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  1 / 51849 MEDLINE  
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[PMID]:29342185
[Au] Autor:Deshpande P; Dapkekar A; Oak M; Paknikar K; Rajwade J
[Ad] Endereço:Nanobioscience group, Agharkar Research Institute, Pune, India.
[Ti] Título:Nanocarrier-mediated foliar zinc fertilization influences expression of metal homeostasis related genes in flag leaves and enhances gluten content in durum wheat.
[So] Source:PLoS One;13(1):e0191035, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Wheat is the staple food for most of the world's population; however, it is a poor source of zinc. Foliar fertilization of zinc via zinc loaded chitosan nanocarriers (Zn-CNP) post-anthesis has proved to be a promising approach for grain zinc enhancement in durum wheat as evidenced in our earlier study. However, the molecular mechanism of uptake of zinc via Zn-CNP remains unclear. METHODS/PRINCIPLE FINDINGS: Foliar application of Zn-CNP was performed at post anthesis stages in two durum wheat cultivars (MACS 3125 and UC1114, containing the Gpc-B1 gene), and expression levels of several metal-related genes were analyzed during early senescence. Zn-CNP application indeed caused changes in gene expression as revealed by qPCR data on representative genes involved in metal homeostasis, phloem transporters, and leaf senescence. Furthermore, zinc-regulated transporters and iron (Fe)-regulated transporter-like protein (ZIP) family [ZIP1, ZIP7, ZIP15], CA (carbonic anhydrase), and DMAS (2'-deoxymugineic acid synthase) in flag leaves exhibited significant correlation with zinc content in the seeds. The analysis of grain endosperm proteins showed enhancement of gamma gliadins while other gluten subunits decreased. Gene expression within ZIP family members varied with the type of cultivar mostly attributed to the Gpc-B1, concentration of external zinc ions as well as the type of tissue analyzed. Correlation analysis revealed the involvement of the selected genes in zinc enhancement. CONCLUSION: At the molecular level, uptake of zinc via Zn-CNP nanocarrier was comparable to the uptake of zinc via common zinc fertilizers i.e. ZnSO4.
[Mh] Termos MeSH primário: Genes de Plantas
Homeostase
Metais/metabolismo
Nanopartículas
Triticum/genética
Zinco/administração & dosagem
[Mh] Termos MeSH secundário: Glutens/metabolismo
Folhas de Planta/genética
Folhas de Planta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Metals); 8002-80-0 (Glutens); J41CSQ7QDS (Zinc)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191035


  2 / 51849 MEDLINE  
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[PMID]:29324800
[Au] Autor:Harrington-Kandt R; Stylianou E; Eddowes LA; Lim PJ; Stockdale L; Pinpathomrat N; Bull N; Pasricha J; Ulaszewska M; Beglov Y; Vaulont S; Drakesmith H; McShane H
[Ad] Endereço:Jenner Institute, University of Oxford, Oxford, United Kingdom.
[Ti] Título:Hepcidin deficiency and iron deficiency do not alter tuberculosis susceptibility in a murine M.tb infection model.
[So] Source:PLoS One;13(1):e0191038, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tuberculosis (TB), caused by the macrophage-tropic pathogen Mycobacterium tuberculosis (M.tb) is a highly prevalent infectious disease. Since an immune correlate of protection or effective vaccine have yet to be found, continued research into host-pathogen interactions is important. Previous literature reports links between host iron status and disease outcome for many infections, including TB. For some extracellular bacteria, the iron regulatory hormone hepcidin is essential for protection against infection. Here, we investigated hepcidin (encoded by Hamp1) in the context of murine M.tb infection. Female C57BL/6 mice were infected with M.tb Erdman via aerosol. Hepatic expression of iron-responsive genes was measured by qRT-PCR and bacterial burden determined in organ homogenates. We found that hepatic Hamp1 mRNA levels decreased post-infection, and correlated with a marker of BMP/SMAD signalling pathways. Next, we tested the effect of Hamp1 deletion, and low iron diets, on M.tb infection. Hamp1 knockout mice did not have a significantly altered M.tb mycobacterial load in either the lungs or spleen. Up to 10 weeks of dietary iron restriction did not robustly affect disease outcome despite causing iron deficiency anaemia. Taken together, our data indicate that unlike with many other infections, hepcidin is decreased following M.tb infection, and show that hepcidin ablation does not influence M.tb growth in vivo. Furthermore, because even severe iron deficiency did not affect M.tb mycobacterial load, we suggest that the mechanisms M.tb uses to scavenge iron from the host must be extremely efficient, and may therefore represent potential targets for drugs and vaccines.
