. Inhibition of the mRNA-degradation function of Ire1 is correlated with further differences in the splicing patterns and a reduction in the mRNA factors for snRNA transcription. Some of the >4000 splicing changes seen at 18 h after LPS stimulation persist into the late stages of antibody secretion, up to 72 h. Meanwhile some early splicing changes are supplanted by new splicing changes introduced by the up-regulation of ELL2, a transcription elongation factor. ELL2 is necessary for immunoglobulin secretion and does this by changing mRNA processing patterns of immunoglobulin heavy chain and >5000 other genes.

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Bułdak, Łukasz, Estera Skudrzyk, Grzegorz Machnik, Aleksandra Bołdys, Rafał Jakub Bułdak, and Bogusław Okopień. "Exenatide improves antioxidant capacity and reduces the expression of LDL receptors and PCSK9 in human insulin-secreting 1.1E7 cell line subjected to hyperglycemia and oxidative stress." Postępy Higieny i Medycyny Doświadczalnej 76, no. 1 (January 1, 2022): 16–23. http://dx.doi.org/10.2478/ahem-2021-0037.

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Abstract Introduction GLP-1 receptor agonists (e.g., exenatide) are novel drugs used in the treatment of diabetes. These drugs, working with other mechanisms of action, improve glycemic control by increasing secretion of insulin and improving survival of pancreatic islet beta cells. Alterations in the oxidative stress level or the expression of proteins associated with cholesterol uptake might be responsible for those findings. Currently, there are few in vitro studies on the impact of exenatide antioxidant capacity in human islet beta cell lines and none that assess the influence of exenatide on LDL receptors and PCSK9 under hyperglycemia and oxidative stress. Therefore, we evaluated the impact of exenatide on antioxidant capacity, insulin secretion, and proteins involved in cholesterol metabolism. Materials and Method An in vitro culture of insulin-secreting cells 1.1E7 was subjected to hyperglycemia and oxidative stress. Assessment was made of the expression of enzymes associated with oxidative stress (NADPH oxidase, catalase, glutathione peroxidase, superoxide dismutase, iNOS) and cholesterol uptake (LDL receptors, PCSK9). Additionally, insulin and nitrite levels in culture media were quantified. Results We showed that exenatide improves expression of catalase and reduces the amount of nitrite in cell cultures in a protein kinase A–dependent manner. Those results were accompanied by a drop in the expression of LDL receptors and PCSK9. Insulin secretion was modestly increased in the culture condition. Conclusions Our findings show potential protective mechanisms exerted by exenatide in human insulin-secreting pancreatic beta cell line (1.1E7), which may be exerted through increased antioxidant capacity and reduced accumulation of cholesterol.

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Wang, Huan, Shuting Zhao, Zexin Qi, Changgang Yang, Dan Ding, Binbin Xiao, Shihong Wang, and Chunwu Yang. "Regulation of Root Exudation in Wheat Plants in Response to Alkali Stress." Plants 13, no. 9 (April 28, 2024): 1227. http://dx.doi.org/10.3390/plants13091227.

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Soil alkalization is an important environmental factor limiting crop production. Despite the importance of root secretion in the response of plants to alkali stress, the regulatory mechanism is unclear. In this study, we applied a widely targeted metabolomics approach using a local MS/MS data library constructed with authentic standards to identify and quantify root exudates of wheat under salt and alkali stresses. The regulatory mechanism of root secretion in alkali-stressed wheat plants was analyzed by determining transcriptional and metabolic responses. Our primary focus was alkali stress-induced secreted metabolites (AISMs) that showed a higher secretion rate in alkali-stressed plants than in control and salt-stressed plants. This secretion was mainly induced by high-pH stress. We discovered 55 AISMs containing –COOH groups, including 23 fatty acids, 4 amino acids, 1 amino acid derivative, 7 dipeptides, 5 organic acids, 9 phenolic acids, and 6 others. In the roots, we also discovered 29 metabolites with higher levels under alkali stress than under control and salt stress conditions, including 2 fatty acids, 3 amino acid derivatives, 1 dipeptide, 2 organic acids, and 11 phenolic acids. These alkali stress-induced accumulated carboxylic acids may support continuous root secretion during the response of wheat plants to alkali stress. In the roots, RNAseq analysis indicated that 5 6-phosphofructokinase (glycolysis rate-limiting enzyme) genes, 16 key fatty acid synthesis genes, and 122 phenolic acid synthesis genes have higher expression levels under alkali stress than under control and salt stress conditions. We propose that the secretion of multiple types of metabolites with a –COOH group is an important pH regulation strategy for alkali-stressed wheat plants. Enhanced glycolysis, fatty acid synthesis, and phenolic acid synthesis will provide more energy and substrates for root secretion during the response of wheat to alkali stress.

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Cornelius, Jamie M., Creagh W. Breuner, and Thomas P. Hahn. "Coping with the extremes: stress physiology varies between winter and summer in breeding opportunists." Biology Letters 8, no. 2 (October 19, 2011): 312–15. http://dx.doi.org/10.1098/rsbl.2011.0865.

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Seasonal changes in stress steroid hormone secretions are thought to reflect investment in self-maintenance versus reproduction. The capricious conditions hypothesis (CCH) posits that reduced corticosterone (CORT) secretion during stress coincident with parental phases of breeding is necessary in harsh environments because a full response would otherwise trigger repeated nest abandonments. To test this hypothesis, we measured seasonal changes in stress physiology in free-living red crossbills ( Loxia curvirostra ), an opportunistically breeding songbird that regularly breeds in summer and winter. This species allows unique comparisons of breeding physiology under very different seasonal environmental conditions within locations. We found strong support for the CCH: red crossbills showed reduced CORT secretion only when in high reproductive condition in the winter, when compared with summer breeders and winter non-breeders. These data demonstrate that behavioural status and local environmental conditions interact to affect mechanisms underlying investment trade-offs, presumably in a way that maximizes lifetime reproductive success.

