Base de dados : MEDLINE
Pesquisa : D06.472.699 [Categoria DeCS]
Referências encontradas : 3363 [refinar]
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[PMID]:27776915
[Au] Autor:Mendler M; Riedinger C; Schlotterer A; Volk N; Fleming T; Herzig S; Nawroth PP; Morcos M
[Ad] Endereço:Department of Medicine 1 and Clinical Chemistry, University of Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany. Electronic address: michael.mendler@med.uni-heidelberg.de.
[Ti] Título:Reduction in ins-7 gene expression in non-neuronal cells of high glucose exposed Caenorhabditis elegans protects from reactive metabolites, preserves neuronal structure and head motility, and prolongs lifespan.
[So] Source:J Diabetes Complications;31(2):304-310, 2017 Feb.
[Is] ISSN:1873-460X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Glucose derived metabolism generates reactive metabolites affecting the neuronal system and lifespan in C. elegans. Here, the role of the insulin homologue ins-7 and its downstream effectors in the generation of high glucose induced neuronal damage and shortening of lifespan was studied. RESULTS: In C. elegans high glucose conditions induced the expression of the insulin homologue ins-7. Abrogating ins-7 under high glucose conditions in non-neuronal cells decreased reactive oxygen species (ROS)-formation and accumulation of methylglyoxal derived advanced glycation endproducts (AGEs), prevented structural neuronal damage and normalised head motility and lifespan. The restoration of lifespan by decreased ins-7 expression was dependent on the concerted action of sod-3 and glod-4 coding for the homologues of iron-manganese superoxide dismutase and glyoxalase 1, respectively. CONCLUSIONS: Under high glucose conditions mitochondria-mediated oxidative stress and glycation are downstream targets of ins-7. This impairs the neuronal system and longevity via a non-neuronal/neuronal crosstalk by affecting sod-3 and glod-4, thus giving further insight into the pathophysiology of diabetic complications.
[Mh] Termos MeSH primário: Proteínas de Caenorhabditis elegans/antagonistas & inibidores
Proteínas de Caenorhabditis elegans/metabolismo
Caenorhabditis elegans/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Glucose/envenenamento
Lactoilglutationa Liase/metabolismo
Estresse Oxidativo
Hormônios Peptídicos/antagonistas & inibidores
Superóxido Dismutase/metabolismo
[Mh] Termos MeSH secundário: Animais
Comportamento Animal
Caenorhabditis elegans/enzimologia
Caenorhabditis elegans/crescimento & desenvolvimento
Proteínas de Caenorhabditis elegans/agonistas
Proteínas de Caenorhabditis elegans/genética
Retroalimentação Fisiológica
Técnicas de Silenciamento de Genes
Técnicas de Inativação de Genes
Produtos Finais de Glicação Avançada/metabolismo
Lactoilglutationa Liase/antagonistas & inibidores
Lactoilglutationa Liase/genética
Longevidade
Mutação
Neuroproteção
Concentração Osmolar
Hormônios Peptídicos/agonistas
Hormônios Peptídicos/genética
Hormônios Peptídicos/metabolismo
Interferência de RNA
Espécies Reativas de Oxigênio/metabolismo
Superóxido Dismutase/antagonistas & inibidores
Superóxido Dismutase/genética
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Caenorhabditis elegans Proteins); 0 (Glycation End Products, Advanced); 0 (Ins-7 protein, C elegans); 0 (Peptide Hormones); 0 (Reactive Oxygen Species); EC 1.15.1.1 (Sod-3 protein, C elegans); EC 1.15.1.1 (Superoxide Dismutase); EC 4.4.1.5 (Lactoylglutathione Lyase); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


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[PMID]:28456825
[Au] Autor:Lu Q; Lu L; Chen W; Lu P
[Ad] Endereço:Department of Ophthalmology, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
[Ti] Título:Expression of angiopoietin-like protein 8 correlates with VEGF in patients with proliferative diabetic retinopathy.
[So] Source:Graefes Arch Clin Exp Ophthalmol;255(8):1515-1523, 2017 Aug.