[Mh] Termos MeSH primário: Anemia Ferropriva/complicações
Modelos Animais de Doenças
Suscetibilidade a Doenças
Hepcidinas/deficiência
Mycobacterium tuberculosis/patogenicidade
Tuberculose/patologia
[Mh] Termos MeSH secundário: Animais
Feminino
Hepcidinas/genética
Homeostase
Ferro/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Camundongos Knockout
Tuberculose/complicações
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hepcidins); E1UOL152H7 (Iron)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191038


  3 / 51849 MEDLINE  
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[PMID]:28463898
[Au] Autor:Gastaldelli A; Gaggini M; DeFronzo R
[Ad] Endereço:aCardiometabolic Risk Laboratory, Institute of Clinical Physiology, National Research Council, Pisa, Italy bUniversity of Texas Health Science Center at San Antonio, TX, USA.
[Ti] Título:Glucose kinetics: an update and novel insights into its regulation by glucagon and GLP-1.
[So] Source:Curr Opin Clin Nutr Metab Care;20(4):300-309, 2017 Jul.
[Is] ISSN:1473-6519
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:PURPOSE OF REVIEW: Glucagon and GLP-1 share the same origin (i.e., proglucagon); primarily GLP-1 is generated from intestinal L-cells and glucagon from pancreatic α-cell, but intestinal glucagon and pancreatic GLP-1 secretion is likely. Glucose kinetics are tightly regulated by pancreatic hormones insulin and glucagon, but other hormones, including glucagon-like peptide-1 (GLP-1), also play an important role. The purpose of this review is to describe the recent findings on the mechanisms by which these two hormones regulate glucose kinetics. RECENT FINDINGS: Recent findings showed new important mechanisms of action of glucagon and GLP-1 in the regulation of glucose metabolism. Knock out of glucagon receptors protects against hyperglycemia without causing hypoglycemia. GLP-1 not only stimulates insulin secretion, but it has also an independent effect on the liver and inhibits glucose production. Moreover, when coinfused with glucagon, GLP-1 limits the hyperglycemic effects. Both hormones have also central effects on gastric emptying (delayed), intestinal motility (reduced), and satiety (increased). SUMMARY: The implications of these findings are very important for the management of type 2 diabetes given that GLP-1 receptor agonist are currently approved for the treatment of hyperglycemia and glucagon receptor antagonists and GLP-1/glucagon dual agonists are under development.
[Mh] Termos MeSH primário: Peptídeo 1 Semelhante ao Glucagon/fisiologia
Glucagon/fisiologia
Glucose/metabolismo
[Mh] Termos MeSH secundário: Animais
Diabetes Mellitus Tipo 2/tratamento farmacológico
Jejum
Esvaziamento Gástrico/fisiologia
Motilidade Gastrointestinal/fisiologia
Glucagon/sangue
Glucagon/farmacologia
Peptídeo 1 Semelhante ao Glucagon/farmacologia
Receptor do Peptídeo Semelhante ao Glucagon 1/agonistas
Receptor do Peptídeo Semelhante ao Glucagon 1/fisiologia
Gluconeogênese/efeitos dos fármacos
Glucose/biossíntese
Homeostase
Seres Humanos
Hiperglicemia/tratamento farmacológico
Cinética
Fígado/efeitos dos fármacos
Fígado/metabolismo
Receptores de Glucagon/antagonistas & inibidores
Receptores de Glucagon/fisiologia
Saciação/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Glucagon-Like Peptide-1 Receptor); 0 (Receptors, Glucagon); 89750-14-1 (Glucagon-Like Peptide 1); 9007-92-5 (Glucagon); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1097/MCO.0000000000000384


  4 / 51849 MEDLINE  
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[PMID]:29441919
[Au] Autor:Lim HW; Kim K; Lim CJ
[Ti] Título:Contribution of ginsenoside Re to cellular redox homeostasis via upregulating glutathione and superoxide dismutase in HaCaT keratinocytes under normal conditions.
