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Pesquisa : D12.644.276.374.200.120.050 [Categoria DeCS]
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  1 / 1927 MEDLINE  
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[PMID]:29309811
[Au] Autor:Park EJ; Park SJ; Kim S; Lee K; Chang J
[Ad] Endereço:Graduate school of East-West Medical Science, Kyung Hee University, Yongin-si, Gyeonggi-do, 17104, Republic of Korea. Electronic address: pejtoxic@hanmail.net.
[Ti] Título:Lung fibroblasts may play an important role in clearing apoptotic bodies of bronchial epithelial cells generated by exposure to PHMG-P-containing solution.
[So] Source:Toxicol Lett;286:108-119, 2018 Apr.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Polyhexamethylene guanidine (PHMG) has been widely used in the industry owing to its excellent biocidal, anti-corrosive, and anti-biofouling properties. In Korea, consumers exposed to PHMG-phosphate (PHMG-P)-containing humidifier disinfectant have begun to suffer from fibrotic lung injury-related symptoms for unknown reasons. However, no appropriate treatment has yet been found because the detail toxic mechanism has not been identified. Herein, we first studied the toxic mechanism of PHMG-P-containing solution using human normal bronchial epithelial cells (BEAS-2B cells). When exposed for 24 h, PHMG-P-containing solution rapidly decreased cell viability from around 6 h after exposure and significantly increased of the phosphatidylserine exposure and the LDH release. At 6 h of exposure, the material contained in the solution was found to be bound to the cell membrane and the inner wall of vacuoles, and damaged the cell membrane and organelles. In addition, a significant increase of IFN-γ was observed among cytokines, the expression of apoptosis-, autophagy-, and membrane and DNA damage-related proteins was also enhanced. Meanwhile, the level of intracellular ROS and the secretion of IL-8 and CXCL-1, which are chemokines for professional phagocytes, decreased. Thus, we treated dead BEAS-2B cells to lung fibroblasts (HFL-1), non-professional phagocytes, and then we observed that the dead cells rapidly attached to HFL-1 cells and were taken up. Additionally, increased secretion of IL-8 and CXCL-1 was observed in the cells. Based on these results, we suggest that pulmonary exposure to PHMG-P induces apoptosis of bronchial epithelial cells and lung fibroblasts might play an important role in the clearance of the apoptotic debris.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Brônquios/efeitos dos fármacos
Citofagocitose
Desinfetantes/toxicidade
Células Epiteliais/efeitos dos fármacos
Fibroblastos/metabolismo
Guanidinas/toxicidade
[Mh] Termos MeSH secundário: Brônquios/metabolismo
Brônquios/ultraestrutura
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Quimiocina CXCL1/metabolismo
Relação Dose-Resposta a Droga
Células Epiteliais/metabolismo
Células Epiteliais/ultraestrutura
Fibroblastos/ultraestrutura
Seres Humanos
Interferon gama/metabolismo
Interleucina-8/metabolismo
L-Lactato Desidrogenase/metabolismo
Fosfatidilserinas/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL1 protein, human); 0 (Chemokine CXCL1); 0 (Disinfectants); 0 (Guanidines); 0 (IFNG protein, human); 0 (IL8 protein, human); 0 (Interleukin-8); 0 (Phosphatidylserines); 31961-54-3 (polyhexamethyleneguanidine); 82115-62-6 (Interferon-gamma); EC 1.1.1.27 (L-Lactate Dehydrogenase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180109
[St] Status:MEDLINE


  2 / 1927 MEDLINE  
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[PMID]:28458362
[Au] Autor:Tanaka K; Yoshitomi T; Hirahara K
[Ad] Endereço:Biologics & Immuno-Oncology Laboratories, Daiichi Sankyo Co., Ltd.
[Ti] Título:Elucidation of Distinct Roles of Guinea Pig CXCR1 and CXCR2 in Neutrophil Migration toward IL-8 and GROα by Specific Antibodies.
