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[PMID]:28449913
[Au] Autor:Hux VJ; Roberts JM; Okun ML
[Ad] Endereço:Magee-Womens Research Institute, USA; Department of Obstetrics and Gynecology, The Ohio State University, USA.
[Ti] Título:Allostatic load in early pregnancy is associated with poor sleep quality.
[So] Source:Sleep Med;33:85-90, 2017 May.
[Is] ISSN:1878-5506
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Allostatic load (AL) measures the cumulative impact of chronic stress and is associated with adverse health outcomes. A novel scoring system has previously been developed for AL in early pregnancy that is associated with pre-eclampsia. It was hypothesized that AL, as identified by the present model, is associated with psychosocial stressors and, specifically, poor sleep quality. METHODS: Women were selected from a low-risk, community-dwelling study population who enrolled at <15 weeks gestation. Nine physiologic components were divided among the domains of cardiovascular, metabolic, and inflammatory function. Spearman's rank correlations were used to examine the association of AL with age, income, the Revised Prenatal Distress Questionnaire (NuPDQ), Inventory of Depressive Symptoms (IDS), and Pittsburgh Sleep Quality Index (PSQI). The Wilcoxon rank-sum test was used to compare AL by race and educational attainment. RESULTS: A total of 103 women were identified, with: a mean age of 29.8 ± 5.0 years, 17.5% black, and mean gestational age 12.2 ± 1.1 weeks. Allostatic load was positively correlated with the PSQI (ρ = 0.23, p = 0.018). There were no associations with age, income, prenatal distress, race, or depression scores. College-educated women had lower AL compared with those with less education (0.57 ± 0.43 vs 0.81 ± 0.55, p = 0.045). CONCLUSION: Higher AL, measured by the pregnancy-specific model, was associated with poorer sleep quality and lower educational attainment, both of which were considered to be chronic stressors. These relationships were consistent with previous findings in non-pregnant populations, and suggest that AL may be useful for capturing the physiologic impact of chronic stress in early pregnancy.
[Mh] Termos MeSH primário: Alostase/fisiologia
Complicações na Gravidez/epidemiologia
Distúrbios do Início e da Manutenção do Sono/psicologia
Transtornos do Sono-Vigília/psicologia
Estresse Psicológico/complicações
[Mh] Termos MeSH secundário: Adulto
Afroamericanos
Feminino
Idade Gestacional
Seres Humanos
Renda
Gravidez
Distúrbios do Início e da Manutenção do Sono/complicações
Distúrbios do Início e da Manutenção do Sono/epidemiologia
Transtornos do Sono-Vigília/complicações
Transtornos do Sono-Vigília/epidemiologia
Fatores Socioeconômicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


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[PMID]:27770781
[Au] Autor:Beydoun MA; Beydoun HA; Mode N; Dore GA; Canas JA; Eid SM; Zonderman AB
[Ad] Endereço:NIH Biomedical Research Center, National Institute on Aging, IRP, 251 Bayview Blvd. Suite 100 Room #:04B118, Baltimore, MD, 21224, USA. baydounm@mail.nih.gov.
[Ti] Título:Racial disparities in adult all-cause and cause-specific mortality among us adults: mediating and moderating factors.
[So] Source:BMC Public Health;16(1):1113, 2016 10 22.