[So] Source:Pharmazie;71(7):413-419, 2016 Jul 07.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Ginsenoside Re (Re) is one of the main ginsenosides which are known to be responsible for diverse pharmacological properties of ginseng, widely used as a dietary supplement and a general tonic. The present work was undertaken to evaluate the antioxidative property of Re by analyzing reactive oxygen species (ROS), nitric oxide (NO), pro-matrix metalloproteinase-2 (proMMP-2) and -9 (proMMP-9), total glutathione (GSH) and superoxide dismutase (SOD) in normal, unstressed HaCaT keratinocytes. When HaCaT cells were subjected to Re, Re suppressed the ROS and NO levels in a concentration-dependent manner. Re at concentrations used exhibited no cytotoxicity on the cellular viabilities of HaCaT cells. It was also able to attenuate proMMP-2 and -9 at both activity and protein levels. On the contrary, Re was capable of enhancing the total GSH and SOD activity levels. The findings suggest that Re has an antioxidative property through the upregulation of some antioxidant components, including total GSH and SOD, in HaCaT keratinocytes, which then can play its underlying role in maintaining the cellular redox homeostasis.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Ginsenosídeos/farmacologia
Glutationa/biossíntese
Homeostase/efeitos dos fármacos
Queratinócitos/efeitos dos fármacos
Superóxido Dismutase/biossíntese
[Mh] Termos MeSH secundário: Sobrevivência Celular/efeitos dos fármacos
Glutationa/efeitos dos fármacos
Seres Humanos
Metaloproteinase 2 da Matriz/efeitos dos fármacos
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/efeitos dos fármacos
Metaloproteinase 9 da Matriz/metabolismo
Óxido Nítrico/antagonistas & inibidores
Oxirredução
Espécies Reativas de Oxigênio/metabolismo
Superóxido Dismutase/efeitos dos fármacos
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antioxidants); 0 (Ginsenosides); 0 (Reactive Oxygen Species); 31C4KY9ESH (Nitric Oxide); 46F3R0BL3I (ginsenoside Re); EC 1.15.1.1 (Superoxide Dismutase); EC 3.4.24.24 (MMP2 protein, human); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.35 (MMP9 protein, human); EC 3.4.24.35 (Matrix Metalloproteinase 9); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6518


  5 / 51849 MEDLINE  
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[PMID]:28968939
[Au] Autor:Gu Q; Chen Z; Cui W; Zhang Y; Hu H; Yu X; Wang Q; Shen W
[Ad] Endereço:College of Life Sciences, Laboratory Center of Life Sciences, Nanjing Agricultural University, Nanjing 210095, China.
[Ti] Título:Methane alleviates alfalfa cadmium toxicity via decreasing cadmium accumulation and reestablishing glutathione homeostasis.
[So] Source:Ecotoxicol Environ Saf;147:861-871, 2018 Jan.
[Is] ISSN:1090-2414
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Although methane (CH ) generation triggered by some environmental stimuli, displays the protective response against oxidative stress in plants, whether and how CH regulates plant tolerance against cadmium stress is largely unknown. Here, we discovered that cadmium (Cd) stimulated the production of CH in alfalfa root tissues. The pretreatment with exogenous CH could alleviate seedling growth inhibition. Less amounts of Cd accumulation was also observed. Consistently, in comparison with Cd stress alone, miR159 transcript was down-regulated by CH , and expression levels of its target gene ABC transporter was increased. By contrast, miR167 transcript was up-regulated, showing a relatively negative correlation with its target gene Nramp6. Meanwhile, Cd-triggered redox imbalance was improved by CH , evidenced by the reduced lipid peroxidation and hydrogen peroxide accumulation, as well as the induction of representative antioxidant genes. Further results showed that Cd-triggered decrease of the ratio of reduced/oxidized (homo)glutathione was rescued by CH . Additionally, CH -triggered alleviation of seedling growth was sensitive to a selective inhibitor of glutathione biosynthesis. Overall, above results revealed that CH -alleviated Cd accumulation at least partially, required the modulation of heavy metal transporters via miR159 and miR167. Finally, the role of glutathione homeostasis elicited by CH was preliminarily suggested.
