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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


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[PMID]:28478039
[Au] Autor:Ye Y; Chen Q; Li J; Jin L; Zheng J; Li X; Lin Z; Gong F
[Ad] Endereço:School of Pharmacy, Wenzhou Medical University, Chashan College Park, Wenzhou, Zhejiang, China.
[Ti] Título:CXCL16 deficiency attenuates diabetic nephropathy through decreasing oxidative stress and inflammation.
[So] Source:Biochem Biophys Res Commun;491(3):848-854, 2017 Sep 23.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Soluble C-X-C chemokine ligand 16 (CXCL16) is related to the inflammatory response in liver injury and involved in the pathogenesis of renal dysfunction in diabetes patients. However, the exact role of elevated CXCL16 in diabetic nephropathy (DN) remains unclear. In this study, we investigated the role of CXCL16 in streptozcin (STZ)-induced diabetic nephropathy (DN) in mice. The results showed that fasting blood glucose (FBG) and 24 h urinary protein, triglyceride, and cholesterol levels increased in diabetic mice, and these changes were partially ameliorated in CXCL16 KO mice. Meanwhile, the results also showed that ROS generation was suppressed and the expression levels of inflammatory factors and infiltration factors were inhibited both in vivo and in vitro using DN models. In addition, the total AKT protein and p-AKT levels were decreased in CXCL16-depleted HK-2 cells that were treated with LPS. These findings suggest that the CXCL16 gene product promotes inflammatory factors and cell infiltration factors, and inhibits the expression of antioxidant factors to accelerate the development of DN, and CXCL16 deficiency attenuates DN may be involved in the AKT signaling pathway.
[Mh] Termos MeSH primário: Glicemia/imunologia
Quimiocina CXCL6/imunologia
Nefropatias Diabéticas/imunologia
Inflamação/imunologia
Estresse Oxidativo/imunologia
Espécies Reativas de Oxigênio/imunologia
[Mh] Termos MeSH secundário: Animais
Quimiocina CXCL16
Nefropatias Diabéticas/induzido quimicamente
Nefropatias Diabéticas/patologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Estreptozocina
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Chemokine CXCL16); 0 (Chemokine CXCL6); 0 (Cxcl16 protein, mouse); 0 (Reactive Oxygen Species); 5W494URQ81 (Streptozocin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170508
[St] Status:MEDLINE


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[PMID]:28396316
[Au] Autor:Choudhury RH; Dunk CE; Lye SJ; Aplin JD; Harris LK; Jones RL
[Ad] Endereço:Maternal and Fetal Health Research Centre, Division of Developmental Biology and Medicine, School of Medical Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9WL, United Kingdom; ruhul.choudhury@postgrad.manchester.ac.uk.
[Ti] Título:Extravillous Trophoblast and Endothelial Cell Crosstalk Mediates Leukocyte Infiltration to the Early Remodeling Decidual Spiral Arteriole Wall.
[So] Source:J Immunol;198(10):4115-4128, 2017 May 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Decidual spiral arteriole (SpA) remodeling is essential to ensure optimal uteroplacental blood flow during human pregnancy, yet very little is known about the regulatory mechanisms. Uterine decidual NK (dNK) cells and macrophages infiltrate the SpAs and are proposed to initiate remodeling before colonization by extravillous trophoblasts (EVTs); however, the trigger for their infiltration is unknown. Using human first trimester placenta, decidua, primary dNK cells, and macrophages, we tested the hypothesis that EVTs activate SpA endothelial cells to secrete chemokines that have the potential to recruit maternal immune cells into SpAs. Gene array, real-time PCR, and ELISA analyses showed that treatment of endothelial cells with EVT conditioned medium significantly increased production of two chemokines, CCL14 and CXCL6. CCL14 induced chemotaxis of both dNK cells and decidual macrophages, whereas CXCL6 also induced dNK cell migration. Analysis of the decidua basalis from early pregnancy demonstrated expression of CCL14 and CXCL6 by endothelial cells in remodeling SpAs, and their cognate receptors are present in both dNK cells and macrophages. Neutralization studies identified IL-6 and CXCL8 as factors secreted by EVTs that induce endothelial cell CCL14 and CXCL6 expression. This study has identified intricate crosstalk between EVTs, SpA cells, and decidual immune cells that governs their recruitment to SpAs in the early stages of remodeling and has identified potential key candidate factors involved. This provides a new understanding of the interactions between maternal and fetal cells during early placentation and highlights novel avenues for research to understand defective SpA remodeling and consequent pregnancy pathology.
