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Pesquisa : D12.776.157.125.050.050 [Categoria DeCS]
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[PMID]:29205962
[Au] Autor:Lin JY; Mao X; Wu HJ; Xue AM
[Ad] Endereço:Department of Forensic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
[Ti] Título:[Genes Expression in the Early Stage of Acute Renal Ischemia-reperfusion Injury in Rats].
[So] Source:Fa Yi Xue Za Zhi;32(6):401-405, 2016 Dec.
[Is] ISSN:1004-5619
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVES: To study the differential genes expression in the early stage of acute renal ischemia-reperfusion injury and explore potential molecular mechanisms. METHODS: The ischemia-reperfusion model was made via clamping renal artery of rat. The microarray detection and bioinformatics analyzing of the genes expression were performed. Differentially expressed genes were screened and related cellular activities and signaling pathways were analyzed in early stage of acute kidney injury. Meanwhile, molecules closely relative to acute kidney injury were explored by establishing a biological network of the differentially expressed genes, and the results were verified by real-time PCR. RESULTS: A total of 151 genes showed differential expression in this study, including 132 up-regulated and 19 down-regulated genes. Cell proliferation, cytokines mediated signaling transduction and immune responses were greatly enriched by GO and KEGG analysis. The results of real-time PCR showed that compared with control groups, three selected genes ( , and ) which related to the acute kidney injury had an obvious differential expression in the early stage of disease. The multiple of increase was essentially the same as the multiple detected by microarray. CONCLUSIONS: This study shows differential gene expression profile, related biological processes and signaling pathways involved in the early stage of acute kidney injury. , and may play a role in the pathogenesis of acute kidney injury.
[Mh] Termos MeSH primário: Lesão Renal Aguda/genética
Traumatismo por Reperfusão/genética
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Anexina A1/genética
Proteínas Reguladoras de Apoptose/genética
Expressão Gênica
Rim/patologia
Fator 6 Semelhante a Kruppel/genética
Ratos
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A1); 0 (Apoptosis Regulatory Proteins); 0 (Klf6 protein, rat); 0 (Kruppel-Like Factor 6); 0 (Phlda1 protein, rat)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE
[do] DOI:10.3969/j.issn.1004-5619.2016.06.001


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[PMID]:28471519
[Au] Autor:Hughes EL; Becker F; Flower RJ; Buckingham JC; Gavins FNE
[Ad] Endereço:Centre for Brain Sciences, Department of Medicine, Imperial College London, London, W12 0NN, UK.
[Ti] Título:Mast cells mediate early neutrophil recruitment and exhibit anti-inflammatory properties via the formyl peptide receptor 2/lipoxin A receptor.
[So] Source:Br J Pharmacol;174(14):2393-2408, 2017 Jul.
[Is] ISSN:1476-5381
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: In recent years, studies have focused on the resolution of inflammation, which can be achieved by endogenous anti-inflammatory agonists such as Annexin A1 (AnxA1). Here, we investigated the effects of mast cells (MCs) on early LPS-induced neutrophil recruitment and the involvement of the AnxA1-formyl peptide receptor 2/ALX (FPR2/ALX or lipoxin A receptor) pathway. EXPERIMENTAL APPROACH: Intravital microscopy (IVM) was used to visualize and quantify the effects of LPS (10 µg per mouse i.p.) on murine mesenteric cellular interactions. Furthermore, the role that MCs play in these inflammatory responses was determined in vivo and in vitro, and effects of AnxA1 mimetic peptide Ac2-26 were assessed. KEY RESULTS: LPS increased both neutrophil endothelial cell interactions within the mesenteric microcirculation and MC activation (determined by IVM and ruthenium red dye uptake), which in turn lead to the early stages of neutrophil recruitment. MC recruitment of neutrophils could be blocked by preventing the pro-inflammatory activation (using cromolyn sodium) or enhancing an anti-inflammatory phenotype (using Ac2-26) in MCs. Furthermore, MCs induced neutrophil migration in vitro, and MC stabilization enhanced the release of AnxA1 from neutrophils. Pharmacological approaches (such as the administration of FPR pan-antagonist Boc2, or the FPR2/ALX antagonist WRW4) revealed neutrophil FPR2/ALX to be important in this process. CONCLUSIONS AND IMPLICATIONS: Data presented here provide evidence for a role of MCs, which are ideally positioned in close proximity to the vasculature, to act as sentinel cells in neutrophil extravasation and resolution of inflammation via the AnxA1-FPR2/ALX pathway.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Mastócitos/efeitos dos fármacos