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Bridgeman, Stephanie, Gaewyn Ellison, Philip Newsholme, and Cyril Mamotte. "The HDAC Inhibitor Butyrate Impairs β Cell Function and Activates the Disallowed Gene Hexokinase I." International Journal of Molecular Sciences 22, no. 24 (December 11, 2021): 13330. http://dx.doi.org/10.3390/ijms222413330.

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Histone deacetylase (HDAC) inhibitors such as butyrate have been reported to reduce diabetes risk and protect insulin-secreting pancreatic β cells in animal models. However, studies on insulin-secreting cells in vitro have found that butyrate treatment resulted in impaired or inappropriate insulin secretion. Our study explores the effects of butyrate on insulin secretion by BRIN BD-11 rat pancreatic β cells and examined effects on the expression of genes implicated in β cell function. Robust HDAC inhibition with 5 mM butyrate or trichostatin A for 24 h in β cells decreased basal insulin secretion and content, as well as insulin secretion in response to acute stimulation. Treatment with butyrate also increased expression of the disallowed gene hexokinase I, possibly explaining the impairment to insulin secretion, and of TXNIP, which may increase oxidative stress and β cell apoptosis. In contrast to robust HDAC inhibition (>70% after 24 h), low-dose and acute high-dose treatment with butyrate enhanced nutrient-stimulated insulin secretion. In conclusion, although protective effects of HDAC inhibition have been observed in vivo, potent HDAC inhibition impairs β cell function in vitro. The chronic low dose and acute high dose butyrate treatments may be more reflective of in vivo effects.

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Shen, Hong, Weibin Jing, Tiancheng Ai, Ying Lu, and Jianxun Cheng. "Differential secretion of lactate and activity of plasma membrane H+-ATPase in the roots of soybean seedlings in response to low-oxygen stress." Australian Journal of Botany 54, no. 5 (2006): 471. http://dx.doi.org/10.1071/bt05141.

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Plants display a series of tolerance mechanism following exposure to low-oxygen stress. Increased secretion of end production of carbohydrate catabolism and synthesis of stress-related proteins are important mechanisms enabling the plant to develop tolerance to anoxia stress. In this study, the secretion of lactate and the activity of plasma membrane H+-ATPase in a wild-type (WTS) and a cultivated soybean (CTS) were investigated in response to low-oxygen stress. Low oxygen (0.1% O2, anoxia) increased the secretion of lactate and reduced the activity of plasma membrane H+-ATPase and ATP content in a time-dependent manner. WTS showed greater root elongation and higher survivability than CTS. The higher lactate secretion coincided with the lower accumulation of lactate in WTS than in CTS. Anoxia decreased the cellular pH in soybean roots. Hypoxia (5% O2) increased the secretion of lactate and the activity of plasma membrane H+-ATPase. In comparison to anoxia, hypoxia stress induced increases of 57.4 and 29.7% of endogenous abscisic acid (ABA) in the root apices of WTS and CTS, respectively. Exogenous application of ABA showed a stimulatory effect on the activity of plasma membrane H+-ATPase and the secretion of citrate from soybean roots. However, cycloheximide, an inhibitor of protein synthesis, abolished ABA effects. These results suggest that the modulation of the secretion of lactate and activity of plasma membrane H+-ATPase in soybean roots is associated with the mechanisms of tolerance to low-oxygen stress. ABA might be involved in the hypoxia signal transmitted in soybean roots.

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Szczepanska-Sadowska, Ewa, Agnieszka Wsol, Agnieszka Cudnoch-Jedrzejewska, and Tymoteusz Żera. "Complementary Role of Oxytocin and Vasopressin in Cardiovascular Regulation." International Journal of Molecular Sciences 22, no. 21 (October 24, 2021): 11465. http://dx.doi.org/10.3390/ijms222111465.

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The neurons secreting oxytocin (OXY) and vasopressin (AVP) are located mainly in the supraoptic, paraventricular, and suprachiasmatic nucleus of the brain. Oxytocinergic and vasopressinergic projections reach several regions of the brain and the spinal cord. Both peptides are released from axons, soma, and dendrites and modulate the excitability of other neuroregulatory pathways. The synthesis and action of OXY and AVP in the peripheral organs (eye, heart, gastrointestinal system) is being investigated. The secretion of OXY and AVP is influenced by changes in body fluid osmolality, blood volume, blood pressure, hypoxia, and stress. Vasopressin interacts with three subtypes of receptors: V1aR, V1bR, and V2R whereas oxytocin activates its own OXTR and V1aR receptors. AVP and OXY receptors are present in several regions of the brain (cortex, hypothalamus, pons, medulla, and cerebellum) and in the peripheral organs (heart, lungs, carotid bodies, kidneys, adrenal glands, pancreas, gastrointestinal tract, ovaries, uterus, thymus). Hypertension, myocardial infarction, and coexisting factors, such as pain and stress, have a significant impact on the secretion of oxytocin and vasopressin and on the expression of their receptors. The inappropriate regulation of oxytocin and vasopressin secretion during ischemia, hypoxia/hypercapnia, inflammation, pain, and stress may play a significant role in the pathogenesis of cardiovascular diseases.

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Zinkevičiūtė, Rūta, Raimundas Ražanskas, Algirdas Kaupinis, Neringa Macijauskaitė, Evaldas Čiplys, Gunnar Houen, and Rimantas Slibinskas. "Yeast Secretes High Amounts of Human Calreticulin without Cellular Stress." Current Issues in Molecular Biology 44, no. 5 (April 19, 2022): 1768–87. http://dx.doi.org/10.3390/cimb44050122.

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The ER chaperone calreticulin (CALR) also has extracellular functions and can exit the mammalian cell in response to various factors, although the mechanism by which this takes place is unknown. The yeast Saccharomyces cerevisiae efficiently secretes human CALR, and the analysis of this process in yeast could help to clarify how it gets out of eukaryotic cells. We have achieved a secretion titer of about 140 mg/L CALR in our S. cerevisiae system. Here, we present a comparative quantitative whole proteome study in CALR-secreting yeast using non-equilibrium pH gradient electrophoresis (NEPHGE)-based two-dimensional gel electrophoresis (2DE) as well as liquid chromatography mass spectrometry in data-independent analysis mode (LC-MSE). A reconstructed carrier ampholyte (CA) composition of NEPHGE-based first-dimension separation for 2DE could be used instead of formerly commercially available gels. Using LC-MSE, we identified 1574 proteins, 20 of which exhibited differential expression. The largest group of differentially expressed proteins were structural ribosomal proteins involved in translation. Interestingly, we did not find any signs of cellular stress which is usually observed in recombinant protein-producing yeast, and we did not identify any secretory pathway proteins that exhibited changes in expression. Taken together, high-level secretion of human recombinant CALR protein in S. cerevisiae does not induce cellular stress and does not burden the cellular secretory machinery. There are only small changes in the cellular proteome of yeast secreting CALR at a high level.

