Supplemental Material for Hippocampal Injection of the Exercise-Induced Myokine Irisin Suppresses Acute Stress-Induced Neurobehavioral Impairment in a Sex-Dependent Manner

2020 ◽  
Keyword(s):  
Acute Stress ◽  
Dependent Manner ◽  
Exercise Induced

Hippocampal injection of the exercise-induced myokine irisin suppresses acute stress-induced neurobehavioral impairment in a sex-dependent manner.

2020 ◽  
Vol 134 (3) ◽  
pp. 233-247
Author(s):  
Mohammad Jodeiri Farshbaf ◽  
Sagufta Garasia ◽  
Dominica P. K. Moussoki ◽  
Amit K. Mondal ◽  
Daniel Cherkowsky ◽  
...  
Keyword(s):  
Acute Stress ◽  
Dependent Manner ◽  
Exercise Induced

Physical exercise increases autophagic signaling through ULK1 in human skeletal muscle

2015 ◽  
Vol 118 (8) ◽  
pp. 971-979 ◽  
Author(s):  
Andreas Buch Møller ◽  
Mikkel Holm Vendelbo ◽  
Britt Christensen ◽  
Berthil Forrest Clasen ◽  
Ann Mosegaard Bak ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Physical Exercise ◽  
Light Chain ◽  
Human Skeletal Muscle ◽  
Transgenic Animal ◽  
Dependent Manner ◽  
Healthy Humans ◽  
Transgenic Animal Models ◽  
Exercise Induced

Data from transgenic animal models suggest that exercise-induced autophagy is critical for adaptation to physical training, and that Unc-51 like kinase-1 (ULK1) serves as an important regulator of autophagy. Phosphorylation of ULK1 at Ser555 stimulates autophagy, whereas phosphorylation at Ser757 is inhibitory. To determine whether exercise regulates ULK1 phosphorylation in humans in vivo in a nutrient-dependent manner, we examined skeletal muscle biopsies from healthy humans after 1-h cycling exercise at 50% maximal O2 uptake on two occasions: 1) during a 36-h fast, and 2) during continuous glucose infusion at 0.2 kg/h. Physical exercise increased ULK1 phosphorylation at Ser555 and decreased lipidation of light chain 3B. ULK1 phosphorylation at Ser555 correlated positively with AMP-activated protein kinase-α Thr172 phosphorylation and negatively with light chain 3B lipidation. ULK1 phosphorylation at Ser757 was not affected by exercise. Fasting increased ULK1 and p62 protein expression, but did not affect exercise-induced ULK1 phosphorylation. These data demonstrate that autophagy signaling is activated in human skeletal muscle after 60 min of exercise, independently of nutritional status, and suggest that initiation of autophagy constitutes an important physiological response to exercise in humans.

scholarly journals Acute Exercise Induced Mitochondrial H2O2Production in Mouse Skeletal Muscle: Association with p66Shcand FOXO3a Signaling and Antioxidant Enzymes

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Ping Wang ◽  
Chun Guang Li ◽  
Zhengtang Qi ◽  
Di Cui ◽  
Shuzhe Ding
Keyword(s):  
Skeletal Muscle ◽  
Antioxidant Enzymes ◽  
Acute Exercise ◽  
Exercise Group ◽  
Time Dependent ◽  
Dependent Manner ◽  
Complex Interplay ◽  
Muscle Tissues ◽  
Exercise Muscle ◽  
Exercise Induced

Exercise induced skeletal muscle phenotype change involves a complex interplay between signaling pathways and downstream regulators. This study aims to investigate the effect of acute exercise on mitochondrial H2O2production and its association withp66Shc, FOXO3a, and antioxidant enzymes. Male ICR/CD-1 mice were subjected to an acute exercise. Muscle tissues (gastrocnemius and quadriceps femoris) were taken after exercise to measure mitochondrial H2O2content, expression ofp66Shcand FOXO3a, and the activity of antioxidant enzymes. The results showed that acute exercise significantly increased mitochondrial H2O2content and expressions ofp66Shcand FOXO3a in a time-dependent manner, with a linear correlation between the increase in H2O2content andp66Shcor FOXO3a expression. The activity of mitochondrial catalase was slightly reduced in the 90 min exercise group, but it was significantly higher in groups with 120 and 150 min exercise compared to that of 90 min exercise group. The activity of SOD was not significantly affected. The results indicate that acute exercise increases mitochondrial H2O2production in the skeletal muscle, which is associated with the upregulation ofp66Shcand FOXO3a. The association ofp66Shcand FOXO3a signaling with exercise induced H2O2generation may play a role in regulating cellular oxidative stress during acute exercise.