[Is] ISSN:1471-2458
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Studies uncovering factors beyond socio-economic status (SES) that would explain racial and ethnic disparities in mortality are scarce. METHODS: Using prospective cohort data from the Third National Health and Nutrition Examination Survey (NHANES III), we examined all-cause and cause-specific mortality disparities by race, mediation through key factors and moderation by age (20-49 vs. 50+), sex and poverty status. Cox proportional hazards, discrete-time hazards and competing risk regression models were conducted (N = 16,573 participants, n = 4207 deaths, Median time = 170 months (1-217 months)). RESULTS: Age, sex and poverty income ratio-adjusted hazard rates were higher among Non-Hispanic Blacks (NHBs) vs. Non-Hispanic Whites (NHW). Within the above-poverty young men stratum where this association was the strongest, the socio-demographic-adjusted HR = 2.59, p < 0.001 was only partially attenuated by SES and other factors (full model HR = 2.08, p = 0.003). Income, education, diet quality, allostatic load and self-rated health, were among key mediators explaining NHB vs. NHW disparity in mortality. The Hispanic paradox was observed consistently among women above poverty (young and old). NHBs had higher CVD-related mortality risk compared to NHW which was explained by factors beyond SES. Those factors did not explain excess risk among NHB for neoplasm-related death (fully adjusted HR = 1.41, 95 % CI: 1.02-2.75, p = 0.044). Moreover, those factors explained the lower risk of neoplasm-related death among MA compared to NHW, while CVD-related mortality risk became lower among MA compared to NHW upon multivariate adjustment. CONCLUSIONS: In sum, racial/ethnic disparities in all-cause and cause-specific mortality (particularly cardiovascular and neoplasms) were partly explained by socio-demographic, SES, health-related and dietary factors, and differentially by age, sex and poverty strata.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/mortalidade
Grupos de Populações Continentais
Grupos Étnicos
Disparidades nos Níveis de Saúde
Neoplasias/mortalidade
Pobreza
Classe Social
[Mh] Termos MeSH secundário: Adulto
Idoso
Alostase
Causas de Morte
Dieta
Escolaridade
Feminino
Seres Humanos
Renda
Masculino
Meia-Idade
Inquéritos Nutricionais
Modelos de Riscos Proporcionais
Estudos Prospectivos
Risco
Estados Unidos/epidemiologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., INTRAMURAL
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171227
[Lr] Data última revisão:
171227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:28880949
[Au] Autor:Coplan JD; Gupta NK; Karim A; Rozenboym A; Smith ELP; Kral JG; Rosenblum LA
[Ad] Endereço:Department of Psychiatry and Behavioral Sciences, Biological Science Unit, State University of New York (SUNY) Downstate Medical Center, Brooklyn, New York, United States of America.
[Ti] Título:Maternal hypothalamic-pituitary-adrenal axis response to foraging uncertainty: A model of individual vs. social allostasis and the "Superorganism Hypothesis".
[So] Source:PLoS One;12(9):e0184340, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Food insecurity is a major global contributor to developmental origins of adult disease. The allostatic load of maternal food uncertainty from variable foraging demand (VFD) activates corticotropin-releasing factor (CRF) without eliciting hypothalamic-pituitary-adrenal (HPA) activation measured on a group level. Individual homeostatic adaptations of the HPA axis may subserve second-order homeostasis, a process we provisionally term "social allostasis." We postulate that maternal food insecurity induces a "superorganism" state through coordination of individual HPA axis response. METHODS: Twenty-four socially-housed bonnet macaque maternal-infant dyads were exposed to 16 weeks of alternating two-week epochs of low or high foraging demand shown to compromise normative maternal-infant rearing. Cerebrospinal fluid (CSF) CRF concentrations and plasma cortisol were measured pre- and post-VFD. Dyadic distance was measured, and blinded observers performed pre-VFD social ranking assessments. RESULTS: Despite marked individual cortisol responses (mean change = 20%) there was an absence of maternal HPA axis group mean response to VFD (0%). Whereas individual CSF CRF concentrations change = 56%, group mean did increase 25% (p = 0.002). Our "dyadic vulnerability" index (low infant weight, low maternal weight, subordinate maternal social status and reduced dyadic distance) predicted maternal cortisol decreases (p < 0.0001) whereas relatively "advantaged" dyads exhibited maternal cortisol increases in response to VFD exposure. COMMENT: In response to a chronic stressor, relative dyadic vulnerability plays a significant role in determining the directionality and magnitude of individual maternal HPA axis responses in the service of maintaining a "superorganism" version of HPA axis homeostasis, provisionally termed "social allostasis."
[Mh] Termos MeSH primário: Comportamento Alimentar/fisiologia
Macaca radiata/fisiologia
Comportamento Materno/fisiologia
[Mh] Termos MeSH secundário: Alostase
Animais
Hormônio Liberador da Corticotropina/sangue
Hormônio Liberador da Corticotropina/líquido cefalorraquidiano
Feminino
Hidrocortisona/sangue
Hidrocortisona/líquido cefalorraquidiano
Sistema Hipotálamo-Hipofisário/metabolismo
Sistema Hipotálamo-Hipofisário/fisiologia
Sistema Hipófise-Suprarrenal/metabolismo
Sistema Hipófise-Suprarrenal/fisiologia
Incerteza
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
9015-71-8 (Corticotropin-Releasing Hormone); WI4X0X7BPJ (Hydrocortisone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170908
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184340


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[PMID]:28870356
[Au] Autor:Barr DA
[Ad] Endereço:Department of Pediatrics, Stanford University School of Medicine, Stanford, CA. Electronic address: barr@stanford.edu.