[Mh] Termos MeSH primário: Cádmio/toxicidade
Glutationa/metabolismo
Homeostase/efeitos dos fármacos
Medicago sativa/efeitos dos fármacos
Metano/farmacologia
Poluentes do Solo/toxicidade
[Mh] Termos MeSH secundário: Antioxidantes/metabolismo
Cádmio/metabolismo
Peroxidação de Lipídeos/efeitos dos fármacos
Medicago sativa/crescimento & desenvolvimento
Medicago sativa/metabolismo
Metano/metabolismo
MicroRNAs/metabolismo
Oxirredução
Estresse Oxidativo/efeitos dos fármacos
Poluentes do Solo/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (MicroRNAs); 0 (Soil Pollutants); 00BH33GNGH (Cadmium); GAN16C9B8O (Glutathione); OP0UW79H66 (Methane)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE


  6 / 51849 MEDLINE  
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[PMID]:28946120
[Au] Autor:Zhao F; Jiang G; Wei P; Wang H; Ru S
[Ad] Endereço:Marine Life Science College, Ocean University of China, 5 Yushan Road, Qingdao, 266003 Shandong Province, PR China.
[Ti] Título:Bisphenol S exposure impairs glucose homeostasis in male zebrafish (Danio rerio).
[So] Source:Ecotoxicol Environ Saf;147:794-802, 2018 Jan.
[Is] ISSN:1090-2414
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Bisphenol S (BPS) is a substitute of the plastic additive bisphenol A (BPA). Its concentrations detected in surface waters and urine samples are on the same order of magnitude as BPA. Human exposure to BPA has been implicated in the development of diabetes mellitus; however, whether BPS can disrupt glucose homeostasis and increase blood glucose concentration remains unclear. We extensively investigated the effects of environmentally relevant concentrations of BPS on glucose metabolism in male zebrafish (Danio rerio) and the underlying mechanisms of these effects. Male zebrafish were exposed to 1, 10, or 100µg/L of BPS for 28 d. Fasting blood glucose (FBG) levels, glycogen levels in the liver and muscle, and mRNA levels of key glucose metabolic enzymes and the activities of the encoded proteins in tissues were evaluated to assess the effect of BPS on glucose metabolism. Plasma insulin levels and expression of preproinsulin and glucagon genes in the visceral tissue were also evaluated. Compared with the control group, exposure to 1 and 10µg/L of BPS significantly increased FBG levels but decreased insulin levels. Gluconeogenesis and glycogenolysis in the liver were promoted, and glycogen synthesis in the liver and muscle and glycolysis in the muscle were inhibited. Exposure to 100µg/L of BPS did not significantly alter plasma insulin and blood glucose levels, but nonetheless pronouncedly interfered with gluconeogenesis, glycogenolysis, glycolysis, and glycogen synthesis. Our data indicates that BPS at environmentally relevant concentrations impairs glucose homeostasis of male zebrafish possibly by hampering the physiological effect of insulin; higher BPS doses also pronouncedly interfered with glucose metabolism.
[Mh] Termos MeSH primário: Glucose/metabolismo
Homeostase/efeitos dos fármacos
Fenóis/toxicidade
Sulfonas/toxicidade
Poluentes Químicos da Água/toxicidade
Peixe-Zebra/metabolismo
[Mh] Termos MeSH secundário: Animais
Relação Dose-Resposta a Droga
Glucagon/genética
Glicogênio/biossíntese
Insulina/sangue
Insulina/genética
Fígado/efeitos dos fármacos
Fígado/metabolismo
Masculino
Músculos/efeitos dos fármacos
Músculos/metabolismo
Precursores de Proteínas/sangue
Precursores de Proteínas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insulin); 0 (Phenols); 0 (Protein Precursors); 0 (Sulfones); 0 (Water Pollutants, Chemical); 61116-24-3 (preproinsulin); 80-09-1 (bis(4-hydroxyphenyl)sulfone); 9005-79-2 (Glycogen); 9007-92-5 (Glucagon); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170926
[St] Status:MEDLINE


  7 / 51849 MEDLINE  
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[PMID]:28462525
[Au] Autor:Tummers B; Green DR
[Ad] Endereço:Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN, USA.
[Ti] Título:Caspase-8: regulating life and death.
[So] Source:Immunol Rev;277(1):76-89, 2017 05.