[Is] ISSN:1435-702X
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To investigate the vitreous and serum levels of angiopoietin-like protein 8 (ANGPTL-8) and vascular endothelial growth factor (VEGF) in patients with proliferative diabetic retinopathy (PDR). The serum levels of these factors were also analyzed in patients with diabetes and no diabetic retinopathy (NDR) and with non-proliferative diabetic retinopathy (NPDR), to detect the possible correlation between the ANGPTL-8 levels and hyperlipidemia. METHODS: Vitreous samples were obtained from 28 patients with PDR and from 12 patients without diabetes and with idiopathic macular hole (IMH). Serum samples were also obtained from 26 patients with NDR and 22 patients with NPDR. ANGPTL-8 levels and other factors were determined using an enzyme-linked immunosorbent assay. RESULTS: The ANGPTL-8 and VEGF levels in the vitreous and serum of the patients with PDR were higher than those in the patients with IMH, and were significantly correlated. The vitreous and serum ANGPTL-8 levels were more correlated with the triglyceride and low-density lipoprotein cholesterol levels than with the high-density lipoprotein cholesterol or total cholesterol levels in the patients with PDR. CONCLUSIONS: The vitreous and serum ANGPTL-8 levels were both upregulated in patients with PDR. There was an association between the elevation in the ANGPTL-8 levels and angiogenic and hyperlipidemic factors in the patients with PDR. These results suggest that ANGPTL-8 is a potential new diagnostic marker and therapeutic target for PDR treatment.
[Mh] Termos MeSH primário: Proteínas Semelhantes a Angiopoietina/biossíntese
Retinopatia Diabética/metabolismo
Hormônios Peptídicos/biossíntese
Neovascularização Retiniana/metabolismo
Fator A de Crescimento do Endotélio Vascular/metabolismo
Corpo Vítreo/metabolismo
[Mh] Termos MeSH secundário: Biomarcadores/metabolismo
Retinopatia Diabética/complicações
Retinopatia Diabética/diagnóstico
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Masculino
Meia-Idade
Neovascularização Retiniana/complicações
Neovascularização Retiniana/diagnóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ANGPTL8 protein, human); 0 (Angiopoietin-like Proteins); 0 (Biomarkers); 0 (Peptide Hormones); 0 (Vascular Endothelial Growth Factor A)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE
[do] DOI:10.1007/s00417-017-3676-z


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[PMID]:29028796
[Au] Autor:Dressano K; Ceciliato PHO; Silva AL; Guerrero-Abad JC; Bergonci T; Ortiz-Morea FA; Bürger M; Silva-Filho MC; Moura DS
[Ad] Endereço:Laboratório de Bioquímica de Proteínas, Departamento de Ciências Biológicas, Escola Superior de Agricultura Luiz de Queiroz, Universidade de São Paulo (ESALQ/USP), Piracicaba, SP, Brazil.
[Ti] Título:BAK1 is involved in AtRALF1-induced inhibition of root cell expansion.
[So] Source:PLoS Genet;13(10):e1007053, 2017 Oct.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The rapid alkalinization factor (RALF) peptide negatively regulates cell expansion, and an antagonistic relationship has been demonstrated between AtRALF1, a root-specific RALF isoform in Arabidopsis, and brassinosteroids (BRs). An evaluation of the response of BR signaling mutants to AtRALF1 revealed that BRI1-associated receptor kinase1 (bak1) mutants are insensitive to AtRALF1 root growth inhibition activity. BAK1 was essential for the induction of AtRALF1-responsive genes but showed no effect on the mobilization of Ca2+ and alkalinization responses. Homozygous plants accumulating AtRALF1 and lacking the BAK1 gene did not exhibit the characteristic semi-dwarf phenotype of AtRALF1-overexpressors. Biochemical evidence indicates that AtRALF1 and BAK1 physically interact with a Kd of 4.6 µM and acridinium-labeled AtRALF1 was used to demonstrate that part of the specific binding of AtRALF1 to intact seedlings and to a microsomal fraction derived from the roots of Arabidopsis plants is BAK1-dependent. Moreover, AtRALF1 induces an increase in BAK1 phosphorylation, suggesting that the binding of AtRALF1 to BAK1 is functional. These findings show that BAK1 contains an additional AtRALF1 binding site, indicating that this protein may be part of a AtRALF1-containing complex as a co-receptor, and it is required for the negative regulation of cell expansion.