[Mh] Termos MeSH primário: Arteríolas/fisiologia
Decídua/fisiologia
Células Endoteliais/metabolismo
Células Matadoras Naturais/fisiologia
Macrófagos/fisiologia
Trofoblastos/metabolismo
[Mh] Termos MeSH secundário: Arteríolas/citologia
Arteríolas/imunologia
Movimento Celular/imunologia
Células Cultivadas
Quimiocina CXCL6/biossíntese
Quimiocina CXCL6/imunologia
Quimiocinas CC/biossíntese
Quimiocinas CC/imunologia
Meios de Cultura/química
Decídua/imunologia
Células Endoteliais/efeitos dos fármacos
Células Endoteliais/imunologia
Feminino
Seres Humanos
Interleucina-6/imunologia
Interleucina-6/secreção
Interleucina-8/imunologia
Interleucina-8/secreção
Macrófagos/imunologia
Placenta/citologia
Placenta/imunologia
Gravidez
Primeiro Trimestre da Gravidez
Trofoblastos/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL14 protein, human); 0 (CXCL6 protein, human); 0 (Chemokine CXCL6); 0 (Chemokines, CC); 0 (Culture Media); 0 (IL6 protein, human); 0 (IL8 protein, human); 0 (Interleukin-6); 0 (Interleukin-8)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170412
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601175


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[PMID]:27706571
[Au] Autor:Ai S; Lin YY; Zheng J; Qiu CX; Liu YJ; Lin X
[Ad] Endereço:People's Hospital Affiliated to Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, China.
[Ti] Título:Effects of Shenkangling intervention on the MAPK pathway in rats with doxorubicin-induced nephropathy.
[So] Source:Genet Mol Res;15(3), 2016 Aug 19.
[Is] ISSN:1676-5680
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Shenkangling plays a role of Yishenhuoxue effect for the treatment of children with nephrotic syndrome. The aim of this study was to investigate the effects of Shenkangling intervention on the mitogen-activated protein kinase (MAPK) pathway in rats with Adriamycin-induced nephropathy (AN) and its underlying mechanism of action. Nephrosis was induced in healthy Sprague-Dawley rats by doxorubicin and the rats were untreated or treated with prednisone, simvastatin, Shenkangling, or a combination thereof. Using real-time PCR, the mRNA expression levels of Chemokine (C-X-C motif) ligand 16 (CXCL16), A Disintegrin and metalloproteinase domain-containing protein 10 (ADAM10), and ADAM17 in the renal tissues of these rats were found to be decreased by the various treatments compared to those in the untreated doxorubicin-induced nephrosis rats. To quantify the activation of the MAPK pathway, western blotting was used to detect the phosphorylation levels of MAPK pathway-associated proteins (p38, ERK1/2, SAPK/JNK) and nuclear factor (NF)-κB p65, which were reduced by the various treatments compared to those in the untreated doxorubicin-induced rats. Serum levels of transforming growth factor (TGF)-ß1, tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, and IL-6, quantified by ELISA, were decreased by the various treatments compared to the levels in the untreated doxorubicin-induced nephrosis rats. The rats treated with prednisone, simvastatin, and Shenkangling showed the best outcome. The Chinese medicine Shenkangling that is known for nourishing the kidney and promoting blood circulation reduced urinary protein levels, increased serum albumin levels, and reduced cholesterol levels by reducing the release of CXCL16, ADAM10, ADAM17, TGF-ß1, TNF-α, IL-1ß, IL- 6, and other inflammatory mediators and inhibiting the activation of the MAPK signaling pathway, thereby effectively improving the state of nephropathy in AN rats. These results indicate that Shenkangling can be used clinically to treat nephropathy.