Mastócitos/metabolismo
Infiltração de Neutrófilos/efeitos dos fármacos
Receptores de Formil Peptídeo/metabolismo
[Mh] Termos MeSH secundário: Animais
Anexina A1/química
Anexina A1/farmacologia
Anti-Inflamatórios/química
Cromolina Sódica/química
Cromolina Sódica/farmacologia
Células Endoteliais/efeitos dos fármacos
Microscopia Intravital
Lipopolissacarídeos/química
Lipopolissacarídeos/farmacologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Neutrófilos/efeitos dos fármacos
Peptídeos/química
Peptídeos/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A1); 0 (Anti-Inflammatory Agents); 0 (Fpr1 protein, mouse); 0 (Lipopolysaccharides); 0 (Peptides); 0 (Receptors, Formyl Peptide); 0 (annexin A1 peptide (2-26)); 0 (formyl peptide receptor 2, mouse); Q2WXR1I0PK (Cromolyn Sodium)
[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:170505
[St] Status:MEDLINE
[do] DOI:10.1111/bph.13847


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[PMID]:29065150
[Au] Autor:Quattrocelli M; Capote J; Ohiri JC; Warner JL; Vo AH; Earley JU; Hadhazy M; Demonbreun AR; Spencer MJ; McNally EM
[Ad] Endereço:Center for Genetic Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States of America.
[Ti] Título:Genetic modifiers of muscular dystrophy act on sarcolemmal resealing and recovery from injury.
[So] Source:PLoS Genet;13(10):e1007070, 2017 Oct.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Genetic disruption of the dystrophin complex produces muscular dystrophy characterized by a fragile muscle plasma membrane leading to excessive muscle degeneration. Two genetic modifiers of Duchenne Muscular Dystrophy implicate the transforming growth factor ß (TGFß) pathway, osteopontin encoded by the SPP1 gene and latent TGFß binding protein 4 (LTBP4). We now evaluated the functional effect of these modifiers in the context of muscle injury and repair to elucidate their mechanisms of action. We found that excess osteopontin exacerbated sarcolemmal injury, and correspondingly, that loss of osteopontin reduced injury extent both in isolated myofibers and in muscle in vivo. We found that ablation of osteopontin was associated with reduced expression of TGFß and TGFß-associated pathways. We identified that increased TGFß resulted in reduced expression of Anxa1 and Anxa6, genes encoding key components of the muscle sarcolemma resealing process. Genetic manipulation of Ltbp4 in dystrophic muscle also directly modulated sarcolemmal resealing, and Ltbp4 alleles acted in concert with Anxa6, a distinct modifier of muscular dystrophy. These data provide a model in which a feed forward loop of TGFß and osteopontin directly impacts the capacity of muscle to recover from injury, and identifies an intersection of genetic modifiers on muscular dystrophy.
[Mh] Termos MeSH primário: Genes Modificadores
Proteínas de Ligação a TGF-beta Latente/fisiologia
Músculo Esquelético/fisiologia
Distrofia Muscular Animal/genética
Osteopontina/metabolismo
[Mh] Termos MeSH secundário: Animais
Anexina A1/genética
Anexina A1/metabolismo
Anexina A6/genética
Anexina A6/metabolismo
Feminino
Regulação da Expressão Gênica
Masculino
Camundongos
Camundongos Endogâmicos DBA
Camundongos Knockout
Músculo Esquelético/lesões
Distrofia Muscular Animal/metabolismo
Distrofia Muscular Animal/patologia
Osteopontina/genética
Receptores de Fatores de Crescimento Transformadores beta/genética
Receptores de Fatores de Crescimento Transformadores beta/metabolismo
Recuperação de Função Fisiológica
Sarcolema/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A1); 0 (Annexin A6); 0 (LTBP-4 protein, mouse); 0 (Latent TGF-beta Binding Proteins); 0 (Receptors, Transforming Growth Factor beta); 0 (Spp1 protein, mouse); 0 (annexin A1, mouse); 106441-73-0 (Osteopontin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171119
[Lr] Data última revisão:
171119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171025
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007070


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Teixeira, Mauro Martins
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[PMID]:28786708
[Au] Autor:Perucci LO; Sugimoto MA; Gomes KB; Dusse LM; Teixeira MM; Sousa LP
[Ad] Endereço:a Departamento de Análises Clínicas e Toxicológicas, Faculdade de Farmácia , Universidade Federal de Minas Gerais , Belo Horizonte , Minas Gerais , Brazil.