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Masumi, Kamiyama, Ookawa Mana, Saito Rika, Tange Noa, Hashizume Mariyo, Matsunaga Misuzu, Yokota Riko, Yoshihara Ayaka, and Iwamoto Tamami. "Isoflavones Inhibit Hydrogen Peroxide-Induced Angiotensinogen Secretion in Mesangial Cells." Current Topics in Nutraceutical Research 22, no. 2 (February 3, 2024): 624–28. http://dx.doi.org/10.37290/ctnr2641-452x.22:624-628.

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The mechanisms underlying increased angiotensinogen secretion in diabetic nephropathy are unknown. This study aimed to examine the mechanism of increased angiotensinogen secretion in mesangial cells. Additionally, we explored the effects of antioxidant compounds, such as isoflavones, on angiotensin secretion. Angiotensinogen expression and secretion were evaluated in mesangial cells treated with hydrogen peroxide. We investigated the effects of pretreatment with catalase, daidzein, and equol and inhibitors of mitogen-activated protein kinase, stress-stimulated kinase p38, or c-Jun NH2-terminal kinase. The 1,1-diphenyl-2-picrylhydrazyl radical scavenging assay revealed that daidzein and equol have antioxidant properties. Hydrogen peroxide stimulated angiotensinogen expression and secretion in mesangial cells in a concentrationdependent manner. Catalase, daidzein, and equol reduced the enhanced angiotensinogen expression and secretion induced by hydrogen peroxide. We examined the mitogen-activated protein kinase cascade to explore cell signaling mechanisms involved in angiotensinogen induction. We hypothesize that stress-stimulated kinase p38 and c-Jun NH2-terminal kinase were crucial in the mechanisms. We found that hydrogen peroxide enhanced angiotensinogen expression and secretion in mesangial cells. However, daidzein and equol decreased this enhancement. Increased angiotensinogen secretion will enhance stress-stimulated kinase p38 and c-Jun NH2-terminal kinase.

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Hannibal, Kara E., and Mark D. Bishop. "Chronic Stress, Cortisol Dysfunction, and Pain: A Psychoneuroendocrine Rationale for Stress Management in Pain Rehabilitation." Physical Therapy 94, no. 12 (December 1, 2014): 1816–25. http://dx.doi.org/10.2522/ptj.20130597.

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Pain is a primary symptom driving patients to seek physical therapy, and its attenuation commonly defines a successful outcome. A large body of evidence is dedicated to elucidating the relationship between chronic stress and pain; however, stress is rarely addressed in pain rehabilitation. A physiologic stress response may be evoked by fear or perceived threat to safety, status, or well-being and elicits the secretion of sympathetic catecholamines (epinephrine and norepinepherine) and neuroendocrine hormones (cortisol) to promote survival and motivate success. Cortisol is a potent anti-inflammatory that functions to mobilize glucose reserves for energy and modulate inflammation. Cortisol also may facilitate the consolidation of fear-based memories for future survival and avoidance of danger. Although short-term stress may be adaptive, maladaptive responses (eg, magnification, rumination, helplessness) to pain or non–pain-related stressors may intensify cortisol secretion and condition a sensitized physiologic stress response that is readily recruited. Ultimately, a prolonged or exaggerated stress response may perpetuate cortisol dysfunction, widespread inflammation, and pain. Stress may be unavoidable in life, and challenges are inherent to success; however, humans have the capability to modify what they perceive as stressful and how they respond to it. Exaggerated psychological responses (eg, catastrophizing) following maladaptive cognitive appraisals of potential stressors as threatening may exacerbate cortisol secretion and facilitate the consolidation of fear-based memories of pain or non–pain-related stressors; however, coping, cognitive reappraisal, or confrontation of stressors may minimize cortisol secretion and prevent chronic, recurrent pain. Given the parallel mechanisms underlying the physiologic effects of a maladaptive response to pain and non–pain-related stressors, physical therapists should consider screening for non–pain-related stress to facilitate treatment, prevent chronic disability, and improve quality of life.

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Nishizawa, Toshihiro, Hidekazu Suzuki, Tatsuhiro Masaoka, Yohei Nomoto, Yuriko Minegishi, Hiroshi Hosoda, Mikiji Mori, et al. "Emotional Stress Enhanced Ghrelin Secretion from the Stomach." Journal of Clinical Biochemistry and Nutrition 38, no. 1 (2006): 33–37. http://dx.doi.org/10.3164/jcbn.38.33.

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Saito, T., H. Itoh, T. Chun, T. Igaki, Y. Mori, J. Yamashita, K. Doi, et al. "Oxidative Stress Suppresses the Endothelial Secretion of Endothelin." Journal of Cardiovascular Pharmacology 31 (1998): S345—S347. http://dx.doi.org/10.1097/00005344-199800001-00096.

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Levine, S. P., B. L. Towell, A. M. Suarez, L. K. Knieriem, M. M. Harris, and J. N. George. "Platelet activation and secretion associated with emotional stress." Circulation 71, no. 6 (June 1985): 1129–34. http://dx.doi.org/10.1161/01.cir.71.6.1129.

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Gibbs, Daniel M. "Stress-Specific Modulation of ACTH Secretion by Oxytocin." Neuroendocrinology 42, no. 6 (1986): 456–58. http://dx.doi.org/10.1159/000124487.

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Aguilera, Greti. "Regulation of Pituitary ACTH Secretion during Chronic Stress." Frontiers in Neuroendocrinology 15, no. 4 (December 1994): 321–50. http://dx.doi.org/10.1006/frne.1994.1013.