[Mh] Termos MeSH primário: Medicamentos de Ervas Chinesas/farmacologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Síndrome Nefrótica/tratamento farmacológico
[Mh] Termos MeSH secundário: Proteína ADAM10/genética
Proteína ADAM17/genética
Animais
Quimiocina CXCL6/genética
Doxorrubicina/toxicidade
Interleucina-1beta/sangue
Interleucina-6/sangue
Masculino
NF-kappa B/metabolismo
Síndrome Nefrótica/sangue
Síndrome Nefrótica/induzido quimicamente
Síndrome Nefrótica/enzimologia
Proteinúria/tratamento farmacológico
Proteinúria/enzimologia
Proteinúria/metabolismo
Ratos
Ratos Sprague-Dawley
Fator de Crescimento Transformador beta1/sangue
Fator de Necrose Tumoral alfa/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CXCL6); 0 (Drugs, Chinese Herbal); 0 (Interleukin-1beta); 0 (Interleukin-6); 0 (NF-kappa B); 0 (Transforming Growth Factor beta1); 0 (Tumor Necrosis Factor-alpha); 80168379AG (Doxorubicin); EC 3.4.24.81 (ADAM10 Protein); EC 3.4.24.81 (ADAM10 protein, rat); EC 3.4.24.86 (ADAM17 Protein); EC 3.4.24.86 (Adam17 protein, rat)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170403
[Lr] Data última revisão:
170403
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161006
[St] Status:MEDLINE
[do] DOI:10.4238/gmr.15038131


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[PMID]:27520585
[Au] Autor:Moazzeni H; Akbari MT; Yazdani S; Elahi E
[Ad] Endereço:Department of Medical Genetics, Faculty of Medical Sciences, Tarbiat Modares University, P.O. Box. 14115-331, Tehran, Iran.
[Ti] Título:Expression of CXCL6 and BBS5 that may be glaucoma relevant genes is regulated by PITX2.
[So] Source:Gene;593(1):76-83, 2016 Nov 15.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The transcription factor PITX2 is implicated in glaucoma pathology. In an earlier study we had used microarray analysis to identify genes in the trabecular meshwork (TM) that are affected by knock down of PITX2. Here, those studies were pursued to identify genes that are direct targets of PITX2 and that may be relevant to glaucoma. Initially, bioinformatics tools were used to select among the genes that had been affected by PITX2 knock down those that have PITX2 binding sites and that may be involved in glaucoma related functions. Subsequently, the effect of PITX2 was tested using the dual luciferase assay in four cell cultures including two primary TM cultures co-transfected with vectors containing promoter fragments of six candidate genes upstream of a luciferase gene and a vector that expressed PITX2. Finally, the effect of PITX2 on endogenous expression of two genes was assessed by over expression and knock down of PITX2 in TM cells. Thirty four genes were found to contain PITX2 binding sites in their putative promoter regions, and 16 were found to be associated with TM-specific and/or glaucoma associated functions. Results of dual luciferase assays confirmed that two of six genes tested were directly targeted by PITX2. The two genes were CXCL6 (chemokine (C-X-C motif) ligand 6) and BBS5 (Bardet-Biedl syndrome 5). Over expression and knock down of PITX2 showed that this transcription factor affects endogenous expression of these two genes in TM cells. CXCL6 encodes a pro-inflammatory cytokine, and many studies have suggested that cytokines and other immune system functions are involved in glaucoma pathogenesis. BBS5 is a member of the BBS family of genes that affect ciliary functions, and ciliary bodies in the anterior chamber of the eye produce the aqueous fluid that affects intraocular pressure. Immune related functions and intraocular pressure are both important components of glaucoma pathology. The role of PITX2 in glaucoma may be mediated partly by regulating the expression of CXCL6 and BBS5 and thus affecting immune functions and intraocular pressure.