[Ti] Título:Annexin A1 and specialized proresolving lipid mediators: promoting resolution as a therapeutic strategy in human inflammatory diseases.
[So] Source:Expert Opin Ther Targets;21(9):879-896, 2017 Sep.
[Is] ISSN:1744-7631
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: The timely resolution of inflammation is essential to restore tissue homeostasis and to avoid chronic inflammatory diseases. Resolution of inflammation is an active process modulated by various proresolving mediators, including annexin A1 (AnxA1) and specialized proresolving lipid mediators (SPMs), which counteract excessive inflammatory responses and stimulate proresolving mechanisms. Areas covered: The protective effects of AnxA1 and SPMs have been extensively explored in pre-clinical animal models. However, studies investigating the function of these molecules in human diseases are just emerging. This review highlights recent advances on the role of proresolving mediators, and pharmacological opportunities of promoting resolution pathways in preclinical models and patients with various human diseases. Expert opinion: Dysregulation or 'failure' in proresolving mechanisms might be involved in the pathogenesis of chronic inflammatory diseases. Altered levels of proresolving mediators were found in a wide range of human diseases. In some cases, AnxA1 and SPMs are up-regulated in human blood and tissues but fail to engage in proresolving signaling and, hence, to regulate excessive inflammation. Thus, the new concept of 'resolution pharmacology' could be applied to compensate deficiency of endogenous proresolving mediators' generation and/or possible failures in the engagement of resolution pathways observed in many chronic inflammatory diseases.
[Mh] Termos MeSH primário: Anexina A1/metabolismo
Desenho de Drogas
Inflamação/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/farmacologia
Seres Humanos
Inflamação/patologia
Mediadores da Inflamação/metabolismo
Metabolismo dos Lipídeos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Annexin A1); 0 (Anti-Inflammatory Agents); 0 (Inflammation Mediators)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170904
[Lr] Data última revisão:
170904
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170809
[St] Status:MEDLINE
[do] DOI:10.1080/14728222.2017.1364363


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[PMID]:28655761
[Au] Autor:Lima KM; Vago JP; Caux TR; Negreiros-Lima GL; Sugimoto MA; Tavares LP; Arribada RG; Carmo AAF; Galvão I; Costa BRC; Soriani FM; Pinho V; Solito E; Perretti M; Teixeira MM; Sousa LP
[Ad] Endereço:From the Programa de Pós-Graduação em Biologia Celular, Departamento de Morfologia, Instituto de Ciências Biológicas.
[Ti] Título:The resolution of acute inflammation induced by cyclic AMP is dependent on annexin A1.