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Milcarek, Christine. "Linking Endoplasmic Reticular Stress, ELL2, and Alternative Splicing." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 123.9. http://dx.doi.org/10.4049/jimmunol.202.supp.123.9.

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Abstract RNA splicing patterns in antibody-secreting cells are shaped by endoplasmic reticulum stress, ELL2 transcription elongation factor induction, and changes in the levels of snRNAs. Endoplasmic reticulum stress induces the unfolded protein response; among these stress proteins is Ire1, whose auto-phosphorylation drives it to acquire a regulated mRNA decay activity. The mRNA-modifying function of phosphorylated Ire1 non-canonically splices Xbp1 and yet degrades other cellular mRNAs with related motifs, in a cell-specific manner. Naïve splenic B cells will activate Ire1 phosphorylation early on after lipopolysaccharide (LPS) stimulation, within 18 h; large-scale changes in mRNA content and splicing patterns result. Inhibition of the mRNA-degradation function of Ire1 is correlated with further differences in the splicing patterns and a reduction in the mRNA factors for snRNA transcription. Some of the >4000 splicing changes seen at 18 h after LPS stimulation persist into the late stages of antibody secretion, up to 72 h. Meanwhile some early splicing changes are supplanted by new splicing changes introduced by the up-regulation of ELL2 which is necessary for immunoglobulin secretion; it does this by changing mRNA processing patterns of immunoglobulin heavy chain and >5000 other genes. unexpectedly, ubiquitination of c-myc by the ELL family members also plays a role in plasma-blast survival.

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Lee, Younghay, Sun-Hye Shin, Kyung-Ah Cho, Yu-Hee Kim, So-Youn Woo, Han Su Kim, Sung-Chul Jung, et al. "Administration of Tonsil-Derived Mesenchymal Stem Cells Improves Glucose Tolerance in High Fat Diet-Induced Diabetic Mice via Insulin-Like Growth Factor-Binding Protein 5-Mediated Endoplasmic Reticulum Stress Modulation." Cells 8, no. 4 (April 23, 2019): 368. http://dx.doi.org/10.3390/cells8040368.

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Type 2 diabetes mellitus (T2DM) is a prevalent chronic metabolic disorder accompanied by high blood glucose, insulin resistance, and relative insulin deficiency. Endoplasmic reticulum (ER) stress induced by high glucose and free fatty acids has been suggested as one of the main causes of β-cell dysfunction and death in T2DM. Stem cell-derived insulin-secreting cells were recently suggested as a novel therapy for diabetes. In the present study, we demonstrate the therapeutic potential of tonsil-derived mesenchymal stem cells (TMSCs) to treat high-fat diet (HFD)-induced T2DM. To explore whether TMSC administration can alleviate T2DM, TMSCs were intraperitoneally injected in HFD-induced T2DM mice once every 2 weeks. TMSC injection markedly improved glucose tolerance and glucose-stimulated insulin secretion and prevented HFD-induced pancreatic β-cell hypertrophy and cell death. In addition, TMSC injection relieved the ER-stress response and preserved gene expression related to glucose sensing and insulin secretion. Moreover, administration of TMSC-derived conditioned medium induced similar therapeutic outcomes, suggesting paracrine effects. Finally, proteomic analysis revealed high secretion of insulin-like growth factor-binding protein 5 by TMSCs, and its expression was critical for the protective effects of TMSCs against HFD-induced glucose intolerance and ER-stress response in pancreatic islets. TMSC administration can alleviate HFD-induced-T2DM via preserving pancreatic islets and their function. These results provide novel evidence of TMSCs as an ER-stress modulator that may be a novel, alternative cell therapy for T2DM.

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Bataille, Amy M., Carla L. Maffeo, and J. Larry Renfro. "Avian renal proximal tubule urate secretion is inhibited by cellular stress-induced AMP-activated protein kinase." American Journal of Physiology-Renal Physiology 300, no. 6 (June 2011): F1327—F1338. http://dx.doi.org/10.1152/ajprenal.00680.2010.

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Urate is a potent antioxidant at high concentrations but it has also been associated with a wide variety of health risks. Plasma urate concentration is determined by ingestion, production, and urinary excretion; however, factors that regulate urate excretion remain uncertain. The objective of this study was to determine whether cellular stress, which has been shown to affect other renal transport properties, modulates urate secretion in the avian renal proximal tubule. Chick kidney proximal tubule epithelial cell primary culture monolayers were used to study the transepithelial transport of radiolabeled urate. This model allowed examination of the processes, such as multidrug resistance protein 4 (Mrp4, Abcc4), which subserve urate secretion in a functional, intact, homologous system. Our results show that the recently implicated urate efflux transporter, breast cancer resistance protein ( ABCG2), does not significantly contribute to urate secretion in this system. Exposure to a high concentration of zinc for 6 h induced a cellular stress response and a striking decrease in transepithelial urate secretion. Acute exposure to zinc had no effect on transepithelial urate secretion or isolated membrane vesicle urate transport, suggesting involvement of a cellular stress adaptation. Activation of AMP-activated protein kinase (AMPK), a candidate modulator of ATP-dependent urate efflux, by 5′-aminoimidazole-4-carboxamide 1-β-d-ribo-furanoside caused a decrease in urate secretion similar to that seen with zinc-induced cellular stress. This effect was prevented with the AMPK inhibitor compound C. Notably, the decrease in urate secretion seen with zinc-induced cellular stress was also prevented by compound C, implicating AMPK in regulation of renal uric acid excretion.

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Newman, Jonathon R., and Diane Wagner. "The influence of water availability and defoliation on extrafloral nectar secretion in quaking aspen (Populus tremuloides)." Botany 91, no. 11 (November 2013): 761–67. http://dx.doi.org/10.1139/cjb-2013-0147.