[Ti] Título:The Childhood Roots of Cardiovascular Disease Disparities.
[So] Source:Mayo Clin Proc;92(9):1415-1421, 2017 Sep.
[Is] ISSN:1942-5546
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A recent national review of the social determinants of cardiovascular disease (CVD) underscored the growing recognition that poor socioeconomic conditions early in life place children at higher risk for CVD as adults. There is growing evidence that chronic elevation of allostatic load as a consequence of high levels of early childhood stress can trigger early atherosclerotic changes in children independently of behaviors. Elevated levels of circulating cortisol have been documented in children as young as 4 years who were raised in highly stressful circumstances. Chronic elevation of cortisol is associated with increased release of inflammatory proteins such as interleukin 6, which can lead to fibrosis and scarring in the vessel walls of the arterial circulation, resulting in increased intima-media thickness. Increased intima-media thickness of the carotid artery has been found in individuals with low socioeconomic status as early as age 18 years and has been associated with increased CVD risk throughout the adult years. The American Academy of Pediatrics has recommended that it is the task of pediatricians and other health care professionals to screen for toxic stress among children during their early years and to take steps known to reduce stress reactivity, thereby helping these children to reduce their risk of early atherosclerotic changes and increased CVD throughout the life course.
[Mh] Termos MeSH primário: Alostase/fisiologia
Doenças Cardiovasculares/etiologia
Espessura Intima-Media Carotídea/efeitos adversos
Disparidades nos Níveis de Saúde
Classe Social
Determinantes Sociais da Saúde
Estresse Psicológico/fisiopatologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Aterosclerose/diagnóstico por imagem
Aterosclerose/etiologia
Doenças Cardiovasculares/diagnóstico por imagem
Criança
Seres Humanos
Hidrocortisona/análise
Tempo
Ultrassonografia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
WI4X0X7BPJ (Hydrocortisone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170913
[Lr] Data última revisão:
170913
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170906
[St] Status:MEDLINE


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[PMID]:28862266
[Au] Autor:Gray JD; Kogan JF; Marrocco J; McEwen BS
[Ad] Endereço:Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, The Rockefeller University, 1230 York Avenue, New York, NY 10065. USA.
[Ti] Título:Genomic and epigenomic mechanisms of glucocorticoids in the brain.
[So] Source:Nat Rev Endocrinol;13(11):661-673, 2017 Nov.
[Is] ISSN:1759-5037
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Following the discovery of glucocorticoid receptors in the hippocampus and other brain regions, research has focused on understanding the effects of glucocorticoids in the brain and their role in regulating emotion and cognition. Glucocorticoids are essential for adaptation to stressors (allostasis) and in maladaptation resulting from allostatic load and overload. Allostatic overload, which can occur during chronic stress, can reshape the hypothalamic-pituitary-adrenal axis through epigenetic modification of genes in the hippocampus, hypothalamus and other stress-responsive brain regions. Glucocorticoids exert their effects on the brain through genomic mechanisms that involve both glucocorticoid receptors and mineralocorticoid receptors directly binding to DNA, as well as by non-genomic mechanisms. Furthermore, glucocorticoids synergize both genomically and non-genomically with neurotransmitters, neurotrophic factors, sex hormones and other stress mediators to shape an organism's present and future responses to a stressful environment. Here, we discuss the mechanisms of glucocorticoid action in the brain and review how glucocorticoids interact with stress mediators in the context of allostasis, allostatic load and stress-induced neuroplasticity.
[Mh] Termos MeSH primário: Encéfalo/metabolismo
Glucocorticoides/metabolismo
Transtornos Mentais/genética
Plasticidade Neuronal/genética
Receptores de Glucocorticoides/genética
Estresse Fisiológico/genética
Estresse Psicológico/genética
[Mh] Termos MeSH secundário: Adaptação Fisiológica
Alostase
Animais
Epigenômica
Regulação da Expressão Gênica
Genômica
Seres Humanos
Sistema Hipotálamo-Hipofisário/metabolismo
Transtornos Mentais/metabolismo
Sistema Hipófise-Suprarrenal/metabolismo
Receptores de Glucocorticoides/metabolismo
Receptores de Mineralocorticoides/genética
Receptores de Mineralocorticoides/metabolismo
Fatores Sexuais
Estresse Psicológico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Glucocorticoids); 0 (Receptors, Glucocorticoid); 0 (Receptors, Mineralocorticoid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170902
[St] Status:MEDLINE
[do] DOI:10.1038/nrendo.2017.97


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[PMID]:28813505
[Au] Autor:Robertson T; Beveridge G; Bromley C
[Ad] Endereço:Centre for Public Health and Population Health Research, Faculty of Health Sciences & Sport, University of Stirling, Stirling, Scotland.