[Mh] Termos MeSH primário: Proteínas de Arabidopsis/genética
Arabidopsis/genética
Hormônios Peptídicos/genética
Raízes de Plantas/genética
Proteínas Serina-Treonina Quinases/genética
[Mh] Termos MeSH secundário: Arabidopsis/crescimento & desenvolvimento
Proteínas de Transporte/genética
Ciclo Celular/genética
Proliferação Celular/genética
Regulação da Expressão Gênica de Plantas/genética
Fenótipo
Fosforilação
Reguladores de Crescimento de Planta/metabolismo
Raízes de Plantas/crescimento & desenvolvimento
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arabidopsis Proteins); 0 (Carrier Proteins); 0 (Peptide Hormones); 0 (Plant Growth Regulators); 0 (RALF1 protein, Arabidopsis); EC 2.7.1.- (BAK1 protein, Arabidopsis); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171014
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007053


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[PMID]:28911868
[Au] Autor:Prinz P; Scharner S; Friedrich T; Schalla M; Goebel-Stengel M; Rose M; Stengel A
[Ad] Endereço:Department for Psychosomatic Medicine, Charité-Universitätsmedizin Berlin, Germany.
[Ti] Título:Central and peripheral expression sites of phoenixin-14 immunoreactivity in rats.
[So] Source:Biochem Biophys Res Commun;493(1):195-201, 2017 Nov 04.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Phoenixin is a pleiotropic peptide involved in reproduction, anxiety and recently also implicated in the control of food intake. Besides the 20-amino acid phoenixin, the 14-amino acid phoenixin-14 also shows bioactive properties. However, the expression sites of phoenixin-14 in the brain and peripheral tissues are not yet described in detail. Therefore, a mapping of the brain and peripheral tissues from male and female Sprague-Dawley rats with a specific phoenixin-14 antibody was performed using western blot and immunohistochemistry. High density of phoenixin-14 immunoreactivity was detected in the medial division of the brain central amygdaloid nucleus, in the spinal trigeminal tract and in the spinocerebellar tract as well as in cells between the crypts of duodenum, jejunum and ileum. Medium density immunoreactivity was observed in the bed nucleus of the stria terminalis, in the area postrema, the nucleus of the solitary tract and the dorsal motor nucleus of the vagus nerve as well as in the peripheral parts of the islets of Langerhans in the pancreas. A low density of phoenixin-14 immunoreactivity was detected in the arcuate nucleus, the supraoptic nucleus and the raphe pallidus. After pre-absorption of the antibody with phoenixin-14 peptide, no immunosignals were observed indicating specificity of the antibody. Taken together, the widespread distribution of phoenixin-14 immunoreactivity gives additional rise to the pleiotropic functions of the peptide such as possible effects in gastrointestinal motility, immune functions and glucose homeostasis.
[Mh] Termos MeSH primário: Encéfalo/imunologia
Hormônios Hipotalâmicos/imunologia
Intestinos/imunologia
Hormônios Peptídicos/imunologia
Medula Espinal/imunologia
[Mh] Termos MeSH secundário: Animais
Feminino
Masculino
Especificidade de Órgãos/imunologia
Ratos
Ratos Sprague-Dawley
Caracteres Sexuais
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hypothalamic Hormones); 0 (Peptide Hormones); 0 (phoenixin-14, rat)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE


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[PMID]:28784291
[Au] Autor:Billard E; Létourneau M; Hébert TE; Chatenet D
[Ad] Endereço:INRS - Institut Armand-Frappier, Groupe de Recherche en Ingénierie des Peptides et en Pharmacothérapie (GRIPP), Université du Québec, Ville de Laval, Québec, Canada.
[Ti] Título:Insight into the role of urotensin II-related peptide tyrosine residue in UT activation.
[So] Source:Biochem Pharmacol;144:100-107, 2017 Nov 15.