scholarly journals Acute Stress Affects the Expression of Hippocampal Mu Oscillations in an Age-Dependent Manner

2017 ◽  
Vol 9 ◽  
Author(s):  
Samir Takillah ◽  
Jérémie Naudé ◽  
Steve Didienne ◽  
Claude Sebban ◽  
Brigitte Decros ◽  
...  
Keyword(s):  
Acute Stress ◽  
Dependent Manner ◽  
Age Dependent

scholarly journals Chronic Stress During Adolescence Blunts the Exercise-Induced Expression of Thyroid Hormone-Target Genes in Metabolically Active Tissues of Male and Female Rats

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A974-A974
Author(s):  
Marco Antonio Parra-Montes de Oca ◽  
Karen Lissette Garduño-Morales ◽  
Patricia Joseph-Bravo
Keyword(s):  
Skeletal Muscle ◽  
Thyroid Hormone ◽  
Chronic Stress ◽  
Voluntary Exercise ◽  
Female Rats ◽  
Dependent Manner ◽  
Male And Female ◽  
Male And Female Rats ◽  
Exercise Induced ◽  
Hpt Axis

Abstract Voluntary exercise activates HPT axis1, that contributes to energy mobilization and energy expenditure. Chronic stress in adulthood inhibits HPT response to voluntary wheel running in a sex dependent manner, inhibiting lipolysis of WAT2. We evaluated the effect of chronic stress during adolescence on HPT axis response to voluntary exercise in adulthood3, with emphasis on metabolic response in skeletal muscle and WAT. Wistar male and female rats (N=36 per sex) were divided in an undisturbed group (Control, C; n=18) and one chronic variable stress during adolescence group (CVS; n=18) (males: PND 30-70; females: PND 30-60). As adults (males: PND 84; females: PND: 74) rats were divided in: 1) exercise group: rats placed individually in a cage with a running wheel per 14 nights, 2) sedentary group with ad libitum feeding, 3) sedentary pair-fed group offered the same amount of food consumed by the exercised group, and kept in individual cages during 14 nights (6 rats/group). WAT weight was determined at sacrifice, hormones quantified by RIA and ELISA, gene expression by RT-PCR. Exercise-induced loss of fat mass was not detected in CVS rats. Exercise decreased corticosterone levels in C males and females of both treatments, supporting sex difference on HPA axis reprogramming by CVS. HPT axis response to voluntary exercise is attenuated by CVS also in a sex dimorphic manner: CVS decreased Trh expression in hypothalamic paraventricular nucleus and no changes in thyroid hormones concentration in males, whereas in females, slightly increased TSH, T4 and T3 levels. Sex also influenced the response of skeletal muscle and WAT to CVS. Dio2 and Pgc1a slightly increased expression in skeletal muscle of males, not of females. Adrb3 expression in WAT increased in females, but not in males; exercise-induced stimulation of Hsl expression was not observed in either sex after CVS. These results suggest that CVS imposed during rat adolescence inhibits the responses to voluntary exercise of HPT axis activity of thyroid hormone-targets in WAT and skeletal muscle in sex dependent manner. These changes could lead to reduced mobilization and the utilization of energy fuels coincident with the fatigue observed after exercise in patients with subclinical or clinical hypothyroidism. (Funded: CONACYT 284883, DGAPA IN213419)1Uribe, Endocrinology 155:2020-2030, 2014.2Parra, Front Endocrinol 10(418):1-13, 2019.3Parra, J Endocr Soc 4(Abstract Supp) Abstract SAT-451, 2020.