[Ti] Título:Allostatic load as a predictor of all-cause and cause-specific mortality in the general population: Evidence from the Scottish Health Survey.
[So] Source:PLoS One;12(8):e0183297, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Allostatic load is a multiple biomarker measure of physiological 'wear and tear' that has shown some promise as marker of overall physiological health, but its power as a risk predictor for mortality and morbidity is less well known. This study has used data from the 2003 Scottish Health Survey (SHeS) (nationally representative sample of Scottish population) linked to mortality records to assess how well allostatic load predicts all-cause and cause-specific mortality. From the sample, data from 4,488 men and women were available with mortality status at 5 and 9.5 (rounded to 10) years after sampling in 2003. Cox proportional hazard models estimated the risk of death (all-cause and the five major causes of death in the population) according to allostatic load score. Multiple imputation was used to address missing values in the dataset. Analyses were also adjusted for potential confounders (sex, age and deprivation). There were 258 and 618 deaths over the 5-year and 10-year follow-up period, respectively. In the fully-adjusted model, higher allostatic load (poorer physiological 'health') was not associated with an increased risk of all-cause mortality after 5 years (HR = 1.07, 95% CI 0.94 to 1.22; p = 0.269), but it was after 10 years (HR = 1.08, 95% CI 1.01 to 1.16; p = 0.026). Allostatic load was not associated with specific causes of death over the same follow-up period. In conclusions, greater physiological wear and tear across multiple physiological systems, as measured by allostatic load, is associated with an increased risk of death, but may not be as useful as a predictor for specific causes of death.
[Mh] Termos MeSH primário: Alostase
Causas de Morte
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Feminino
Inquéritos Epidemiológicos
Seres Humanos
Masculino
Meia-Idade
Modelos de Riscos Proporcionais
Escócia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170817
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183297


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[PMID]:28709033
[Au] Autor:Egorov AI; Griffin SM; Converse RR; Styles JN; Sams EA; Wilson A; Jackson LE; Wade TJ
[Ad] Endereço:National Health and Environmental Effects Research Laboratory, United States Environmental Protection Agency, Research Triangle Park, NC, USA. Electronic address: egorov.andrey@epa.gov.
[Ti] Título:Vegetated land cover near residence is associated with reduced allostatic load and improved biomarkers of neuroendocrine, metabolic and immune functions.
[So] Source:Environ Res;158:508-521, 2017 10.
[Is] ISSN:1096-0953
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Greater exposure to urban green spaces has been linked to reduced risks of depression, cardiovascular disease, diabetes and premature death. Alleviation of chronic stress is a hypothesized pathway to improved health. Previous studies linked chronic stress with a biomarker-based composite measure of physiological dysregulation known as allostatic load. OBJECTIVE: This study's objective was to assess the relationship between vegetated land cover near residences and allostatic load. METHODS: This cross-sectional population-based study involved 206 adult residents of the Durham-Chapel Hill, North Carolina metropolitan area. Exposure was quantified using high-resolution metrics of trees and herbaceous vegetation within 500m of each residence derived from the U.S. Environmental Protection Agency's EnviroAtlas land cover dataset. Eighteen biomarkers of immune, neuroendocrine, and metabolic functions were measured in serum or saliva samples. Allostatic load was defined as a sum of potentially unhealthy biomarker values dichotomized at 10th or 90th percentile of sample distribution. Regression analysis was conducted using generalized additive models with two-dimensional spline smoothing function of geographic coordinates, weighted measures of vegetated land cover allowing decay of effects with distance, and geographic and demographic covariates. RESULTS: An inter-quartile range increase in distance-weighted vegetated land cover was associated with 37% (95% Confidence Limits 46%; 27%) reduced allostatic load; significantly reduced adjusted odds of having low level of norepinephrine, dopamine, and dehydroepiandrosterone, and high level of epinephrine, fibrinogen, vascular cell adhesion molecule-1, and interleukin-8 in serum, and α-amylase in saliva; and reduced odds of previously diagnosed depression. CONCLUSIONS: The observed effects of vegetated land cover on allostatic load and individual biomarkers are consistent with prevention of depression, cardiovascular disease and premature mortality.