[Is] ISSN:1873-2968
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:While sharing common biological activity, the two endogenous ligands of the G protein-coupled receptor UT, e.g. urotensin II (UII) and urotensin II-related peptide (URP), also exhibit distinct effects that could be explained by distinct interactions with their cognate receptor (UT). Accordingly, introduction of a similar substitution at the intracyclic Tyr residue in UII and URP led to compounds with divergent pharmacologic profiles. Hypothesizing that the Tyr residue of URP is a key-element to understand the specific activation of UT by URP, we undertook a study of the structure-activity relationship in which this particular residue was replaced by non-natural and constrained amino acids. Each compound was evaluated for its ability to bind UT, to induce rat aortic ring contraction and to activate Gq and G signaling pathways. We identified [Pep ]URP, that binds UT with an affinity similar to that of URP, but behaves as a biased ligand. Used as an antagonist, this peptide is also able to selectively reduce the maximal aortic contraction of URP but not UII. Our results suggest that the orientation of the Tyr residue can stabilize at least two different conformations of UT, leading to biased signaling and a probe-dependent allosteric effect.
[Mh] Termos MeSH primário: Aorta Torácica/metabolismo
Hormônios Peptídicos/metabolismo
Tirosina/metabolismo
Urotensinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Aorta Torácica/efeitos dos fármacos
Sítios de Ligação/fisiologia
Relação Dose-Resposta a Droga
Células HEK293
Seres Humanos
Masculino
Hormônios Peptídicos/farmacologia
Ratos
Ratos Sprague-Dawley
Relação Estrutura-Atividade
Vasoconstrição/efeitos dos fármacos
Vasoconstrição/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Peptide Hormones); 0 (Urotensins); 0 (urotensin II-related peptide, rat); 42HK56048U (Tyrosine); 9047-55-6 (urotensin II)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170809
[St] Status:MEDLINE


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[PMID]:28777197
[Au] Autor:Coquerel D; Chagnon F; Sainsily X; Dumont L; Murza A; Côté J; Dumaine R; Sarret P; Marsault É; Salvail D; Auger-Messier M; Lesur O
[Ad] Endereço:1Centre de Recherche du CHUS (CRCHUS) et Unité des Soins Intensifs Médicaux, Département de Médecine, Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, Sherbrooke, QC, Canada. 2Institut de Pharmacologie de Sherbrooke (IPS) and Département de Pharmacologie-Physiologie, Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, Sherbrooke, QC, Canada. 3IPS Thérapeutique, Sherbrooke, QC, Canada.
[Ti] Título:ELABELA Improves Cardio-Renal Outcome in Fatal Experimental Septic Shock.
[So] Source:Crit Care Med;45(11):e1139-e1148, 2017 Nov.
[Is] ISSN:1530-0293
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Apelin-13 was recently proposed as an alternative to the recommended ß-adrenergic drugs for supporting endotoxin-induced myocardial dysfunction. Since Apelin-13 signals through its receptor (Apelin peptide jejunum) to exert singular inotropic/vasotropic actions and to optimize body fluid balance, this candidate pathway might benefit septic shock management. Whether the newly discovered ELABELA (ELA), a second endogenous ligand of the Apelin peptide jejunum receptor highly expressed in the kidney, further improves cardio-renal impairment remains unknown. DESIGN, SETTING, AND SUBJECTS: Interventional study in a rat model of septic shock (128 adult males) to assess the effects of ELA and Apelin-13 on vascular and cardio-renal function. Experiments were performed in a tertiary care University-based research institute. INTERVENTIONS: Polymicrobial sepsis-induced cardiac dysfunction was produced by cecal ligation puncture to assess hemodynamic efficacy, cardioprotection, and biomechanics under acute or continuous infusions of the apelinergic agonists ELA or Apelin-13 (39 and 15 µg/kg/hr, respectively) versus normal saline. MEASUREMENTS AND MAIN RESULTS: Apelinergic agonists improved 72-hour survival after sepsis induction, with ELA providing the best clinical outcome after 24 hours. Apelinergic agonist infusion counteracted cecal ligation puncture-induced myocardial dysfunction by improving left ventricular pressure-volume relationship. ELA-treated cecal ligation puncture rats were the only group to 1) display a significant improvement in left ventricular filling as shown by increased E-wave velocity and left ventricular end-diastolic volume, 2) exhibit a higher plasma volume, and 3) limit kidney injury and free-water clearance. These beneficial renal effects were superior to Apelin-13, likely because full-length ELA enabled a distinctive regulation of pituitary vasopressin release. CONCLUSIONS: Activation of the apelinergic system by exogenous ELA or Apelin-13 infusion improves cardiovascular function and survival after cecal ligation puncture-induced sepsis. However, ELA proved better than Apelin-13 by improving fluid homeostasis, cardiovascular hemodynamics recovery, and limiting kidney dysfunction in a vasopressinergic-dependent manner.