[Mh] Termos MeSH primário: Câmara Anterior/metabolismo
Quimiocina CXCL6/biossíntese
Proteínas do Olho/metabolismo
Regulação da Expressão Gênica
Glaucoma/metabolismo
Proteínas de Homeodomínio/metabolismo
Proteínas/metabolismo
Elementos de Resposta
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Quimiocina CXCL6/genética
Cílios/genética
Cílios/metabolismo
Proteínas do Olho/genética
Feminino
Glaucoma/genética
Glaucoma/patologia
Proteínas de Homeodomínio/genética
Seres Humanos
Pressão Intraocular/genética
Masculino
Proteínas/genética
Fatores de Transcrição/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BBS5 protein, human); 0 (CXCL6 protein, human); 0 (Chemokine CXCL6); 0 (Eye Proteins); 0 (Homeodomain Proteins); 0 (Proteins); 0 (Transcription Factors); 184787-43-7 (homeobox protein PITX2)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:171008
[Lr] Data última revisão:
171008
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160814
[St] Status:MEDLINE


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[PMID]:27496882
[Au] Autor:Ma Z; Jin X; He L; Wang Y
[Ad] Endereço:Selzman Institute for Kidney Health and Section of Nephrology, Department of Medicine, Baylor College of Medicine, Houston, Texas; Section of Nephrology, Department of Medicine, Shuguang Hospital, Shanghai, China; and.
[Ti] Título:CXCL16 regulates renal injury and fibrosis in experimental renal artery stenosis.
[So] Source:Am J Physiol Heart Circ Physiol;311(3):H815-21, 2016 Sep 01.
[Is] ISSN:1522-1539
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recent studies have shown that inflammation plays a critical role in the initiation and progression of hypertensive kidney disease, including renal artery stenosis. However, the signaling mechanisms underlying the induction of inflammation are poorly understood. We found that CXCL16 was induced in the kidney in a murine model of renal artery stenosis. To determine whether CXCL16 is involved in renal injury and fibrosis, wild-type and CXCL16 knockout mice were subjected to renal artery stenosis induced by placing a cuff on the left renal artery. Wild-type and CXCL16 knockout mice had comparable blood pressure at baseline. Renal artery stenosis caused an increase in blood pressure that was similar between wild-type and CXCL16 knockout mice. CXCL16 knockout mice were protected from RAS-induced renal injury and fibrosis. CXCL16 deficiency suppressed bone marrow-derived fibroblast accumulation and myofibroblast formation in the stenotic kidneys, which was associated with less expression of extracellular matrix proteins. Furthermore, CXCL16 deficiency inhibited infiltration of F4/80(+) macrophages and CD3(+) T cells in the stenotic kidneys compared with those of wild-type mice. Taken together, our results indicate that CXCL16 plays a pivotal role in the pathogenesis of renal artery stenosis-induced renal injury and fibrosis through regulation of bone marrow-derived fibroblast accumulation and macrophage and T-cell infiltration.
[Mh] Termos MeSH primário: Lesão Renal Aguda/genética
Quimiocina CXCL6/genética
Fibroblastos
Rim/patologia
Macrófagos/imunologia
Obstrução da Artéria Renal/genética
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Lesão Renal Aguda/imunologia
Animais
Pressão Sanguínea
Western Blotting
Células da Medula Óssea
Quimiocina CXCL16
Quimiocina CXCL6/imunologia
Modelos Animais de Doenças
Fibrose/genética
Fibrose/imunologia
Imunofluorescência
Frequência Cardíaca
Hipertensão/complicações
Hipertensão/imunologia
Rim/imunologia
Rim/metabolismo
Masculino
Camundongos
Camundongos Knockout
Reação em Cadeia da Polimerase em Tempo Real
Obstrução da Artéria Renal/imunologia
Insuficiência Renal Crônica/etiologia
Insuficiência Renal Crônica/imunologia
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CXCL16); 0 (Chemokine CXCL6); 0 (Cxcl16 protein, mouse)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160807
[St] Status:MEDLINE
[do] DOI:10.1152/ajpheart.00948.2015


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[PMID]:27211287
[Au] Autor:Kiku Y; Nagasawa Y; Tanabe F; Sugawara K; Watanabe A; Hata E; Ozawa T; Nakajima KI; Arai T; Hayashi T
[Ad] Endereço:Hokkaido Research Station, National Institute of Animal Health, NARO, Sapporo, Hokkaido 062-0045, Japan.