[So] Source:J Biol Chem;292(33):13758-13773, 2017 Aug 18.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Annexin A1 (AnxA1) is a glucocorticoid-regulated protein known for its anti-inflammatory and pro-resolving effects. We have shown previously that the cAMP-enhancing compounds rolipram (ROL; a PDE4 inhibitor) and Bt cAMP (a cAMP mimetic) drive caspase-dependent resolution of neutrophilic inflammation. In this follow-up study, we investigated whether AnxA1 could be involved in the pro-resolving properties of these compounds using a model of LPS-induced inflammation in BALB/c mice. The treatment with ROL or Bt cAMP at the peak of inflammation shortened resolution intervals, improved resolution indices, and increased AnxA1 expression. studies showed that ROL and Bt cAMP induced AnxA1 expression and phosphorylation, and this effect was prevented by PKA inhibitors, suggesting the involvement of PKA in ROL-induced AnxA1 expression. Akin to these findings, H89 prevented ROL- and Bt cAMP-induced resolution of inflammation, and it was associated with decreased levels of intact AnxA1. Moreover, two different strategies to block the AnxA1 pathway (by using -Boc-Met-Leu-Phe, a nonselective AnxA1 receptor antagonist, or by using an anti-AnxA1 neutralizing antiserum) prevented ROL- and Bt cAMP-induced resolution and neutrophil apoptosis. Likewise, the ability of ROL or Bt cAMP to induce neutrophil apoptosis was impaired in AnxA-knock-out mice. Finally, in settings, ROL and Bt cAMP overrode the survival-inducing effect of LPS in human neutrophils in an AnxA1-dependent manner. Our results show that AnxA1 is at least one of the endogenous determinants mediating the pro-resolving properties of cAMP-elevating agents and cAMP-mimetic drugs.
[Mh] Termos MeSH primário: Anexina A1/agonistas
Bucladesina/uso terapêutico
AMP Cíclico/agonistas
Infiltração de Neutrófilos/efeitos dos fármacos
Inibidores da Fosfodiesterase 4/uso terapêutico
Pleurisia/tratamento farmacológico
Rolipram/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Anexina A1/antagonistas & inibidores
Anexina A1/genética
Anexina A1/metabolismo
Apoptose/efeitos dos fármacos
Bucladesina/antagonistas & inibidores
Células Cultivadas
AMP Cíclico/análogos & derivados
AMP Cíclico/antagonistas & inibidores
AMP Cíclico/metabolismo
Proteínas Quinases Dependentes de AMP Cíclico/antagonistas & inibidores
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Seres Humanos
Lipopolissacarídeos/toxicidade
Macrófagos/efeitos dos fármacos
Macrófagos/imunologia
Macrófagos/metabolismo
Macrófagos/patologia
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Knockout
Neutrófilos/efeitos dos fármacos
Neutrófilos/imunologia
Neutrófilos/metabolismo
Neutrófilos/patologia
Inibidores da Fosfodiesterase 4/química
Fosforilação/efeitos dos fármacos
Pleurisia/imunologia
Pleurisia/metabolismo
Pleurisia/patologia
Inibidores de Proteínas Quinases/farmacologia
Processamento de Proteína Pós-Traducional/efeitos dos fármacos
Células RAW 264.7
Rolipram/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A1); 0 (Lipopolysaccharides); 0 (Phosphodiesterase 4 Inhibitors); 0 (Protein Kinase Inhibitors); 0 (annexin A1, mouse); 63X7MBT2LQ (Bucladesine); E0399OZS9N (Cyclic AMP); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); K676NL63N7 (Rolipram)
[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:170629
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.800391


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[PMID]:28551657
[Au] Autor:Wang W; Zhong W; Chen C; Meng Q; Wei J
[Ad] Endereço:Department of Radiation Oncology, Indiana University School of Medicine, Indianapolis, IN, U.S.A. ww32@iu.edu.
[Ti] Título:Circulating Antibodies to Linear Peptide Antigens Derived from ANXA1 and FOXP3 in Lung Cancer.
[So] Source:Anticancer Res;37(6):3151-3155, 2017 06.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Our previous studies revealed that concentrations of circulating antibodies to annexin A1 (ANXA1) and forkhead-box P3 (FOXP3) increased significantly in patients with non-small cell lung cancer (NSCLC). This study was thus undertaken to replicate our initial findings with different sample sets. PATIENTS AND METHODS: Antibodies were tested in 108 patients with NSCLC and 216 controls, who were divided into the discovery (49 vs. 108) and validation (60 vs. 108) group based on the time of enrolment. RESULTS: Analysis of the discovery group showed a significant increase in circulating anti-ANXA1 IgG levels in the patient group compared with the control group (p=0.005) but the validation group simply exhibited a trend toward an increase in IgG levels in NSCLC (p=0.238), generating a combined p-value of 0.009. CONCLUSION: The findings of this study support the notion that circulating IgG antibodies to ANXA1 could be used as a biomarker for early diagnosis of NSCLC but failed to replicate such findings for FOXP3.