[Mh] Termos MeSH primário: Peptídeos e Proteínas de Sinalização Intercelular/farmacologia
Hormônios Peptídicos/farmacologia
Choque Séptico/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Biomarcadores
Citocinas/imunologia
Modelos Animais de Doenças
Ecocardiografia
Hemodinâmica/efeitos dos fármacos
Masculino
Ratos
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cytokines); 0 (ELA peptide, human); 0 (Intercellular Signaling Peptides and Proteins); 0 (Peptide Hormones); 0 (apelin-13 peptide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171025
[Lr] Data última revisão:
171025
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170805
[St] Status:MEDLINE
[do] DOI:10.1097/CCM.0000000000002639


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[PMID]:28739636
[Au] Autor:Ganz T; Jung G; Naeim A; Ginzburg Y; Pakbaz Z; Walter PB; Kautz L; Nemeth E
[Ad] Endereço:Department of Medicine and.
[Ti] Título:Immunoassay for human serum erythroferrone.
[So] Source:Blood;130(10):1243-1246, 2017 Sep 07.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Erythroferrone (ERFE) is a glycoprotein hormone secreted by erythroblasts in response to stimulation by erythropoietin (EPO). We previously demonstrated that ERFE messenger RNA expression and serum protein concentration increase in mice subjected to hemorrhage or EPO therapy, that ERFE acts on hepatocytes to suppress hepcidin, and that the resulting decrease in hepcidin augments iron delivery for intensified erythropoiesis. We also showed that ERFE contributes to pathological hepcidin suppression and iron overload in mice with nontransfused ß-thalassemia. We now report the development and technical validation of a rabbit monoclonal antibody-based sandwich immunoassay for human ERFE. We use this assay to show that blood loss or EPO administration increases serum ERFE concentrations in humans, and that patients with both nontransfused and transfused ß-thalassemia have very high serum ERFE levels, which decrease after blood transfusion. The assay should be useful for human studies of normal and disordered erythropoiesis and its effect on iron homeostasis.
[Mh] Termos MeSH primário: Imunoensaio/métodos
Hormônios Peptídicos/sangue
[Mh] Termos MeSH secundário: Adulto
Idoso
Doadores de Sangue
Eritropoese
Hepcidinas/sangue
Seres Humanos
Masculino
Meia-Idade
Adulto Jovem
Talassemia beta/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fam132b protein, human); 0 (Hepcidins); 0 (Peptide Hormones)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171008
[Lr] Data última revisão:
171008
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2017-04-777987


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[PMID]:28583915
[Au] Autor:Chen H; Wang L; Wang W; Cheng C; Zhang Y; Zhou Y; Wang C; Miao X; Wang J; Wang C; Li J; Zheng L; Huang K
[Ad] Endereço:Tongji School of Pharmacy.
[Ti] Título:ELABELA and an ELABELA Fragment Protect against AKI.
[So] Source:J Am Soc Nephrol;28(9):2694-2707, 2017 Sep.
[Is] ISSN:1533-3450
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Renal ischemia-reperfusion (I/R) injury is the most common cause of AKI, which associates with high mortality and has no effective therapy. ELABELA (ELA) is a newly identified 32-residue hormone peptide highly expressed in adult kidney. To investigate whether ELA has protective effects on renal I/R injury, we administered the mature peptide (ELA32) or the 11-residue furin-cleaved fragment (ELA11) to hypoxia-reperfusion (H/R)-injured or adriamycin-treated renal tubular cells ELA32 and ELA11 significantly inhibited the elevation of the DNA damage response, apoptosis, and inflammation in H/R-injured renal tubular cells and suppressed adriamycin-induced DNA damage response. Similarly, overexpression of ELA32 or ELA11 significantly inhibited H/R-induced cell death, DNA damage response, and inflammation. Notably, treatment of mice with ELA32 or ELA11 but not an ELA11 mutant with a cysteine to alanine substitution at the N terminus (AE11C) inhibited I/R injury-induced renal fibrosis, inflammation, apoptosis, and the DNA damage response and markedly reduced the renal tubular lesions and renal dysfunction. Together, our results suggest that ELA32 and ELA11 may be therapeutic candidates for treating AKI.