Metallothionein gene regulation in the preimplantation rabbit blastocyst

Development ◽  
1987 ◽  
Vol 100 (3) ◽  
pp. 463-469
Author(s):  
G.K. Andrews ◽  
Y.M. Huet ◽  
L.D. Lehman ◽  
S.K. Dey
Keyword(s):  
Gene Expression ◽  
Acute Stress ◽  
Relative Rate ◽  
Exchange Chromatography ◽  
Dependent Manner ◽  
Fold Induction ◽  
Acute Stress Response ◽  
Rabbit Blastocyst

Expression of metallothionein (MT) genes in the preimplantation rabbit blastocyst was analysed by determination of the levels of MT mRNA and relative rates of MT synthesis. MT was found to be constitutively expressed at low levels in the blastocyst. Exposure of the day-6 blastocyst to zinc ions in vitro rapidly increased the level of MT gene expression in a dose-dependent manner, with a ten-fold induction in the relative rate of synthesis at 400 microM-Zn2+. Ion-exchange chromatography of pulse-labelled blastocyst protein showed that the relative rates of synthesis of both MT-I and MT-II were markedly increased following zinc treatment, with MT-I being the predominant isometallothionein. Zinc induction of MT synthesis in the blastocyst was also detected on day 4 of gestation just after the morula-to-blastocyst transition. In contrast to the zinc effects on MT, in vitro exposure to 10 microM-Cd2+ resulted in a large induction of MT mRNA but only a modest increase in the relative rate of MT synthesis. Cadmium was found to be toxic to the day-6 blastocyst, and 10 microM-Cd2+ induced an acute stress response as indicated by a dramatic induction of heat-shock protein (HSP-70) gene expression.

scholarly journals Differential Adaptive Responses to Chronic Stress of Maternally Stressed Male Mice Offspring

Endocrinology ◽  
2005 ◽  
Vol 146 (7) ◽  
pp. 3202-3210 ◽  
Author(s):  
Sooyoung Chung ◽  
Gi Hoon Son ◽  
Sung Ho Park ◽  
Eonyoung Park ◽  
Kun Ho Lee ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Hpa Axis ◽  
Acute Stress ◽  
Feedback Inhibition ◽  
Corticosterone Level ◽  
Dependent Manner ◽  
Male Mice ◽  
Adaptive Responses ◽  
Repeated Restraint Stress ◽  
Postnatal Stress

Abstract It is well established that stress in early life can alter the activity of the hypothalamus-pituitary-adrenal (HPA) axis, but most studies to date have focused on HPA reactivity in response to a single acute stress. The present study addressed whether stress in pregnant mice could influence the adaptive responses of their offspring to chronic stress. Male offspring were exclusively used in this study. Elevated plus maze tests revealed that 14 d of repeated restraint stress (6 h per day; from postnatal d 50–63) significantly increased anxiety-like behavior in maternally stressed mice. NBI 27914, a CRH receptor antagonist, completely eliminated anxiety-related behaviors in a dose-dependent manner, indicating an involvement of a hyperactive CRH system. In accordance with increased anxiety, CRH contents in the hypothalamus and amygdala were significantly higher in these mice. Despite an increased basal activity of the CRH-ACTH system, the combination of chronic prenatal and postnatal stress resulted in a significant reduction of basal plasma corticosterone level, presumably because of a defect in adrenal function. Along with alterations in hypothalamic and hippocampal corticosteroid receptors, it was also demonstrated that a dysfunction in negative feedback inhibition of the HPA axis could be deteriorated by chronic stress in maternally stressed male mice. Taken together, these results indicate that exposure to maternal stress in the womb can affect an animal’s coping capacity to chronic postnatal stress.

scholarly journals Acute stress enhances heterodimerization and binding of corticosteroid receptors at glucocorticoid target genes in the hippocampus

2016 ◽  
Vol 113 (40) ◽  
pp. 11336-11341 ◽  
Author(s):  
Karen R. Mifsud ◽  
Johannes M. H. M. Reul
Keyword(s):  
Glucocorticoid Receptors ◽  
Target Genes ◽  
Acute Stress ◽  
Stressful Event ◽  
Dependent Manner ◽  
Fk506 Binding Protein ◽  
Receptor Interactions ◽  
Additional Level ◽  
Chip Analysis