[So] Source:Biol Pharm Bull;40(5):729-732, 2017.
[Is] ISSN:1347-5215
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Chemokine receptors CXCR1 and CXCR2 are conserved between guinea pigs and humans, but the distinct role of each receptor in chemotactic responses of neutrophils against chemokine ligands has not been elucidated due in part to the lack of specific inhibitors against these receptors in guinea pigs. In this study, we investigated the roles of guinea pig CXCR1 and CXCR2 on neutrophils in chemotactic responses to guinea pig interleukin (IL)-8 and growth-regulated oncogene (GRO)α by using specific inhibitory antibodies against these receptors. Neutrophil migration induced by IL-8 was partially inhibited by either anti-CXCR1 antibody or anti-CXCR2 antibody. In addition, the migration was inhibited completely when both anti-CXCR1 and anti-CXCR2 antibodies were combined. On the other hand, neutrophil migration induced by GROα was not inhibited by anti-CXCR1 antibody while inhibited profoundly by anti-CXCR2 antibody. These results indicated that CXCR1 and CXCR2 mediated migration induced by the IL-8 synergistically and only CXCR2 mediated migration induced by GROα in guinea pig neutrophils. Our findings on ligand selectivity of CXCR1 and CXCR2 in guinea pigs are consistent with those in humans.
[Mh] Termos MeSH primário: Quimiocina CXCL1/farmacologia
Interleucina-8/farmacologia
Neutrófilos/fisiologia
Receptores de Interleucina-8A/fisiologia
Receptores de Interleucina-8B/fisiologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Bloqueadores/farmacologia
Movimento Celular/efeitos dos fármacos
Quimiocina CXCL1/antagonistas & inibidores
Quimiotaxia/efeitos dos fármacos
Feminino
Cobaias
Doenças do Sistema Imune
Interleucina-8/antagonistas & inibidores
Transtornos Leucocíticos
Neutrófilos/imunologia
Receptores de Interleucina-8A/imunologia
Receptores de Interleucina-8B/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Blocking); 0 (Chemokine CXCL1); 0 (Interleukin-8); 0 (Receptors, Interleukin-8A); 0 (Receptors, Interleukin-8B)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1248/bpb.b16-00918


  3 / 1927 MEDLINE  
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[PMID]:29360827
[Au] Autor:Kim EK; Moon S; Kim DK; Zhang X; Kim J
[Ad] Endereço:Oral Cancer Research Institute, Department of Oral Pathology, Yonsei University College of Dentistry, Seoul, Republic of Korea.
[Ti] Título:CXCL1 induces senescence of cancer-associated fibroblasts via autocrine loops in oral squamous cell carcinoma.
[So] Source:PLoS One;13(1):e0188847, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cancer-associated fibroblasts (CAFs) have emerged as one of the main factors related to cancer progression, however, the conversion mechanism of normal fibroblasts (NOFs) to CAFs has not been well elucidated. The aim of this study was to investigate the underlying mechanism of CAF transformation from NOFs in oral squamous cell carcinoma (OSCC). This study found that NOFs exposed to OSCC cells transformed to senescent cells. The cytokine antibody array showed the highest secretion levels of IL-6 and CXCL1 in NOFs co-cultured with OSCC cells. Despite that both IL-6 and CXCL1 induced the senescent phenotype of CAFs, CXCL1 secretion showed a cancer-specific response to transform NOFs into CAFs in OSCC, whereas IL-6 secretion was eventuated by common co-culture condition. Further, CXCL1 was released from NOFs co-cultured with OSCC cells, however, CXCL1 was undetectable in mono-cultured NOFs or co-cultured OSCC cells with NOFs. Taken together, this study demonstrates that CXCL1 can transform NOFs into senescent CAFs via an autocrine mechanism. These data might contribute to further understanding of CAFs and to development of a potential therapeutic approach targeting cancer cells-CAFs interactions.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/patologia
Senescência Celular/fisiologia
Quimiocina CXCL1/fisiologia
Neoplasias Bucais/patologia
[Mh] Termos MeSH secundário: Western Blotting
Carcinoma de Células Escamosas/metabolismo
Técnicas de Cocultura
Citocinas/metabolismo
Ensaio de Imunoadsorção Enzimática
Fibroblastos/patologia
Seres Humanos
Neoplasias Bucais/metabolismo
Invasividade Neoplásica
Espécies Reativas de Oxigênio/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CXCL1 protein, human); 0 (Chemokine CXCL1); 0 (Cytokines); 0 (Reactive Oxygen Species)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180124
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188847


  4 / 1927 MEDLINE  
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[PMID]:28455419
[Au] Autor:Wang D; Sun H; Wei J; Cen B; DuBois RN
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina.