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In recent years, water stress has led to widespread growth declines and dieback of several North American tree species. In addition to its direct effects on tree physiology, water stress may compromise anti-herbivore defenses. We tested whether extrafloral (EF) sugar secretion rate in Populus tremuloides Michx. (quaking aspen) increases in response to defoliation and whether water stress impairs constitutive and inducible EF sugar secretion. We subjected P. tremuloides ramets of four genotypes to water restriction and defoliation in a factorial design and measured EF sugar secretion rates 2, 4, and 6 days after defoliation. The sugar secretion rate of defoliated ramets was significantly higher than that of undefoliated ramets 6 days after defoliation. Low water availability reduced the sugar secretion rate of one of the four aspen genotypes but did not prevent induction. Populus tremuloides genotypes secreted EF sugar at different average rates, suggesting genetic variation for this trait. The results indicate that EF nectar secretion is inducible in P. tremuloides, which could increase the effectiveness of indirect defense following herbivory. Genotypic differences in the response of P. tremuloides to water stress suggest that some clonal stands may be at a disadvantage when faced with compound stresses of drought and herbivory.

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Brown, L. A. "Glutathione protects signal transduction in type II cells under oxidant stress." American Journal of Physiology-Lung Cellular and Molecular Physiology 266, no. 2 (February 1, 1994): L172—L177. http://dx.doi.org/10.1152/ajplung.1994.266.2.l172.

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Brief exposure of type II cells to 100 microM t-butyl hydroperoxide (tBOOH) inhibits agonist-induced surfactant secretion and second messenger generation presumably through the oxidation of membrane lipids. Since glutathione (GSH) reduces lipid peroxides and protects type II cells from oxidant injury as determined by crude indicators, then GSH should also protect signal transduction. In the current study, tBOOH inhibited ATP-induced adenosine 3',5'-cyclic monophosphate and inositol trisphosphate generation and surfactant secretion. Stimulation of surfactant secretion by forskolin or phorbol acetate was also inhibited by tBOOH. Pretreatment with GSH (1 mM) blocked the tBOOH inhibition. This protection occurred in the presence of gamma-glutamyl transferase and gamma-glutamylcysteine synthetase inhibitors and suggested GSH was transported as an intact molecule. GSH protection was blocked by gamma-L-glutamyl-L-glutamate, an agent that blocks GSH transport. Protection of surfactant secretion and signal transduction was also provided by the constitutive amino acids but not if GSH synthesis was blocked. In the cultured type II cell model, GSH transport and synthesis protected signal transduction and, subsequently, surfactant secretion against oxidant injury.

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Saito, Takatoshi, Hiroshi Itoh, Tae-Hwa Chun, Yasutomo Fukunaga, Jun Yamashita, Kentaro Doi, Tokuji Tanaka, et al. "Coordinate regulation of endothelin and adrenomedullin secretion by oxidative stress in endothelial cells." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 3 (September 1, 2001): H1364—H1371. http://dx.doi.org/10.1152/ajpheart.2001.281.3.h1364.

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To elucidate the significance of oxidative stress in the modulation of endothelial functions, we examined the effects of H2O2 on the expression of two endothelium-derived vasoactive peptides, endothelin (ET) and adrenomedullin (Am), and their interaction. H2O2 dose dependently suppressed ET secretion and ET-1 mRNA expression in bovine carotid endothelial cells (ECs). Menadion sodium bisulfate, a redox cycling drug, also decreased ET secretion in a dose-dependent manner. Catalase, a H2O2 reductase, and dl-α-tocopherol (vitamin E) significantly inhibited H2O2-induced suppression of ET secretion. Downregulation of ET-1 mRNA under oxidative stress was regulated at the transcriptional level. In contrast, H2O2increased Am secretion (and its mRNA expression) accompanied by the augmentation of cAMP production. Am, as well as 8-bromo-cAMP and forskolin decreased ET secretion in a dose-dependent fashion. Furthermore, an anti-Am monoclonal antibody that we developed abolished H2O2-induced suppression of ET secretion at 6–24 h after the addition of H2O2. H2O2 increased the intracellular Ca2+ concentration ([Ca2+]i). Moreover, treatment with ionomycin, a Ca2+ ionophore, and thapsigargin, an inhibitor of endoplasmic reticulum ATPase, decreased ET secretion dose dependently for 3 h. These results suggest that the production of ET was decreased via activation of the Am-cAMP pathway and by the elevation of [Ca2+]i under oxidative stress. These findings elucidate the coordinate expression of two local vascular hormones, ET and Am, under oxidative stress, which may protect against vascular diseases.

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Gai, Yedan, Jinglin Zhang, Chao Wei, Wei Cao, Yan Cui, and Sheng Cui. "miR-375 negatively regulates the synthesis and secretion of catecholamines by targeting Sp1 in rat adrenal medulla." American Journal of Physiology-Cell Physiology 312, no. 5 (May 1, 2017): C663—C672. http://dx.doi.org/10.1152/ajpcell.00345.2016.

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The adrenal gland is an important endocrine gland in balancing homeostasis and the response to stress by synthesizing and secreting catecholamines (CATs), and it has been confirmed that microRNA-375 (miR-375) is highly expressed in adrenal medulla. However, up to now there are few reports about the functions and related mechanisms in adrenal medulla. The present study was thus designed to study the roles and related mechanisms in rat adrenal medulla. Our results showed that miR-375 was specifically expressed in rat adrenal medulla chromaffin cells, and its expression was downregulated when rats were exposed to stress. The further functional studies demonstrated that the inhibition of endogenous miR-375 induced the secretion of CATs in primary rat medulla chromaffin cells and PC12 cells, whereas miR-375 overexpression resulted in a decline of CAT secretion. In addition, our results showed that miR-375 negatively regulated tyrosine hydroxylase (TH) and dopamine-β-hydroxylase (DBH) and mediated adrenomedullary CAT biosynthesis. These functions of miR-375 were accomplished by its binding to the 3′-untranslated region of Sp1, which was involved in the regulation of TH and DBH expressions. These novel findings suggest that miR-375 acts as a potent negative mediator in regulating the synthesis and secretion of CATs in the adrenal medulla during the maintenance of homeostasis under stress.

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Ponikowska, Irena, Przemysław Adamczyk, and Irena Krupka-Matuszczyk. "Thermal Therapy In Patients with Post-pandemic Stress Syndrome as a S upporting Therapy." Acta Balneologica 62, no. 4 (2020): 245–49. http://dx.doi.org/10.36740/abal202004108.