[Ti] Título:The cell wall component lipoteichoic acid of Staphylococcus aureus induces chemokine gene expression in bovine mammary epithelial cells.
[So] Source:J Vet Med Sci;78(9):1505-1510, 2016 Oct 01.
[Is] ISSN:1347-7439
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Staphylococcus aureus (SA) is a major cause of bovine mastitis, but its pathogenic mechanism remains poorly understood. To evaluate the role of lipoteichoic acid (LTA) in the immune or inflammatory response of SA mastitis, we investigated the gene expression profile in bovine mammary epithelial cells stimulated with LTA alone or with formalin-killed SA (FKSA) using cap analysis of gene expression. Seven common differentially expressed genes related to immune or inflammatory mediators were up-regulated under both LTA and FKSA stimulations. Three of these genes encode chemokines (IL-8, CXCL6 and CCL2) functioning as chemoattractant molecules for neutrophils and macrophages. These results suggest that the initial inflammatory response of SA infection in mammary gland may be related with LTA induced chemokine genes.
[Mh] Termos MeSH primário: Quimiocinas/metabolismo
Lipopolissacarídeos/farmacocinética
Glândulas Mamárias Animais/citologia
Ácidos Teicoicos/farmacocinética
[Mh] Termos MeSH secundário: Animais
Bovinos
Quimiocina CCL2/metabolismo
Quimiocina CXCL6/metabolismo
Células Epiteliais/efeitos dos fármacos
Células Epiteliais/metabolismo
Feminino
Expressão Gênica/efeitos dos fármacos
Interleucina-8/metabolismo
Glândulas Mamárias Animais/efeitos dos fármacos
Glândulas Mamárias Animais/metabolismo
Staphylococcus aureus/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CCL2); 0 (Chemokine CXCL6); 0 (Chemokines); 0 (Interleukin-8); 0 (Lipopolysaccharides); 0 (Teichoic Acids); 56411-57-5 (lipoteichoic acid)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170622
[Lr] Data última revisão:
170622
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160524
[St] Status:MEDLINE


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[PMID]:27095254
[Au] Autor:Chen C; Shi L; Li Y; Wang X; Yang S
[Ad] Endereço:Department of Respiratory Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, China.
[Ti] Título:Disease-specific dynamic biomarkers selected by integrating inflammatory mediators with clinical informatics in ARDS patients with severe pneumonia.
[So] Source:Cell Biol Toxicol;32(3):169-84, 2016 06.
[Is] ISSN:1573-6822
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Acute respiratory distress syndrome (ARDS) is a heterogeneous syndrome that occurs as a result of various risk factors, including either direct or indirect lung injury, and systemic inflammation triggered also by severe pneumonia (SP). SP-ARDS-associated morbidity and mortality remains high also due to the lack of disease-specific biomarkers. The present study aimed at identifying disease-specific biomarkers in SP or SP-ARDS by integrating proteomic profiles of inflammatory mediators with clinical informatics. Plasma was sampled from the healthy as controls or patients with SP infected with bacteria or infection-associated SP-ARDS on the day of admission, day 3, and day 7. About 15 or 52 cytokines showed significant difference between SP and SP-ARDS patients with controls or 13 between SP-ARDS with SP alone and controls, including bone morphogenetic protein-15 (BMP-15), chemokine (C-X-C motif) ligand 16 (CXCL16), chemokine (C-X-C motif) receptor 3 (CXCR3), interleukin-6 (IL-6), protein NOV homolog (NOV/CCN3), glypican 3, insulin-like growth factor binding protein 4 (IGFBP-4), IL-5, IL-5 R alpha, IL-22 BP, leptin, MIP-1d, and orexin B with a significant correlation with Digital Evaluation Score System (DESS) scores. ARDS patients with overexpressed IL-6, CXCL16, or IGFBP-4 had significantly longer hospital stay and higher incidence of secondary infection. We also found higher levels of those mediators were associated with poor survival rates in patients with lung cancer and involved in the process of the epithelial mesenchymal transition of alveolar epithelial cells. Our preliminary study suggested that integration of proteomic profiles with clinical informatics as part of clinical bioinformatics is important to validate and optimize disease-specific and disease-staged biomarkers.