[Mh] Termos MeSH primário: Lesão Renal Aguda/metabolismo
Lesão Renal Aguda/prevenção & controle
Proteínas de Transporte/farmacologia
Fragmentos de Peptídeos/farmacologia
Hormônios Peptídicos/farmacologia
RNA Mensageiro/metabolismo
Traumatismo por Reperfusão/metabolismo
Traumatismo por Reperfusão/prevenção & controle
[Mh] Termos MeSH secundário: Lesão Renal Aguda/genética
Lesão Renal Aguda/fisiopatologia
Animais
Apoptose/efeitos dos fármacos
Proteínas Mutadas de Ataxia Telangiectasia/metabolismo
Autofagia/efeitos dos fármacos
Proteínas de Transporte/genética
Proteínas de Transporte/uso terapêutico
Moléculas de Adesão Celular/genética
Hipóxia Celular
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Quinase do Ponto de Checagem 1/metabolismo
Reparo do DNA/efeitos dos fármacos
Expressão Gênica/efeitos dos fármacos
Receptor Celular 1 do Vírus da Hepatite A/genética
Histonas/metabolismo
Seres Humanos
Inflamação/genética
Inflamação/prevenção & controle
Molécula 1 de Adesão Intercelular/genética
Interleucina-6/genética
Túbulos Renais/citologia
Camundongos
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/uso terapêutico
Hormônios Peptídicos/uso terapêutico
Fosfoproteínas/metabolismo
Fosforilação
Ratos
Traumatismo por Reperfusão/genética
Traumatismo por Reperfusão/fisiopatologia
Fator de Crescimento Transformador beta1/genética
Fator de Necrose Tumoral alfa/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apela protein (22-32), human); 0 (Apela protein, mouse); 0 (Carrier Proteins); 0 (Cell Adhesion Molecules); 0 (ELA peptide, human); 0 (Havcr1 protein, mouse); 0 (Havcr1protein, rat); 0 (Hepatitis A Virus Cellular Receptor 1); 0 (Histones); 0 (ICAM1 protein, rat); 0 (Interleukin-6); 0 (Peptide Fragments); 0 (Peptide Hormones); 0 (Phosphoproteins); 0 (RNA, Messenger); 0 (Transforming Growth Factor beta1); 0 (Tumor Necrosis Factor-alpha); 0 (gamma-H2AX protein, rat); 126547-89-5 (Intercellular Adhesion Molecule-1); EC 2.7.- (ataxia telangiectasia and Rad3-related kinase, rat); EC 2.7.11.1 (Ataxia Telangiectasia Mutated Proteins); EC 2.7.11.1 (Checkpoint Kinase 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170607
[St] Status:MEDLINE
[do] DOI:10.1681/ASN.2016111210


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[PMID]:28494926
[Au] Autor:Sharman MJ; Bacci B; Santos L; Mansfield CS
[Ad] Endereço:Faculty of Veterinary and Agricultural Science, The University of Melbourne, Parkville, Victoria, Australia. Electronic address: melloras@alumni.unimelb.edu.au.
[Ti] Título:Gastrokine mRNA expression in gastric tissue from dogs with helicobacter colonisation but without inflammatory change during treatment.
[So] Source:Vet Immunol Immunopathol;187:28-34, 2017 May.