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The viral pandemic causes multidirectional adverse effects and the greatest of which is health. The viral infection itself and severe infectious disease with pulmonary complications are of government concern. However, less is said about the effects of pandemic restrictions, e.g., social isolation leading to a series of severe psychosomatic disorders. In social isolation and quarantine, the classic negative lifestyle factors are working – the lack of exercise, excessive eating, stress, and addiction intensity. In turn, these factors lead to the exacerbation of chronic diseases such as diabetes, obesity, hypertension, heart disease, and others. Stress plays a unique role as it causes a number of stress syndromes, including the most severe form – post-traumatic stress disorder (PTSD). Stress is destructive to the entire body. It causes changes mainly in the autonomic nervous system and the endocrine system. In a stressful situation, the sympathetic nervous system’s activity increases, which leads to disorders in the functioning of many organs. Together with the autonomic nervous system’s stimulation, the secretion of stress hormones such as adrenaline, noradrenaline, and cortisol increases. Increased adrenaline secretion leads to arrhythmias, hypertension, and metabolic changes. Excessive secretion of cortisol increases protein catabolism, glucagon secretion, increases gluconeogenesis, lipolysis, and, consequently, increases blood glucose and cholesterol levels. Post-pandemic stress syndromes should be treated. Classic psychotherapy proposes the most important methods of treating these syndromes. The thermal therapy is the most useful and of pathogenetic significance. Thermal therapy includes heat therapy, hydrotherapy, peloid therapy, massages, music therapy, and physical training. These procedures, included in the appropriate treatment program, positively affect the autonomic nervous system, reduce the secretion of stress hormones, and reduce the level of stress. Thanks to thermal therapy, patients regain their mental balance, eradicate anxiety, improve physical condition, and increase resistance to infections. Moreover, they acquire knowledge about the proper lifestyle and methods to deal with stress.

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Breen, Kellie M., Amy E. Oakley, Andrew V. Pytiak, Alan J. Tilbrook, Elizabeth R. Wagenmaker, and Fred J. Karsch. "Does Cortisol Acting Via the Type II Glucocorticoid Receptor Mediate Suppression of Pulsatile Luteinizing Hormone Secretion in Response to Psychosocial Stress?" Endocrinology 148, no. 4 (April 1, 2007): 1882–90. http://dx.doi.org/10.1210/en.2006-0973.

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This study assessed the importance of cortisol in mediating inhibition of pulsatile LH secretion in sheep exposed to a psychosocial stress. First, we developed an acute psychosocial stress model that involves sequential layering of novel stressors over 3–4 h. This layered-stress paradigm robustly activated the hypothalamic-pituitary-adrenal axis and unambiguously inhibited pulsatile LH secretion. We next used this paradigm to test the hypothesis that cortisol, acting via the type II glucocorticoid receptor (GR), mediates stress-induced suppression of pulsatile LH secretion. Our approach was to determine whether an antagonist of the type II GR (RU486) reverses inhibition of LH pulsatility in response to the layered stress. We used two animal models to assess different aspects of LH pulse regulation. With the first model (ovariectomized ewe), LH pulse characteristics could vary as a function of both altered GnRH pulses and pituitary responsiveness to GnRH. In this case, antagonism of the type II GR did not prevent stress-induced inhibition of pulsatile LH secretion. With the second model (pituitary-clamped ovariectomized ewe), pulsatile GnRH input to the pituitary was fixed to enable assessment of stress effects specifically at the pituitary level. In this case, the layered stress inhibited pituitary responsiveness to GnRH and antagonism of the type II GR reversed the effect. Collectively, these findings indicate acute psychosocial stress inhibits pulsatile LH secretion, at least in part, by reducing pituitary responsiveness to GnRH. Cortisol, acting via the type II GR, is an obligatory mediator of this effect. However, under conditions in which GnRH input to the pituitary is not clamped, antagonism of the type II GR does not prevent stress-induced inhibition of LH pulsatility, implicating an additional pathway of suppression that is independent of cortisol acting via this receptor.

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Jackson, Benjamin T., George J. Piasecki, Herbert E. Cohn, and Wayne R. Cohen. "Control of fetal insulin secretion." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 6 (December 1, 2000): R2179—R2188. http://dx.doi.org/10.1152/ajpregu.2000.279.6.r2179.

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In this study, we investigated the way in which fetal insulin secretion is influenced by interrelated changes in blood glucose and sympathoadrenal activity. Experiments were conducted in late gestation sheep fetuses prepared with chronic peripheral and adrenal catheters. The fetus mounted a brisk insulin response to hyperglycemia but with only a minimal change in the glucose-to-insulin ratio, indicating a tight coupling between insulin secretion and plasma glucose. In well-oxygenated fetuses, α2-adrenergic blockade by idazoxan effected no change in fetal insulin concentration, indicating the absence of a resting sympathetic inhibitory tone for insulin secretion. With hypoxia, fetal norepinephrine (NE) and epinephrine secretion and plasma NE increased markedly; fetal insulin secretion decreased strikingly with the degree of change related to extant plasma glucose concentration. Idazoxan blocked this effect showing the hypoxic inhibition of insulin secretion to be mediated by a specific α2-adrenergic mechanism. α2-Blockade in the presence of sympathetic activation secondary to hypoxic stress also revealed the presence of a potent β-adrenergic stimulatory effect for insulin secretion. However, based on an analysis of data at the completion of the study, this β-stimulatory mechanism was seen to be absent in all six fetuses that had been subjected to a prior experimentally induced hypoxic stress but in only one of nine fetuses not subjected to this perturbation. We speculate that severe hypoxic stress in the fetus may, at least in the short term, have a residual effect in suppressing the β-adrenergic stimulatory mechanism for insulin secretion.

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Song, Wei, Jun Wang, Yumin Zhang, Tao Ma, and Kunzheng Wang. "Effect of Substance P on Differentiation of Bone Marrow Stromal Stem Cells Under Oxidative Stress." Journal of Biomaterials and Tissue Engineering 11, no. 4 (April 1, 2021): 772–77. http://dx.doi.org/10.1166/jbt.2021.2577.