[Mh] Termos MeSH primário: Mediadores da Inflamação/sangue
Pneumonia/sangue
Síndrome do Desconforto Respiratório do Adulto/sangue
[Mh] Termos MeSH secundário: Adulto
Idoso
Biomarcadores/sangue
Estudos de Casos e Controles
Quimiocina CXCL6/sangue
Citocinas/sangue
Feminino
Seres Humanos
Inflamação/sangue
Inflamação/patologia
Interleucina-6/sangue
Masculino
Informática Médica/métodos
Meia-Idade
Pneumonia/diagnóstico
Pneumonia/patologia
Prognóstico
Proteômica
Síndrome do Desconforto Respiratório do Adulto/diagnóstico
Síndrome do Desconforto Respiratório do Adulto/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (CXCL6 protein, human); 0 (Chemokine CXCL6); 0 (Cytokines); 0 (IL6 protein, human); 0 (Inflammation Mediators); 0 (Interleukin-6)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170309
[Lr] Data última revisão:
170309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160421
[St] Status:MEDLINE
[do] DOI:10.1007/s10565-016-9322-4


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[PMID]:27032929
[Au] Autor:Li Z; Zhang Q; Zhang Q; Xu M; Qu Y; Cai X; Lu L
[Ad] Endereço:Department of Gastroenterology and Hepatology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 20080, China.
[Ti] Título:CXCL6 promotes human hepatocyte proliferation through the CXCR1-NFκB pathway and inhibits collagen I secretion by hepatic stellate cells.
[So] Source:Biochem Cell Biol;94(3):229-35, 2016 Jun.
[Is] ISSN:1208-6002
[Cp] País de publicação:Canada
[La] Idioma:eng
[Ab] Resumo:Hepatocyte proliferation and collagen I (COLI) secretion are important processes during liver regeneration. This study aimed to investigate the role of CXCL6 in hepatocyte proliferation and COLI secretion. Serum CXCL6 levels in patients with chronic hepatitis B (CHB) were examined and the effects of CXCL6 on the proliferation of L02 hepatocytes and the secretion of COLI from LX2 human hepatic stellate cells were evaluated. We found that serum CXCL6 levels increased gradually with disease progression of CHB, and there was positive correlation between serum CXCL6 level and alanine transaminase (ALT) and aspartate transaminase (AST). In vitro, CXCL6 promoted L02 proliferation but this was blocked upon CXCR1 knockdown. The level of phospho-IκBα was upregulated by CXCL6 but downregulated by CXCR1 siRNA in L02 cells. CXCL6 inhibited the secretion of COLI by LX2 cells, dependent on CXCR1 and CXCR2. Taken together, these data suggest that increased expression of CXCL6 during CHB could promote hepatocyte proliferation through the CXCR1-NFκB pathway and inhibit the secretion of COLI by hepatic stellate cells.