[Mh] Termos MeSH primário: Anexina A1/imunologia
Antígenos de Neoplasias/imunologia
Autoanticorpos/sangue
Carcinoma Pulmonar de Células não Pequenas/sangue
Fatores de Transcrição Forkhead/imunologia
Imunoglobulina G/sangue
Neoplasias Pulmonares/sangue
[Mh] Termos MeSH secundário: Idoso
Carcinoma Pulmonar de Células não Pequenas/imunologia
Carcinoma Pulmonar de Células não Pequenas/patologia
Estudos de Casos e Controles
Detecção Precoce de Câncer/métodos
Feminino
Seres Humanos
Neoplasias Pulmonares/imunologia
Neoplasias Pulmonares/patologia
Masculino
Meia-Idade
Valor Preditivo dos Testes
Reprodutibilidade dos Testes
Testes Sorológicos
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Annexin A1); 0 (Antigens, Neoplasm); 0 (Autoantibodies); 0 (FOXP3 protein, human); 0 (Forkhead Transcription Factors); 0 (Immunoglobulin G)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170529
[St] Status:MEDLINE


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[PMID]:28414743
[Au] Autor:He J; Yi B; Chen Y; Huang Q; Wang H; Lu K; Fu W
[Ad] Endereço:Department of Anesthesia, Southwest Hospital, The Third Military Medical University, Chongqing, China.
[Ti] Título:The ET-1-mediated carbonylation and degradation of ANXA1 induce inflammatory phenotype and proliferation of pulmonary artery smooth muscle cells in HPS.
[So] Source:PLoS One;12(4):e0175443, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hepatopulmonary syndrome (HPS) is a serious complication of advanced liver disease, which markedly increases mortality. Pulmonary vascular remodelling (PVR) induced by circulating mediators plays an important role in the pathogenesis of HPS, while the underlying mechanism remains undefined. In the present study, we reported that endothelin-1 (ET-1) is up-regulated and annexin A1(ANXA1) is down-regulated in HPS rat, and ET-1 decreases the ANXA1 expression in a dose-dependent manner in rat pulmonary arterial smooth muscle cells (PASMCs). Then, we showed that ANXA1 can decrease nuclear p-ERK1/2 accumulation and decrease the cyclin D1 expression, thus resulting in the subsequent inhibition of PASMCs proliferation. As previously reported, we confirmed that ET-1 decreases the ANXA1 protein levels by the carbonylation and degradation of ANXA1. In conclusion, our research links the signaling cascade of ET1-ANXA1-cell proliferation to a potential therapeutic strategy for blocking IPS-associated PVR.
[Mh] Termos MeSH primário: Anexina A1/metabolismo
Proliferação Celular/fisiologia
Endotelina-1/metabolismo
Síndrome Hepatopulmonar/metabolismo
Inflamação/metabolismo
Miócitos de Músculo Liso/metabolismo
Artéria Pulmonar/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Ciclina D1/metabolismo
Regulação para Baixo/fisiologia
Síndrome Hepatopulmonar/patologia
Inflamação/patologia
Sistema de Sinalização das MAP Quinases/fisiologia
Músculo Liso Vascular/metabolismo
Músculo Liso Vascular/patologia
Miócitos de Músculo Liso/patologia
Fenótipo
Carbonilação Proteica/fisiologia
Artéria Pulmonar/patologia
Ratos
Ratos Sprague-Dawley
Transdução de Sinais/fisiologia
Regulação para Cima/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A1); 0 (Endothelin-1); 136601-57-5 (Cyclin D1)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170505
[Lr] Data última revisão:
170505
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170418
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0175443


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[PMID]:28407017
[Au] Autor:Perretti M; Di Filippo C; D'Amico M; Dalli J
[Ad] Endereço:The William Harvey Research Institute, Barts and The London School of Medicine, Queen Mary University of London, Charterhouse Square, London, United Kingdom.