[Mh] Termos MeSH primário: Alostase
Meio Ambiente
Distribuição Espacial da População
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Metabolismo Basal
Biomarcadores/sangue
Biomarcadores/metabolismo
Estudos Transversais
Feminino
Seres Humanos
Sistema Imunitário
Masculino
Meia-Idade
Sistemas Neurossecretores
North Carolina
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Biomarkers)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170715
[St] Status:MEDLINE


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[PMID]:28687630
[Au] Autor:Qureshi MA; Haynes CM; Pellegrino MW
[Ad] Endereço:From the Department of Biology, University of Texas Arlington, Arlington, Texas 76019 and.
[Ti] Título:The mitochondrial unfolded protein response: Signaling from the powerhouse.
[So] Source:J Biol Chem;292(33):13500-13506, 2017 Aug 18.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mitochondria are multifaceted and indispensable organelles required for cell performance. Accordingly, dysfunction to mitochondria can result in cellular decline and possibly the onset of disease. Cells use a variety of means to recover mitochondria and restore homeostasis, including the activation of retrograde pathways such as the mitochondrial unfolded protein response (UPR ). In this Minireview, we will discuss how cells adapt to mitochondrial stress through UPR regulation. Furthermore, we will explore the current repertoire of biological functions that are associated with this essential stress-response pathway.
[Mh] Termos MeSH primário: Alostase
Mitocôndrias/metabolismo
Modelos Biológicos
Transdução de Sinais
Estresse Fisiológico
Resposta a Proteínas não Dobradas
[Mh] Termos MeSH secundário: Animais
Retículo Endoplasmático/enzimologia
Retículo Endoplasmático/metabolismo
Estresse do Retículo Endoplasmático
Genoma Mitocondrial
Células-Tronco Hematopoéticas/citologia
Células-Tronco Hematopoéticas/enzimologia
Células-Tronco Hematopoéticas/metabolismo
Seres Humanos
Imunidade Inata
Mitocôndrias/enzimologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170709
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.R117.791061


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[PMID]:28637872
[Au] Autor:Yadav V; Gao XH; Willard B; Hatzoglou M; Banerjee R; Kabil O
[Ad] Endereço:From the Department of Biological Chemistry, University of Michigan Medical School, Ann Arbor, Michigan 48109.
[Ti] Título:Hydrogen sulfide modulates eukaryotic translation initiation factor 2α (eIF2α) phosphorylation status in the integrated stress-response pathway.
[So] Source:J Biol Chem;292(32):13143-13153, 2017 Aug 11.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hydrogen sulfide (H S) regulates various physiological processes, including neuronal activity, vascular tone, inflammation, and energy metabolism. Moreover, H S elicits cytoprotective effects against stressors in various cellular models of injury. However, the mechanism of the signaling pathways mediating the cytoprotective functions of H S is not well understood. We previously uncovered a heme-dependent metabolic switch for transient induction of H S production in the trans-sulfuration pathway. Here, we demonstrate that increased endogenous H S production or its exogenous administration modulates major components of the integrated stress response promoting a metabolic state primed for stress response. We show that H S transiently increases phosphorylation of eukaryotic translation initiation factor 2 (eIF2α) resulting in inhibition of general protein synthesis. The H S-induced increase in eIF2α phosphorylation was mediated at least in part by inhibition of protein phosphatase-1 (PP1c) via persulfidation at Cys-127. Overexpression of a PP1c cysteine mutant (C127S-PP1c) abrogated the H S effect on eIF2α phosphorylation. Our data support a model in which H S exerts its cytoprotective effect on ISR signaling by inducing a transient adaptive reprogramming of global mRNA translation. Although a transient increase in endogenous H S production provides cytoprotection, its chronic increase such as in cystathionine ß-synthase deficiency may pose a problem.