A stressful event results in secretion of glucocorticoid hormones, which bind to mineralocorticoid receptors (MRs) and glucocorticoid receptors (GRs) in the hippocampus to regulate cognitive and affective responses to the challenge. MRs are already highly occupied by low glucocorticoid levels under baseline conditions, whereas GRs only become substantially occupied by stress- or circadian-driven glucocorticoid levels. Currently, however, the binding of MRs and GRs to glucocorticoid-responsive elements (GREs) within hippocampal glucocorticoid target genes under such physiological conditions in vivo is unknown. We found that forced swim (FS) stress evoked increased hippocampal RNA expression levels of the glucocorticoid-responsive genes FK506-binding protein 5 (Fkbp5), Period 1 (Per1), and serum- and glucocorticoid-inducible kinase 1 (Sgk1). Chromatin immunoprecipitation (ChIP) analysis showed that this stressor caused substantial gene-dependent increases in GR binding and surprisingly, also MR binding to GREs within these genes. Different acute challenges, including novelty, restraint, and FS stress, produced distinct glucocorticoid responses but resulted in largely similar MR and GR binding to GREs. Sequential and tandem ChIP analyses showed that, after FS stress, MRs and GRs bind concomitantly to the same GRE sites within Fkbp5 and Per1 but not Sgk1. Thus, after stress, MRs and GRs seem to bind to GREs as homo- and/or heterodimers in a gene-dependent manner. MR binding to GREs at baseline seems to be restricted, whereas after stress, GR binding may facilitate cobinding of MR. This study reveals that the interaction of MRs and GRs with GREs within the genome constitutes an additional level of complexity in hippocampal glucocorticoid action beyond expectancies based on ligand–receptor interactions.

scholarly journals Acute stress alters individual risk taking in a time-dependent manner and leads to anti-social risk

2016 ◽  
Vol 45 (7) ◽  
pp. 877-885 ◽  
Author(s):  
S. Bendahan ◽  
L. Goette ◽  
J. Thoresen ◽  
L. Loued-Khenissi ◽  
F. Hollis ◽  
...  
Keyword(s):  
Risk Taking ◽  
Acute Stress ◽  
Time Dependent ◽  
Individual Risk ◽  
Social Risk ◽  
Dependent Manner

scholarly journals Estrogens Mediate Cardiac Hypertrophy in a Stimulus-Dependent Manner

Endocrinology ◽  
2012 ◽  
Vol 153 (9) ◽  
pp. 4480-4490 ◽  
Author(s):  
Christopher D. Haines ◽  
Pamela A. Harvey ◽  
Leslie A. Leinwand
Keyword(s):  
Cardiac Hypertrophy ◽  
Cardiac Function ◽  
Estrogen Signaling ◽  
Dependent Manner ◽  
Cardiac Events ◽  
Established Risk Factor ◽  
Apparent Loss ◽  
Exercise Induced ◽  
Insight Into

The incidence of cardiac hypertrophy, an established risk factor for heart failure, is generally lower in women compared with men, but this advantage is lost after menopause. Although it is widely believed that estrogens are cardioprotective, there are contradictory reports, including increased cardiac events in postmenopausal women receiving estrogens and enhanced cardiac protection from ischemic injury in female mice without estrogens. We exposed aromatase knockout (ArKO) mice, which produce no estrogens, to both pathologic and physiologic stimuli. This model allows an investigation into the effects of a complete, chronic lack of estrogens in male and female hearts. At baseline, female ArKO mice had normal-sized hearts but decreased cardiac function and paradoxically increased phosphorylation of many progrowth kinases. When challenged with the pathological stimulus, isoproterenol, ArKO females developed 2-fold more hypertrophy than wild-type females. In contrast, exercise-induced physiological hypertrophy was unaffected by the absence of estrogens in either sex, although running performance was blunted in ArKO females. Thus, loss of estrogen signaling in females, but not males, impairs cardiac function and sensitizes the heart to pathological insults through up-regulation of multiple hypertrophic pathways. These findings provide insight into the apparent loss of cardioprotection after menopause and suggest that caution is warranted in the long-term use of aromatase inhibitors in the setting of breast cancer prevention.

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