[Ti] Título:CXCL1 Is Critical for Premetastatic Niche Formation and Metastasis in Colorectal Cancer.
[So] Source:Cancer Res;77(13):3655-3665, 2017 Jul 01.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Emerging evidence suggests that the primary tumor influences the development of supportive metastatic microenvironments, referred to as premetastatic niches, in certain distant organs before arrival of metastatic cells. However, the mechanisms underlying the contributions of the primary tumor to premetastatic niche formation are not fully understood. Here, we demonstrate that colorectal carcinoma cells secrete VEGFA, which stimulates tumor-associated macrophages to produce CXCL1 in the primary tumor. Elevation of CXCL1 in premetastatic liver tissue recruited CXCR2-positive myeloid-derived suppressor cells (MDSC) to form a premetastatic niche that ultimately promoted liver metastases. Importantly, premetastatic liver-infiltrating MDSCs induced tumor cell survival without involvement of innate or adaptive immune responses. Our study provides the first evidence that primary malignant cell-secreted VEGFA stimulates tumor-associated macrophages to produce CXCL1, which recruits CXCR2-positive MDSCs to form a premetastatic niche to promote liver metastases. Our findings not only shed light on how the tumor microenvironment contributes to premetastatic niche formation at distant sites, but they also provide comprehensive insights into how MDSCs are recruited to other organs where they contribute to metastatic spread of disease. Moreover, our work also provides a rationale for development of CXCR2 antagonists to inhibit or prevent metastatic spread of disease. .
[Mh] Termos MeSH primário: Quimiocina CXCL1/biossíntese
Neoplasias Colorretais/metabolismo
Neoplasias Colorretais/patologia
Neoplasias Hepáticas/secundário
[Mh] Termos MeSH secundário: Animais
Quimiocina CXCL1/imunologia
Neoplasias Colorretais/imunologia
Células HCT116
Xenoenxertos
Seres Humanos
Neoplasias Hepáticas/imunologia
Neoplasias Hepáticas/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos NOD
Camundongos SCID
Metástase Neoplásica
Células-Tronco Neoplásicas/imunologia
Células-Tronco Neoplásicas/metabolismo
Células-Tronco Neoplásicas/patologia
Nicho de Células-Tronco
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL1 protein, human); 0 (Chemokine CXCL1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180127
[Lr] Data última revisão:
180127
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-16-3199


  5 / 1927 MEDLINE  
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[PMID]:28450382
[Au] Autor:Young HL; Rowling EJ; Bugatti M; Giurisato E; Luheshi N; Arozarena I; Acosta JC; Kamarashev J; Frederick DT; Cooper ZA; Reuben A; Gil J; Flaherty KT; Wargo JA; Vermi W; Smith MP; Wellbrock C; Hurlstone A
[Ad] Endereço:Manchester Cancer Research Centre, Faculty of Biology, Medicine, and Health, School of Medical Sciences, Division of Molecular and Clinical Cancer Studies, The University of Manchester, Manchester M13 9PT, England, UK.
[Ti] Título:An adaptive signaling network in melanoma inflammatory niches confers tolerance to MAPK signaling inhibition.