[Is] ISSN:1873-2534
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Gastrokines (GKNs) are bioactive substances secreted by gastric cells. Evidence supports functional roles for GKNs in gastric homeostasis, immune responses and tumour suppression. Down-regulation has been reported in Helicobacter pylori associated gastritis and other inflammatory gastrointestinal conditions in mice and people. The aim of this study was to evaluate GKN gene expression in dogs positive for other Helicobacter spp. both before and after treatment. Expression of Gkn-1 and Gkn-2 mRNA was studied in endoscopic biopsy samples collected from seven healthy dogs over three time-points pre- (T0) and at 1 and 18 weeks post-treatment for Helicobacter spp. colonisation (T1 & T2). The relative expression software tool (REST) was used to provide efficiency corrected expression ratios for comparisons between groups and these results were compared to a standard 2ΔΔCT methodology. Compared with T1 Gkn1 and Gkn2 mRNA expression was greater at T0 by a mean factor of 2.53 (SE=1.83-3.54) for Gkn1 (P=0.000) and 2.85 (SE=2.23-3.75) for Gkn2 (P=0.000). This difference was attenuated when comparisons were made between T0 and T2. Histopathological evidence of gastritis was not present in any Helicobacter spp. positive sample. When compared to post-eradication samples Gkn gene expression is increased in the presence of Helicobacter spp. in dogs without evidence for concurrent inflammation. Further evaluation is required to determine the relevance of this finding, however given a suspected role in gastric homeostasis, up-regulation of GKN1 and GKN2 could limit development of gastritis in Helicobacter spp. positive dogs.
[Mh] Termos MeSH primário: Doenças do Cão/microbiologia
Hormônios Gastrointestinais/metabolismo
Infecções por Helicobacter/veterinária
Hormônios Peptídicos/metabolismo
Estômago/metabolismo
[Mh] Termos MeSH secundário: Amoxicilina/uso terapêutico
Animais
Antibacterianos/uso terapêutico
Claritromicina/uso terapêutico
Doenças do Cão/tratamento farmacológico
Doenças do Cão/imunologia
Cães
Gastrite/imunologia
Gastrite/metabolismo
Gastrite/microbiologia
Gastrite/veterinária
Expressão Gênica
Infecções por Helicobacter/tratamento farmacológico
Infecções por Helicobacter/imunologia
Infecções por Helicobacter/microbiologia
Reação em Cadeia da Polimerase em Tempo Real/veterinária
Estômago/microbiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Gastrointestinal Hormones); 0 (Peptide Hormones); 804826J2HU (Amoxicillin); H1250JIK0A (Clarithromycin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170513
[St] Status:MEDLINE


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[PMID]:28490095
[Au] Autor:Song H; Wang X; Hu W; Yang X; Diao E; Shen T; Qiang Q
[Ad] Endereço:Jiangsu Collaborative Innovation Center of Regional Modern Agriculture & Environmental Protection, Jiangsu Key Laboratory for Eco-Agricultural Biotechnology around Hongze Lake, Huaiyin Normal University, Huai'an 223300, Jiangsu, China; Huaian Key Laboratory of Food Components and Functional Food
[Ti] Título:A cold-induced phytosulfokine peptide is related to the improvement of loquat fruit chilling tolerance.
[So] Source:Food Chem;232:434-442, 2017 Oct 01.
[Is] ISSN:0308-8146
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A novel peptidomics approach was used to discover cold-induced peptides in loquat fruit. Twenty unique peptides derived from 18 proproteins were identified, and they were involved in sugar signalling, protein metabolism and stress response. The quantitative analysis revealed 7 peptides with more than 2-fold upregulation, especially a 4.96-fold increase detected in the phytosulfokine (PSK) peptide. To further evaluate effects of PSK1 on fruit chilling tolerance, weight loss, firmness and internal browning were investigated in PSK1-treated loquat fruit at 0°C. By contrast, these chilling injury symptoms were effectively reduced by PSK1. PSK1 markedly delayed decreases of ATP content and energy charge. The PSK1-treated fruit exhibited significantly lower activities of cell-wall degrading enzymes and transcripts of genes related to lignin synthesis. Our results demonstrated that PSK1 improves chilling tolerance of loquat fruit by maintaining high energy status and cell integrity. Peptidomics analysis provides a promising tool to discover some key peptides.
[Mh] Termos MeSH primário: Eriobotrya
Frutas
Hormônios Peptídicos
Proteínas de Plantas
[Mh] Termos MeSH secundário: Carboidratos
Parede Celular
Temperatura Baixa
Peptídeos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carbohydrates); 0 (PSK-alpha protein, plant); 0 (Peptide Hormones); 0 (Peptides); 0 (Plant Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170512
[St] Status:MEDLINE



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