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Bone marrow stromal stem cells (BMSCs) can be used to treat bone defects but BMSCs are damaged under oxidative stress. The neuropeptide substance P (SP) involves various cellular activities. However, SP’s role in BMSCs differentiation under oxidative stress is unknown. Rat BMSCs were isolated and assigned into control group; oxidative stress group treated with 200 μM H2O2; and SP group, in which 10 mM SP was added under oxidative stress followed by analysis of SP secretion by ELISA, cell proliferation by MTT method, Caspase3 activity, Bax and Bcl-2 level by Real time PCR, ALP activity ROS and SOD content as well as NF-κB level by Western blot. Under oxidative stress, SP secretion was significantly decreased, BMSCs proliferation was inhibited, Caspase3 activity and Bax expression increased, Bcl-2 and ALP activity was decreased along with increased ROS activity and NF-κB level and reduced SOD activity (P <0.05), adding SP to BMSCs under oxidative stress can significantly promote SP secretion and cell proliferation, reduce Caspase3 activity and Bax expression, increase Bcl-2 expression and ALP activity, decreased ROS activity and NF-κB level, and elevated SOD activity (P <0.05). SP secretion from BMSCs cells was reduced under oxidative stress. Up-regulation of SP in BMSCs cells under oxidative stress can inhibit BMSCs apoptosis and promote cell proliferation and osteogenesis by regulating NF-κB.

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Meyer, Bianca A., and Shirin Doroudgar. "ER Stress-Induced Secretion of Proteins and Their Extracellular Functions in the Heart." Cells 9, no. 9 (September 10, 2020): 2066. http://dx.doi.org/10.3390/cells9092066.

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Endoplasmic reticulum (ER) stress is a result of conditions that imbalance protein homeostasis or proteostasis at the ER, for example ischemia, and is a common event in various human pathologies, including the diseased heart. Cardiac integrity and function depend on the active secretion of mature proteins from a variety of cell types in the heart, a process that requires an intact ER environment for efficient protein folding and trafficking to the secretory pathway. As a consequence of ER stress, most protein secretion by the ER secretory pathway is decreased. Strikingly, there is a select group of proteins that are secreted in greater quantities during ER stress. ER stress resulting from the dysregulation of ER Ca2+ levels, for instance, stimulates the secretion of Ca2+-binding ER chaperones, especially GRP78, GRP94, calreticulin, and mesencephalic astrocyte-derived neurotrophic factor (MANF), which play a multitude of roles outside the cell, strongly depending on the cell type and tissue. Here we review current insights in ER stress-induced secretion of proteins, particularly from the heart, and highlight the extracellular functions of these proteins, ranging from the augmentation of cardiac cell viability to the modulation of pro- and anti-apoptotic, oncogenic, and immune-stimulatory cell signaling, cell invasion, extracellular proteostasis, and more. Many of the roles of ER stress-induced protein secretion remain to be explored in the heart. This article is part of a special issue entitled “The Role of Proteostasis Derailment in Cardiac Diseases.”

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Wu, Danhai, and Kan Wang. "Interleukin-15 Regulates Osteogenic/Adipogenic Differentiation of Bone Marrow Mesenchymal Stem Cells Under Oxidative Stress by Regulating PI3K/Akt/mTOR Signaling Pathway." Journal of Biomaterials and Tissue Engineering 9, no. 12 (December 1, 2019): 1770–75. http://dx.doi.org/10.1166/jbt.2019.2207.

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The oxidative stress process can affect bone marrow mesenchymal stem cells (BMSCs) differentiation. Interleukin (IL-15) regulates fat differentiation of BMSCs. However, the role of IL-15 in osteogenic/adipogenic differentiation of BMSCs under oxidative stress remains unclear. Rat BMSCs were cultured and randomly divided into control group; oxidative stress group and IL-15 treatment group followed by analysis of IL-15 secretion by ELISA, expression of osteocalcin, type I collagen, RUNX2 and OPN mRNA as well as FABP4 and PPARγ 2 by Real time PCR, ALP activity, ROS content and SOD activity, and expression of PI3K/Akt/mTOR signaling proteins by Western blot. In oxidative stress group, IL-15 secretion was significantly decreased, osteocalcin, type I collagen, RUNX2 and OPN mRNA expression was reduced, along with deceased ALP activity and SOD activity, increased ROS content and FABP4 and PPARγ 2 protein expression as well as decreased expression of p-AKT and mTOR in comparison of control (P < 0 05). IL-15 treatment on oxidative stress BMSCs significantly increased IL-15 secretion and the expression of osteocalcin, type I collagen, RUNX2 and OPN mRNA, along with increased ALP activity and SOD activity, decreased FABP4 and PPAR 2 protein expression and ROS content as well as increased expression of p-AKT and mTOR (P < 0 05). IL-15 secretion was reduced in BMSCs under oxidative stress. Promoting IL-15 secretion can improve redox balance through PI3K/Akt/mTOR signaling pathway, promote osteogenic differentiation of BMSCs.

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Osterlund, Chad D., Mariana Rodriguez-Santiago, Elizabeth R. Woodruff, Ryan J. Newsom, Anjali P. Chadayammuri, and Robert L. Spencer. "Glucocorticoid Fast Feedback Inhibition of Stress-Induced ACTH Secretion in the Male Rat: Rate Independence and Stress-State Resistance." Endocrinology 157, no. 7 (May 4, 2016): 2785–98. http://dx.doi.org/10.1210/en.2016-1123.