[So] Source:J Exp Med;214(6):1691-1710, 2017 Jun 05.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mitogen-activated protein kinase (MAPK) pathway antagonists induce profound clinical responses in advanced cutaneous melanoma, but complete remissions are frustrated by the development of acquired resistance. Before resistance emerges, adaptive responses establish a mutation-independent drug tolerance. Antagonizing these adaptive responses could improve drug effects, thereby thwarting the emergence of acquired resistance. In this study, we reveal that inflammatory niches consisting of tumor-associated macrophages and fibroblasts contribute to treatment tolerance through a cytokine-signaling network that involves macrophage-derived IL-1ß and fibroblast-derived CXCR2 ligands. Fibroblasts require IL-1ß to produce CXCR2 ligands, and loss of host IL-1R signaling in vivo reduces melanoma growth. In tumors from patients on treatment, signaling from inflammatory niches is amplified in the presence of MAPK inhibitors. Signaling from inflammatory niches counteracts combined BRAF/MEK (MAPK/extracellular signal-regulated kinase kinase) inhibitor treatment, and consequently, inhibiting IL-1R or CXCR2 signaling in vivo enhanced the efficacy of MAPK inhibitors. We conclude that melanoma inflammatory niches adapt to and confer drug tolerance toward BRAF and MEK inhibitors early during treatment.
[Mh] Termos MeSH primário: Inflamação/enzimologia
Inflamação/patologia
Sistema de Sinalização das MAP Quinases
Melanoma/enzimologia
Melanoma/patologia
Neoplasias Cutâneas/enzimologia
Neoplasias Cutâneas/patologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Quimiocina CXCL1/metabolismo
Fibroblastos/efeitos dos fármacos
Fibroblastos/metabolismo
Seres Humanos
Interleucina-1/metabolismo
Interleucina-1beta/metabolismo
Interleucina-8/metabolismo
Ligantes
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Macrófagos/efeitos dos fármacos
Macrófagos/metabolismo
Camundongos Knockout
Quinases de Proteína Quinase Ativadas por Mitógeno/antagonistas & inibidores
Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo
NF-kappa B/metabolismo
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas B-raf/metabolismo
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Receptores de Interleucina-1/metabolismo
Receptores de Interleucina-8B/metabolismo
Células Estromais/metabolismo
Células Estromais/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CXCL1); 0 (Interleukin-1); 0 (Interleukin-1beta); 0 (Interleukin-8); 0 (Ligands); 0 (NF-kappa B); 0 (Protein Kinase Inhibitors); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Receptors, Interleukin-1); 0 (Receptors, Interleukin-8B); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf); EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180125
[Lr] Data última revisão:
180125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20160855


  6 / 1927 MEDLINE  
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[PMID]:28985357
[Au] Autor:Zhao W; Siegel D; Biton A; Tonqueze OL; Zaitlen N; Ahituv N; Erle DJ
[Ad] Endereço:Lung Biology Center, Department of Medicine, University of California San Francisco, 4th St, San Francisco, CA 94158, USA.
[Ti] Título:CRISPR-Cas9-mediated functional dissection of 3'-UTRs.
[So] Source:Nucleic Acids Res;45(18):10800-10810, 2017 Oct 13.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Many studies using reporter assays have demonstrated that 3' untranslated regions (3'-UTRs) regulate gene expression by controlling mRNA stability and translation. Due to intrinsic limitations of heterologous reporter assays, we sought to develop a gene editing approach to investigate the regulatory activity of 3'-UTRs in their native context. We initially used dual-CRISPR (clustered, regularly interspaced, short palindromic repeats)-Cas9 targeting to delete DNA regions corresponding to nine chemokine 3'-UTRs that destabilized mRNA in a reporter assay. Targeting six chemokine 3'-UTRs increased chemokine mRNA levels as expected. However, targeting CXCL1, CXCL6 and CXCL8 3'-UTRs unexpectedly led to substantial mRNA decreases. Metabolic labeling assays showed that targeting these three 3'-UTRs increased mRNA stability, as predicted by the reporter assay, while also markedly decreasing transcription, demonstrating an unexpected role for 3'-UTR sequences in transcriptional regulation. We further show that CRISPR-Cas9 targeting of specific 3'-UTR elements can be used for modulating gene expression and for highly parallel localization of active 3'-UTR elements in the native context. Our work demonstrates the duality and complexity of 3'-UTR sequences in regulation of gene expression and provides a useful approach for modulating gene expression and for functional annotation of 3'-UTRs in the native context.