[Is] ISSN:1600-065X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Roles for cell death in development, homeostasis, and the control of infections and cancer have long been recognized. Although excessive cell damage results in passive necrosis, cells can be triggered to engage molecular programs that result in cell death. Such triggers include cellular stress, oncogenic signals that engage tumor suppressor mechanisms, pathogen insults, and immune mechanisms. The best-known forms of programmed cell death are apoptosis and a recently recognized regulated necrosis termed necroptosis. Of the two best understood pathways of apoptosis, the extrinsic and intrinsic (mitochondrial) pathways, the former is induced by the ligation of death receptors, a subset of the TNF receptor (TNFR) superfamily. Ligation of these death receptors can also induce necroptosis. The extrinsic apoptosis and necroptosis pathways regulate each other and their balance determines whether cells live. Integral in the regulation and initiation of death receptor-mediated activation of programmed cell death is the aspartate-specific cysteine protease (caspase)-8. This review describes the role of caspase-8 in the initiation of extrinsic apoptosis execution and the mechanism by which caspase-8 inhibits necroptosis. The importance of caspase-8 in the development and homeostasis and the way that dysfunctional caspase-8 may contribute to the development of malignancies in mice and humans are also explored.
[Mh] Termos MeSH primário: Caspase 8/imunologia
Inflamassomos/metabolismo
Mitocôndrias/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose
Homeostase
Seres Humanos
Necrose
Receptores de Morte Celular/metabolismo
Receptores do Fator de Necrose Tumoral/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Inflammasomes); 0 (Receptors, Death Domain); 0 (Receptors, Tumor Necrosis Factor); 0 (Tumor Necrosis Factor-alpha); EC 3.4.22.- (Caspase 8)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1111/imr.12541


  8 / 51849 MEDLINE  
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[PMID]:28449707
[Au] Autor:Llorens F; Thüne K; Sikorska B; Schmitz M; Tahir W; Fernández-Borges N; Cramm M; Gotzmann N; Carmona M; Streichenberger N; Michel U; Zafar S; Schuetz AL; Rajput A; Andréoletti O; Bonn S; Fischer A; Liberski PP; Torres JM; Ferrer I; Zerr I
[Ad] Endereço:Department of Neurology, University Medical Center Göttingen, and German Center for Neurodegenerative Diseases (DZNE), Robert Koch Strasse 40, 37075, Göttingen, Germany. franc.llorens@gmail.com.
[Ti] Título:Altered Ca homeostasis induces Calpain-Cathepsin axis activation in sporadic Creutzfeldt-Jakob disease.
[So] Source:Acta Neuropathol Commun;5(1):35, 2017 04 27.
[Is] ISSN:2051-5960
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Sporadic Creutzfeldt-Jakob disease (sCJD) is the most prevalent form of human prion disease and it is characterized by the presence of neuronal loss, spongiform degeneration, chronic inflammation and the accumulation of misfolded and pathogenic prion protein (PrP ). The molecular mechanisms underlying these alterations are largely unknown, but the presence of intracellular neuronal calcium (Ca ) overload, a general feature in models of prion diseases, is suggested to play a key role in prion pathogenesis.Here we describe the presence of massive regulation of Ca responsive genes in sCJD brain tissue, accompanied by two Ca -dependent processes: endoplasmic reticulum stress and the activation of the cysteine proteases Calpains 1/2. Pathogenic Calpain proteins activation in sCJD is linked to the cleavage of their cellular substrates, impaired autophagy and lysosomal damage, which is partially reversed by Calpain inhibition in a cellular prion model. Additionally, Calpain 1 treatment enhances seeding activity of PrP in a prion conversion assay. Neuronal lysosomal impairment caused by Calpain over activation leads to the release of the lysosomal protease Cathepsin S that in sCJD mainly localises in axons, although massive Cathepsin S overexpression is detected in microglial cells. Alterations in Ca homeostasis and activation of Calpain-Cathepsin axis already occur at pre-clinical stages of the disease as detected in a humanized sCJD mouse model.Altogether our work indicates that unbalanced Calpain-Cathepsin activation is a relevant contributor to the pathogenesis of sCJD at multiple molecular levels and a potential target for therapeutic intervention.