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Normal glucocorticoid secretion is critical for physiological and mental health. Glucocorticoid secretion is dynamically regulated by glucocorticoid-negative feedback; however, the mechanisms of that feedback process are poorly understood. We assessed the temporal characteristics of glucocorticoid-negative feedback in vivo using a procedure for drug infusions and serial blood collection in unanesthetized rats that produced a minimal disruption of basal ACTH plasma levels. We compared the negative feedback effectiveness present when stress onset coincides with corticosterone's (CORT) rapidly rising phase (30 sec pretreatment), high plateau phase (15 min pretreatment), or restored basal phase (60 min pretreatment) as well as effectiveness when CORT infusion occurs after the onset of stress (5 min poststress onset). CORT treatment prior to stress onset acted remarkably fast (within 30 sec) to suppress stress-induced ACTH secretion. Furthermore, fast feedback induction did not require rapid increases in CORT at the time of stress onset (hormone rate independent), and those feedback actions were relatively long lasting (≥15 min). In contrast, CORT elevation after stress onset produced limited and delayed ACTH suppression (stress state resistance). There was a parallel stress-state resistance for CORT inhibition of stress-induced Crh heteronuclear RNA in the paraventricular nucleus but not Pomc heteronuclear RNA in the anterior pituitary. CORT treatment did not suppress stress-induced prolactin secretion, suggesting that CORT feedback is restricted to the control of hypothalamic-pituitary-adrenal axis elements of a stress response. These temporal, stress-state, and system-level features of in vivo CORT feedback provide an important physiological context for ex vivo studies of molecular and cellular mechanisms of CORT-negative feedback.

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Lortz, S., S. Lenzen, and I. Mehmeti. "Impact of scavenging hydrogen peroxide in the endoplasmic reticulum for β cell function." Journal of Molecular Endocrinology 55, no. 1 (June 24, 2015): 21–29. http://dx.doi.org/10.1530/jme-15-0132.

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Oxidative folding of nascent proteins in the endoplasmic reticulum (ER), catalysed by one or more members of the protein disulfide isomerase family and the sulfhydryl oxidase ER oxidoreductin 1 (ERO1), is accompanied by generation of hydrogen peroxide (H2O2). Because of the high rate of insulin biosynthesis and the low expression of H2O2-inactivating enzymes in pancreatic β cells, it has been proposed that the luminal H2O2concentration might be very high. As the role of this H2O2in ER stress and proinsulin processing is still unsolved, an ER-targeted and luminal-active catalase variant, ER-Catalase N244, was expressed in insulin-secreting INS-1E cells. In these cells, the influence of ER-specific H2O2removal on cytokine-mediated cytotoxicity and ER stress, insulin gene expression, insulin content and secretion was analysed. The expression of ER-Catalase N244 reduced the toxicity of exogenously added H2O2significantly with a threefold increase of the EC50value for H2O2. However, the expression of cytokine-induced ER stress genes and viability after incubation with β cell toxic cytokines (IL1β alone or together with TNFα+IFNγ) was not affected by ER-Catalase N244. In control and ER-Catalase N244 expressing cells, insulin secretion and proinsulin content was identical, while removal of luminal H2O2reduced insulin gene expression and insulin content in ER-Catalase N244 expressing cells. These data show that ER-Catalase N244 reduced H2O2toxicity but did not provide protection against pro-inflammatory cytokine-mediated toxicity and ER stress. Insulin secretion was not affected by decreasing H2O2in the ER in spite of a reduced insulin transcription and processing.

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Domes, Gregor, Markus Heinrichs, Ulrike Rimmele, Ursula Reichwald, and Martin Hautzinger. "Acute Stress Impairs Recognition for Positive Words—Association with Stress-induced Cortisol Secretion." Stress 7, no. 3 (September 2004): 173–81. http://dx.doi.org/10.1080/10253890412331273213.

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Carta, Sonia, Federica Penco, Rosa Lavieri, Alberto Martini, Charles Anthony Dinarello, Marco Gattorno, and Anna Rubartelli. "Cell stress increases ATP release in NLRP3 inflammasome-mediated autoinflammatory diseases, resulting in cytokine imbalance." Proceedings of the National Academy of Sciences 112, no. 9 (February 17, 2015): 2835–40. http://dx.doi.org/10.1073/pnas.1424741112.

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Abstract:

Cell stress is implicated in triggering bouts of systemic inflammation in patients with autoinflammatory disorders. Blood monocytes from patients affected by NLRP3-mediated cryopyrin-associated periodic syndromes (CAPS) release greater amounts of IL-1β than monocytes from unaffected subjects. Here we show that stress lowers the threshold of activation; blood monocytes from CAPS patients maintain the high levels of secreted IL-1β (fivefold) and IL-18 (10-fold) when stimulated with 1,000-fold less LPS than that required for full IL-1β secretion in control subjects. Unexpectedly, IL-1α secretion is increased 10-fold, indicating that inflammatory episodes in CAPS may not be entirely a result of IL-1β but may also involve IL-1α. In CAPS monocytes, LPS induces the externalization of copious amounts of ATP (10-fold), which drive IL-1β, IL-18, and IL-1α release via activation of the P2X purinoceptor 7. This enhanced ATP release appears to be the link between cell stress and increased cytokine secretion in CAPS. In the later phase after LPS stimulation, CAPS monocytes undergo oxidative stress, which impairs production of the anti-inflammatory IL-1 receptor antagonist (IL-1Ra). Remarkably, IL-1Ra secretion is fully restored by treatment with antioxidants. In two patients with the same NLRP3 mutation, but different disease severity, monocytes from the mildly affected patient exhibited more efficient redox response, lower ATP secretion, and more balanced cytokine production. Thus, the robustness of the individual antioxidant response increases the tolerance to stress and reduces the negative effect of the disease. Pharmacologic block of P2X purinoceptor 7 and improved stress tolerance may represent novel treatment strategies in stress-associated inflammatory diseases.

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Marra, D., D. Warot, I. Berlin, E. Hispard, and S. Dally. "Psychological stress and cortisol secretion in anhedonic alcoholic men." European Psychiatry 18, no. 8 (December 2003): 415–17. http://dx.doi.org/10.1016/j.eurpsy.2003.06.007.

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AbstractWe investigated plasma cortisol in a psychological stress paradigm in seven weaned anhedonic alcoholics in comparison with seven age-matched healthy controls. Alcoholics had significantly higher mean plasma cortisol at baseline and no increase following a psychological stress paradigm. Anhedonic alcoholics judged the experimental situation less agreeable than controls. Anhedonic alcoholics may have blunted cortisol response to psychological stress.

Journal articles on the topic 'Secretion stress'

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