[Mh] Termos MeSH primário: Regiões 3´ não Traduzidas
Sistemas CRISPR-Cas
Regulação da Expressão Gênica
[Mh] Termos MeSH secundário: Quimiocina CXCL1/genética
Quimiocina CXCL6/genética
Quimiocinas/genética
Elementos Facilitadores Genéticos
Edição de Genes
Genes Reporter
Seres Humanos
Interleucina-8/genética
Estabilidade de RNA
RNA Mensageiro/metabolismo
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (CXCL1 protein, human); 0 (CXCL6 protein, human); 0 (Chemokine CXCL1); 0 (Chemokine CXCL6); 0 (Chemokines); 0 (IL8 protein, human); 0 (Interleukin-8); 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:171007
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx675


  7 / 1927 MEDLINE  
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[PMID]:28922428
[Au] Autor:Jin L; Batra S; Jeyaseelan S
[Ad] Endereço:Laboratory of Lung Biology, Department of Pathobiological Sciences and Center for Experimental Infectious Disease Research, School of Veterinary Medicine, Louisiana State University, Baton Rouge, Louisiana, United States of America.
[Ti] Título:Diminished neutrophil extracellular trap (NET) formation is a novel innate immune deficiency induced by acute ethanol exposure in polymicrobial sepsis, which can be rescued by CXCL1.
[So] Source:PLoS Pathog;13(9):e1006637, 2017 Sep.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Polymicrobial sepsis is the result of an exaggerated host immune response to bacterial pathogens. Animal models and human studies demonstrate that alcohol intoxication is a key risk factor for sepsis-induced mortality. Multiple chemokines, such as CXCL1, CXCL2 and CXCL5 are critical for neutrophil recruitment and proper function of neutrophils. However, it is not quite clear the mechanisms by which acute alcohol suppresses immune responses and whether alcohol-induced immunosuppression can be rescued by chemokines. Thus, we assessed whether acute ethanol challenge via gavage diminishes antibacterial host defense in a sepsis model using cecal ligation and puncture (CLP) and whether this immunosuppression can be rescued by exogenous CXCL1. We found acute alcohol intoxication augments mortality and enhances bacterial growth in mice following CLP. Ethanol exposure impairs critical antibacterial functions of mouse and human neutrophils including reactive oxygen species production, neutrophil extracellular trap (NET) formation, and NET-mediated killing in response to both Gram-negative (E. coli) and Gram-positive (Staphylococcus aureus) pathogens. As compared with WT (C57Bl/6) mice, CXCL1 knockout mice display early mortality following acute alcohol exposure followed by CLP. Recombinant CXCL1 (rCXCL1) in acute alcohol challenged CLP mice increases survival, enhances bacterial clearance, improves neutrophil recruitment, and enhances NET formation (NETosis). Recombinant CXCL1 (rCXCL1) administration also augments bacterial killing by alcohol-treated and E. coli- and S. aureus-infected neutrophils. Taken together, our data unveils novel mechanisms underlying acute alcohol-induced dysregulation of the immune responses in polymicrobial sepsis, and CXCL1 is a critical mediator to rescue alcohol-induced immune dysregulation in polymicrobial sepsis.