[Mh] Termos MeSH primário: Quimiocina CXCL6/metabolismo
Colágeno Tipo I/secreção
Hepatite B Crônica/metabolismo
NF-kappa B/metabolismo
Receptores de Interleucina-8A/metabolismo
[Mh] Termos MeSH secundário: Adulto
Linhagem Celular
Proliferação Celular
Feminino
Células Estreladas do Fígado/secreção
Hepatite B Crônica/patologia
Hepatócitos/citologia
Hepatócitos/metabolismo
Hepatócitos/patologia
Seres Humanos
Masculino
Redes e Vias Metabólicas
Meia-Idade
Receptores de Interleucina-8A/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL6 protein, human); 0 (Chemokine CXCL6); 0 (Collagen Type I); 0 (NF-kappa B); 0 (Receptors, Interleukin-8A)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170620
[Lr] Data última revisão:
170620
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160402
[St] Status:MEDLINE
[do] DOI:10.1139/bcb-2015-0136


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[PMID]:26844528
[Au] Autor:Matter MS; Marquardt JU; Andersen JB; Quintavalle C; Korokhov N; Stauffer JK; Kaji K; Decaens T; Quagliata L; Elloumi F; Hoang T; Molinolo A; Conner EA; Weber A; Heikenwalder M; Factor VM; Thorgeirsson SS
[Ad] Endereço:Laboratory of Experimental Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD.
[Ti] Título:Oncogenic driver genes and the inflammatory microenvironment dictate liver tumor phenotype.
[So] Source:Hepatology;63(6):1888-99, 2016 Jun.
[Is] ISSN:1527-3350
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: The majority of hepatocellular carcinoma develops in the background of chronic liver inflammation caused by viral hepatitis and alcoholic or nonalcoholic steatohepatitis. However, the impact of different types of chronic inflammatory microenvironments on the phenotypes of tumors generated by distinct oncogenes is largely unresolved. To address this issue, we generated murine liver tumors by constitutively active AKT-1 (AKT) and ß-catenin (CAT), followed by induction of chronic liver inflammation by 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) and carbon tetrachloride. Also, the impact of DDC-induced chronic liver inflammation was compared between two liver tumor models using a combination of AKT-CAT or AKT-NRAS(G12V) . Treatment with DDC and carbon tetrachloride significantly facilitated the adenoma-to-carcinoma conversion and accelerated the growth of AKT-CAT tumors. Furthermore, DDC treatment altered the morphology of AKT-CAT tumors and caused loss of lipid droplets. Transcriptome analysis of AKT-CAT tumors revealed that cellular growth and proliferation were mainly affected by chronic inflammation and caused up-regulation of Cxcl16, Galectin-3, and Nedd9, among others. Integration with transcriptome profiles from human hepatocellular carcinomas further demonstrated that AKT-CAT tumors generated in the context of chronic liver inflammation showed enrichment of poor prognosis gene sets or decrease of good prognosis gene sets. In contrast, DDC had a more subtle effect on AKT-NRAS(G12V) tumors and primarily enhanced already existent tumor characteristics as supported by transcriptome analysis. However, it also reduced lipid droplets in AKT-NRAS(G12V) tumors. CONCLUSION: Our study suggests that liver tumor phenotype is defined by a combination of driving oncogenes but also the nature of chronic liver inflammation. (Hepatology 2016;63:1888-1899).
[Mh] Termos MeSH primário: Hepatite Animal/complicações
Neoplasias Hepáticas Experimentais/etiologia
Oncogenes
Proteínas Proto-Oncogênicas c-akt/metabolismo
beta Catenina/metabolismo
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Animais
Tetracloreto de Carbono
Linhagem Celular
Quimiocina CXCL16
Quimiocina CXCL6/metabolismo
Feminino
Galectina 3/metabolismo
Hepatite Animal/induzido quimicamente
Neoplasias Hepáticas Experimentais/metabolismo
Camundongos
Fenótipo
Piridinas
Transcriptoma
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3,5-diethoxycarbonyl-1,4-dihydrocollidine); 0 (Adaptor Proteins, Signal Transducing); 0 (Chemokine CXCL16); 0 (Chemokine CXCL6); 0 (Cxcl16 protein, mouse); 0 (Galectin 3); 0 (NEDD9 protein, mouse); 0 (Pyridines); 0 (beta Catenin); CL2T97X0V0 (Carbon Tetrachloride); EC 2.7.11.1 (Akt1 protein, mouse); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160205
[St] Status:MEDLINE
[do] DOI:10.1002/hep.28487



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