[Mh] Termos MeSH primário: Encéfalo/metabolismo
Cálcio/metabolismo
Calpaína/metabolismo
Catepsinas/metabolismo
Síndrome de Creutzfeldt-Jakob/metabolismo
Homeostase/fisiologia
[Mh] Termos MeSH secundário: Animais
Encéfalo/patologia
Cátions Bivalentes/metabolismo
Células Cultivadas
Síndrome de Creutzfeldt-Jakob/patologia
Modelos Animais de Doenças
Seres Humanos
Lisossomos/metabolismo
Lisossomos/patologia
Mesocricetus
Camundongos Transgênicos
Neurônios/metabolismo
Neurônios/patologia
Proteínas PrPSc/metabolismo
Ratos Wistar
Proteínas Recombinantes/metabolismo
Ovinos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cations, Divalent); 0 (PrPSc Proteins); 0 (Recombinant Proteins); EC 3.4.- (Cathepsins); EC 3.4.22.- (Calpain); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1186/s40478-017-0431-y


  9 / 51849 MEDLINE  
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[PMID]:27773809
[Au] Autor:Jung B; Staudacher JJ; Beauchamp D
[Ad] Endereço:University of Illinois at Chicago, Chicago, Illinois. Electronic address: bjung@uic.edu.
[Ti] Título:Transforming Growth Factor ß Superfamily Signaling in Development of Colorectal Cancer.
[So] Source:Gastroenterology;152(1):36-52, 2017 Jan.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Transforming growth factor (TGF)-ß cytokines signal via a complex network of pathways to regulate proliferation, differentiation, adhesion, migration, and other functions in many cell types. A high percentage of colorectal tumors contain mutations that disrupt TGF-ß family member signaling. We review how TGF-ß family member signaling is altered during development of colorectal cancer, models of study, interaction of pathways, and potential therapeutic strategies.
[Mh] Termos MeSH primário: Neoplasias Colorretais/genética
Neoplasias Colorretais/metabolismo
Receptores de Fatores de Crescimento Transformadores beta/genética
Transdução de Sinais
Proteínas Smad/genética
Fator de Crescimento Transformador beta/genética
Fator de Crescimento Transformador beta/metabolismo
[Mh] Termos MeSH secundário: Ativinas/metabolismo
Animais
Proteínas Morfogenéticas Ósseas/metabolismo
Neoplasias Colorretais/imunologia
Mutação em Linhagem Germinativa
Homeostase
Seres Humanos
Camundongos
Camundongos Knockout
Receptores de Fatores de Crescimento Transformadores beta/imunologia
Proteínas Smad/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Bone Morphogenetic Proteins); 0 (Receptors, Transforming Growth Factor beta); 0 (Smad Proteins); 0 (Transforming Growth Factor beta); 104625-48-1 (Activins)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:28463109
[Au] Autor:Tang X; Roessingh S; Hayley SE; Chu ML; Tanaka NK; Wolfgang W; Song S; Stanewsky R; Hamada FN
[Ad] Endereço:Visual Systems Group, Abrahamson Pediatric Eye Institute, Division of Pediatric Ophthalmology, Cincinnati Children's Hospital Medical Center, Cincinnati, United States.
[Ti] Título:The role of PDF neurons in setting the preferred temperature before dawn in .
[So] Source:Elife;6, 2017 05 02.
[Is] ISSN:2050-084X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Animals have sophisticated homeostatic controls. While mammalian body temperature fluctuates throughout the day, small ectotherms, such as achieve a body temperature rhythm (BTR) through their preference of environmental temperature. Here, we demonstrate that pigment dispersing factor (PDF) neurons play an important role in setting preferred temperature before dawn. We show that small lateral ventral neurons (sLNvs), a subset of PDF neurons, activate the dorsal neurons 2 (DN2s), the main circadian clock cells that regulate temperature preference rhythm (TPR). The number of temporal contacts between sLNvs and DN2s peak before dawn. Our data suggest that the thermosensory anterior cells (ACs) likely contact sLNvs via serotonin signaling. Together, the ACs-sLNs-DN2s neural circuit regulates the proper setting of temperature preference before dawn. Given that sLNvs are important for sleep and that BTR and sleep have a close temporal relationship, our data highlight a possible neuronal interaction between body temperature and sleep regulation.
[Mh] Termos MeSH primário: Temperatura Corporal
Drosophila/fisiologia
Rede Nervosa/fisiologia
Neurônios/fisiologia
[Mh] Termos MeSH secundário: Animais
Relógios Circadianos
Drosophila/efeitos da radiação
Proteínas de Drosophila/metabolismo
Homeostase
Neurônios/química
Neuropeptídeos/metabolismo
Serotonina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Drosophila Proteins); 0 (Neuropeptides); 0 (pdf protein, Drosophila); 333DO1RDJY (Serotonin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE



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