[Mh] Termos MeSH primário: Fator 4 Ativador da Transcrição/metabolismo
Estresse do Retículo Endoplasmático
Fator de Iniciação 2 em Eucariotos/metabolismo
Gasotransmissores/metabolismo
Sulfeto de Hidrogênio/metabolismo
Proteína Fosfatase 1/metabolismo
[Mh] Termos MeSH secundário: Fator 4 Ativador da Transcrição/genética
Alostase
Substituição de Aminoácidos
Animais
Linhagem Celular
Sobrevivência Celular
Células Cultivadas
Cisteína/química
Fator de Iniciação 2 em Eucariotos/genética
Regulação da Expressão Gênica
Seres Humanos
Camundongos
Camundongos Knockout
Mutação
Fosforilação/efeitos dos fármacos
Proteína Fosfatase 1/genética
Processamento de Proteína Pós-Traducional
Proteínas Recombinantes/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Atf4 protein, mouse); 0 (Eukaryotic Initiation Factor-2); 0 (Gasotransmitters); 0 (Recombinant Proteins); 145891-90-3 (Activating Transcription Factor 4); EC 3.1.3.16 (PPP1CA protein, human); EC 3.1.3.16 (Protein Phosphatase 1); K848JZ4886 (Cysteine); YY9FVM7NSN (Hydrogen Sulfide)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170825
[Lr] Data última revisão:
170825
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.778654


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[PMID]:28600454
[Au] Autor:Smith CO; Nehrke K; Brookes PS
[Ad] Endereço:Department of Biochemistry, University of Rochester Medical Center, Rochester, NY, U.S.A.
[Ti] Título:The Slo(w) path to identifying the mitochondrial channels responsible for ischemic protection.
[So] Source:Biochem J;474(12):2067-2094, 2017 Jun 09.
[Is] ISSN:1470-8728
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mitochondria play an important role in tissue ischemia and reperfusion (IR) injury, with energetic failure and the opening of the mitochondrial permeability transition pore being the major causes of IR-induced cell death. Thus, mitochondria are an appropriate focus for strategies to protect against IR injury. Two widely studied paradigms of IR protection, particularly in the field of cardiac IR, are ischemic preconditioning (IPC) and volatile anesthetic preconditioning (APC). While the molecular mechanisms recruited by these protective paradigms are not fully elucidated, a commonality is the involvement of mitochondrial K channel opening. In the case of IPC, research has focused on a mitochondrial ATP-sensitive K channel (mitoK ), but, despite recent progress, the molecular identity of this channel remains a subject of contention. In the case of APC, early research suggested the existence of a mitochondrial large-conductance K (BK, big conductance of potassium) channel encoded by the gene, although more recent work has shown that the channel that underlies APC is in fact encoded by In this review, we discuss both the pharmacologic and genetic evidence for the existence and identity of mitochondrial K channels, and the role of these channels both in IR protection and in regulating normal mitochondrial function.
[Mh] Termos MeSH primário: Alostase
Mitocôndrias Cardíacas/metabolismo
Modelos Biológicos
Isquemia Miocárdica/metabolismo
Traumatismo por Reperfusão Miocárdica/metabolismo
Canais de Potássio/metabolismo
[Mh] Termos MeSH secundário: Animais
Cardiotônicos/farmacologia
Seres Humanos
Ativação do Canal Iônico/efeitos dos fármacos
Precondicionamento Isquêmico Miocárdico
Canais KATP/agonistas
Canais KATP/antagonistas & inibidores
Canais KATP/genética
Canais KATP/metabolismo
Subunidades alfa do Canal de Potássio Ativado por Cálcio de Condutância Alta/agonistas
Subunidades alfa do Canal de Potássio Ativado por Cálcio de Condutância Alta/antagonistas & inibidores
Subunidades alfa do Canal de Potássio Ativado por Cálcio de Condutância Alta/genética
Subunidades alfa do Canal de Potássio Ativado por Cálcio de Condutância Alta/metabolismo
Moduladores de Transporte de Membrana/farmacologia
Mitocôndrias Cardíacas/efeitos dos fármacos
Isquemia Miocárdica/terapia
Traumatismo por Reperfusão Miocárdica/prevenção & controle
Bloqueadores dos Canais de Potássio/farmacologia
Canais de Potássio/agonistas
Canais de Potássio/química
Canais de Potássio/genética
Isoformas de Proteínas/agonistas
Isoformas de Proteínas/antagonistas & inibidores
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
Terminologia como Assunto
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cardiotonic Agents); 0 (KATP Channels); 0 (KCNMA1 protein, human); 0 (KCNT2 protein, human); 0 (Large-Conductance Calcium-Activated Potassium Channel alpha Subunits); 0 (Membrane Transport Modulators); 0 (Potassium Channel Blockers); 0 (Potassium Channels); 0 (Protein Isoforms)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170825
[Lr] Data última revisão:
170825
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170611
[St] Status:MEDLINE
[do] DOI:10.1042/BCJ20160623



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