[Mh] Termos MeSH primário: Quimiocina CXCL1/imunologia
Etanol/toxicidade
Armadilhas Extracelulares/imunologia
Imunidade Inata/imunologia
Sepse/imunologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Quimiocina CXCL1/farmacologia
Modelos Animais de Doenças
Armadilhas Extracelulares/efeitos dos fármacos
Imunofluorescência
Seres Humanos
Imunidade Inata/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Microscopia Eletrônica de Transmissão
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CXCL1); 3K9958V90M (Ethanol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006637


  8 / 1927 MEDLINE  
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[PMID]:28870907
[Au] Autor:Divella R; Daniele A; DE Luca R; Simone M; Naglieri E; Savino E; Abbate I; Gadaleta CD; Ranieri G
[Ad] Endereço:Clinical Pathology Laboratory, National Cancer Research Centre, Giovanni Paolo II Tumor institute, Bari, Italy rosadive@inwind.it.
[Ti] Título:Circulating Levels of VEGF and CXCL1 Are Predictive of Metastatic Organotropismin in Patients with Colorectal Cancer.
[So] Source:Anticancer Res;37(9):4867-4871, 2017 09.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Colorectal cancer is the most common cancer of the gastrointestinal system and has a marked preference to metastasize to distant organs. In this study, we investigated whether levels of circulating serum pro-angiogenic cytokine such as chemokine (C-X-C motif) ligand 1 (melanoma growth-stimulating activity, alpha; CXCL1) and vascular endothelial growth factor (VEGF) have a role in favoring the colonization of metastatic cells at preferential sites and determined their prognostic significance in a cohort of 103 patients with metastatic colorectal cancer. Importantly, we found that the presence of elevated circulating levels of VEGF and CXCL1 are predictive of liver and lung metastasis, respectively. Moreover, the presence of a high serum VEGF level represents a negative prognostic factor for patients with liver metastases, with a worse prognosis than patients with lung metastasis. This suggests an additional role for circulating cytokines as a predictive tool for cancer prognosis and diagnosis, as well as for assessment of tumor sensitivity to anticancer therapy.
[Mh] Termos MeSH primário: Quimiocina CXCL1/sangue
Neoplasias Colorretais/sangue
Neoplasias Colorretais/patologia
Fator A de Crescimento do Endotélio Vascular/sangue
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Feminino
Seres Humanos
Neoplasias Hepáticas/sangue
Neoplasias Hepáticas/secundário
Neoplasias Pulmonares/sangue
Neoplasias Pulmonares/secundário
Masculino
Meia-Idade
Metástase Neoplásica
Prognóstico
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL1 protein, human); 0 (Chemokine CXCL1); 0 (Vascular Endothelial Growth Factor A)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170906
[St] Status:MEDLINE


  9 / 1927 MEDLINE  
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[PMID]:28844502
[Au] Autor:Sowa JE; Slusarczyk J; Trojan E; Chamera K; Leskiewicz M; Regulska M; Kotarska K; Basta-Kaim A
[Ad] Endereço:Institute of Pharmacology, Polish Academy of Sciences, Department of Physiology, 12 Smetna St, 31-343 Krakow, Poland; Institute of Pharmacology, Polish Academy of Sciences, Department of Experimental Neuroendocrinology, 12 Smetna St, 31-343 Krakow, Poland.
[Ti] Título:Prenatal stress affects viability, activation, and chemokine signaling in astroglial cultures.
[So] Source:J Neuroimmunol;311:79-87, 2017 Oct 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:CXCL12/SDF-1α and CX3CL1/fractalkine are constitutively expressed in the brain, which indicates their significant functions. Emerging evidence highlights the role of astrocytes and the immune system in the pathophysiology of stress-related disorders. The aim of this study was to assess whether prenatal stress affects chemokine signaling, cell viability/activation, and the iNOS pathway in astroglial cultures. Our results showed that prenatal stress lowered astrocyte viability and simultaneously increased GFAP expression. Furthermore, CX3CL1 production and the CXCL12/CXCR4-7 axis were also altered by prenatal stress. Taken together, malfunctions caused by prenatal stress may adversely influence brain development, leading to long-term effects on adult brain function and behavior.