[Ti] Título:Characterizing the anti-inflammatory and tissue protective actions of a novel Annexin A1 peptide.
[So] Source:PLoS One;12(4):e0175786, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inflammation in now appreciated to be at the centre of may diseases that affect Western civilization. Current therapeutics for managing these conditions may interfere with the host response leading to immune suppression. We recently developed an annexin (Anx) A1-derived peptide, coined CR-AnxA12-50, which displays potent pro-resolving and tissue protective actions. Herein, we designed a novel peptide using CR-AnxA12-50 as a template that was significantly more resistant to neutrophil-mediated degradation. This peptide, termed CR-AnxA12-48, retained high affinity and specificity to the pro-resolving Lipoxin A4 receptor (ALX) with an IC50 of ~20nM. CR-AnxA12-48 dose dependently (100fM-10nM) promoted the efferocytosis of apoptotic neutrophils, an action that was mediated by the murine orthologue of human ALX. The neutrophil-directed actions were also retained with human primary cells were CR-AnxA12-48 reduced human neutrophil recruitment to activated endothelial cells at concentrations as low as 100 pM. This protective action was mediated by human ALX, since incubation of neutrophils with an anti-ALX antibody reversed this anti-inflammatory actions of CR-AnxA12-48. Administration of this peptide to mice during dermal inflammation led to a significant and dose dependent decrease in neutrophil recruitment. This reduction in neutrophil numbers was more pronounced than that displayed by the parent peptide CR-AnxA12-50. CR-AnxA12-48 was also cardioprotecitve reducing infarct size and systemic chemokine (C-C motif) ligand 5 concentration following ischemia reperfusion injury. These findings identify CR-AnxA12-48 as a new ALX agonist that regulates phagocyte responses and displays tissue-protective actions.
[Mh] Termos MeSH primário: Anexina A1/química
Anti-Inflamatórios/administração & dosagem
Cardiotônicos/administração & dosagem
Inflamação/tratamento farmacológico
Traumatismo por Reperfusão Miocárdica/prevenção & controle
Peptídeos/administração & dosagem
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Animais
Anti-Inflamatórios/farmacologia
Cardiotônicos/farmacologia
Modelos Animais de Doenças
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Inflamação/etiologia
Inflamação/imunologia
Inflamação/metabolismo
Masculino
Camundongos
Neutrófilos/efeitos dos fármacos
Peptídeos/farmacologia
Fagócitos/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Annexin A1); 0 (Anti-Inflammatory Agents); 0 (Cardiotonic Agents); 0 (HSH2D protein, human); 0 (Peptides)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170505
[Lr] Data última revisão:
170505
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170414
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0175786


  9 / 1055 MEDLINE  
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[PMID]:28379492
[Au] Autor:Rossi A; Moro A; Tebaldi T; Cornella N; Gasperini L; Lunelli L; Quattrone A; Viero G; Macchi P
[Ad] Endereço:Laboratory of Molecular and Cellular Neurobiology, Centre for Integrative Biology, University of Trento, via Sommarive 9, 38123 Trento (TN), Italy.
[Ti] Título:Identification and dynamic changes of RNAs isolated from RALY-containing ribonucleoprotein complexes.
[So] Source:Nucleic Acids Res;45(11):6775-6792, 2017 Jun 20.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:RALY is a member of the heterogeneous nuclear ribonucleoprotein family (hnRNP), a large family of RNA-binding proteins involved in many aspects of RNA metabolism. Although RALY interactome has been recently characterized, a comprehensive global analysis of RALY-associated RNAs is lacking and the biological function of RALY remains elusive. Here, we performed RIP-seq analysis to identify RALY interacting RNAs and assessed the role of RALY in gene expression. We demonstrate that RALY binds specific coding and non-coding RNAs and associates with translating mRNAs of mammalian cells. Among the identified transcripts, we focused on ANXA1 and H1FX mRNAs, encoding for Annexin A1 and for the linker variant of the histone H1X, respectively. Both proteins are differentially expressed by proliferating cells and are considered as markers for tumorigenesis. We demonstrate that cells lacking RALY expression exhibit changes in the levels of H1FX and ANXA1 mRNAs and proteins in an opposite manner. We also provide evidence for a direct binding of RALY to the U-rich elements present within the 3΄UTR of both transcripts. Thus, our results identify RALY as a poly-U binding protein and as a regulator of H1FX and ANXA1 in mammalian cells.