[Mh] Termos MeSH primário: Astrócitos/metabolismo
Quimiocinas/metabolismo
Efeitos Tardios da Exposição Pré-Natal/patologia
Transdução de Sinais/fisiologia
Estresse Psicológico/patologia
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Astrócitos/imunologia
Sobrevivência Celular/fisiologia
Células Cultivadas
Córtex Cerebral/patologia
Quimiocina CXCL1/genética
Quimiocina CXCL1/metabolismo
Quimiocina CXCL12/genética
Quimiocina CXCL12/metabolismo
Quimiocinas/genética
Feminino
Proteína Glial Fibrilar Ácida/metabolismo
L-Lactato Desidrogenase/metabolismo
Óxido Nítrico/metabolismo
Gravidez
Ratos
Ratos Sprague-Dawley
Regulação para Cima/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CXCL1); 0 (Chemokine CXCL12); 0 (Chemokines); 0 (Glial Fibrillary Acidic Protein); 31C4KY9ESH (Nitric Oxide); EC 1.1.1.27 (L-Lactate Dehydrogenase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170829
[St] Status:MEDLINE


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[PMID]:28796783
[Au] Autor:Reins RY; Courson J; Lema C; Redfern RL
[Ad] Endereço:The Ocular Surface Institute, College of Optometry, University of Houston, Houston, Texas, United States of America.
[Ti] Título:MyD88 contribution to ocular surface homeostasis.
[So] Source:PLoS One;12(8):e0182153, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cornea must maintain homeostasis, enabling rapid response to injury and microbial insult, to protect the eye from insult and infection. Toll-like receptors (TLRs) are critical to this innate immune response through the recognition and response to pathogens. Myeloid differentiation primary response (MyD88) is a key signaling molecule necessary for Toll-like receptor (TLR) and interleukin-1 receptor (IL-1R)-mediated immune defense and has been shown to be necessary for corneal defense during infection. Here, we examined the intrinsic role of TLR signaling in ocular surface tissues by determining baseline levels of inflammatory mediators, the response to mechanical stimuli, and corneal infection in MyD88-deficient mice (MyD88-/-). In addition, cytokine, chemokine, and matrix metalloproteinase (MMP) expression was determined in ocular surface cells exposed to a panel of TLR agonists. Compared to wild-type (WT) animals, MyD88-/- mice expressed lower MMP-9 levels in the cornea and conjunctiva. Corneal IL-1α, TNFα, and conjunctival IL-1α, IL-2, IL-6, and IL-9 levels were also significantly reduced. Additionally, CXCL1 and RANTES expression was lower in both MyD88-/- tissues compared to WT and IL-1R-/- mice. Interestingly, MyD88-/- mice had lower corneal sensitivities (1.01±0.31 gm/mm2) than both WT (0.59±0.16 gm/mm2) and IL-1R-/- (0.52±0.08 gm/mm2). Following Pseudomonas aeruginosa challenge, MyD88-/- mice had better clinical scores (0.5±0.0) compared to IL-1R-/- (1.5±0.6) and WT (2.3±0.3) animals, but had significantly more corneal bacterial isolates. However, no signs of infection were detected in inoculated uninjured corneas from either MyD88 or IL-1R-deficient mice. This work furthers our understanding of the importance of TLR signaling in corneal defense and immune homeostasis, showing that a lack of MyD88 may compromise the baseline innate response to insult.
[Mh] Termos MeSH primário: Túnica Conjuntiva/metabolismo
Córnea/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
Fator 88 de Diferenciação Mieloide/genética
[Mh] Termos MeSH secundário: Animais
Quimiocina CCL5/metabolismo
Quimiocina CXCL1/metabolismo
Citocinas/metabolismo
Camundongos
Camundongos Knockout
Fator 88 de Diferenciação Mieloide/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CCL5); 0 (Chemokine CXCL1); 0 (Cytokines); 0 (Myd88 protein, mouse); 0 (Myeloid Differentiation Factor 88); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182153



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