[Mh] Termos MeSH primário: Ribonucleoproteínas Nucleares Heterogêneas Grupo C/fisiologia
RNA Mensageiro/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Anexina A1/genética
Anexina A1/metabolismo
Carcinogênese/genética
Carcinogênese/metabolismo
Ciclo Celular
Regulação Neoplásica da Expressão Gênica
Células HEK293
Células HeLa
Seres Humanos
Células Jurkat
Células MCF-7
Polirribossomos/metabolismo
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Annexin A1); 0 (Heterogeneous-Nuclear Ribonucleoprotein Group C); 0 (RALY protein, human); 0 (RNA, Messenger)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170406
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx235


  10 / 1055 MEDLINE  
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[PMID]:28378195
[Au] Autor:Sharma P; Jenkins M; Zarlenga D; Fetterer R; Xiao Z; Tuo W
[Ad] Endereço:Animal Parasitic Diseases Laboratory, BARC.NEA, Beltsville, MD, USA.
[Ti] Título:Characterization of Ostertagia ostertagi annexin-like proteins at different developmental stages.
[So] Source:Parasitol Res;116(5):1515-1522, 2017 May.
[Is] ISSN:1432-1955
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Ostertagiosis remains an economically important parasitic disease in cattle in the temperate regions of the world. Repeated exposures to Ostertagia ostertagi in calves cause significant pathology in the abomasum but elicit little protective immunity. The larvae use the host's gastric glands as a niche for development, where the parasite completes its parasitic stages, while in the gastric glands, the larvae must down-regulate the host inflammatory immune responses. Annexin (ANX) A1, commonly found in most eukaryotes, is heavily involved in controlling anti-inflammatory responses by binding receptors on leukocytes. We hypothesized, therefore, that parasite proteins of the ANX family may be involved in host-parasite interactions during ostertagiosis. BLASTN search with the bovine ANXA1 identified two families of Oos-ANX like proteins (Oos-ANXL), each of which was highly conserved at the genetic level and identical at the amino acid sequence level. Oos-ANXL-1 is encoded by two transcripts and Oos-ANXL-2 by 20 transcripts. The present study characterized one Oos-ANXL, representing the most abundant Oos-ANXL, which was further defined as Oost-ANXL-2.1. Oos-ANXL-2.1 with a coding sequence of 519 bp was PCR-amplified, cloned, and expressed. Oos-ANXL-2.1 was immunolocalized to both L3 and adult, but not L4. The staining appeared to be associated with the gut and hypodermis in L3, but it was specifically localized to the hypodermis in adult worms. Western blots detected three protein bands in parasite lysates using anti-recombinant Oos-ANXL-2.1 antibody. Integrated optical density for each of the 3 Oos-ANXL-2s or the total Oos-ANXL-2s detected by Western blots (P < 0.05) was higher in adult worms than in L3 or L4. The results indicate that the production of Oos-ANXL-2s is developmentally regulated and most abundant in the adult worm. This rather large family of proteins could be a potential vaccine target against O. ostertagi infection and warrants further investigation.
[Mh] Termos MeSH primário: Anexina A1/metabolismo
Anexina A2/imunologia
Doenças dos Bovinos/parasitologia
Interações Hospedeiro-Parasita
Ostertagia/embriologia
Ostertagíase/veterinária
[Mh] Termos MeSH secundário: Abomaso/parasitologia
Sequência de Aminoácidos/genética
Animais
Anexina A1/genética
Anexina A2/genética
Bovinos
Mucosa Gástrica/parasitologia
Larva/metabolismo
Ostertagia/fisiologia
Ligação Proteica
Proteínas Recombinantes/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A1); 0 (Annexin A2); 0 (Recombinant Proteins)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171007
[Lr] Data última revisão:
171007
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170406
[St] Status:MEDLINE
[do] DOI:10.1007/s00436-017-5428-8



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