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[PMID]:28460571
[Au] Autor:Gautam SK; Kumar S; Cannon A; Hall B; Bhatia R; Nasser MW; Mahapatra S; Batra SK; Jain M
[Ad] Endereço:a Department of Biochemistry and Molecular Biology , University of Nebraska Medical Center , Omaha , NE , USA.
[Ti] Título:MUC4 mucin- a therapeutic target for pancreatic ductal adenocarcinoma.
[So] Source:Expert Opin Ther Targets;21(7):657-669, 2017 07.
[Is] ISSN:1744-7631
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Pancreatic cancer (PC) is characterized by mucin overexpression. MUC4 is the most differentially overexpressed membrane-bound mucin that plays a functional role in disease progression and therapy resistance. Area covered: We describe the clinicopathological significance of MUC4, summarize mechanisms contributing to its deregulated expression, review preclinical studies aimed at inhibiting MUC4, and discuss how MUC4 overexpression provides opportunities for developing targeted therapies. Finally, we discuss the challenges for developing MUC4-based therapeutics, and identify areas where efforts should be directed to effectively exploit MUC4 as a therapeutic target for PC. Expert opinion: Studies demonstrating that abrogation of MUC4 expression reduces proliferation and metastasis of PC cells and enhances sensitivity to therapeutic agents affirm its utility as a therapeutic target. Emerging evidence also supports the suitability of MUC4 as a potential immunotherapy target. However, these studies have been limited to in vitro, ex vivo or in vivo approaches using xenograft tumors in immunodeficient murine models. For translational relevance, MUC4-targeted therapies should be evaluated in murine models with intact immune system and accurate tumor microenvironment. Additionally, future studies evaluating MUC4 as a target for immunotherapy must entail characterization of immune response in PC patients and investigate its association with immunosuppression and survival.
[Mh] Termos MeSH primário: Carcinoma Ductal Pancreático/tratamento farmacológico
Mucina-4/genética
Neoplasias Pancreáticas/tratamento farmacológico
[Mh] Termos MeSH secundário: Adenocarcinoma/tratamento farmacológico
Adenocarcinoma/genética
Adenocarcinoma/patologia
Animais
Antineoplásicos/farmacologia
Antineoplásicos/uso terapêutico
Carcinoma Ductal Pancreático/genética
Carcinoma Ductal Pancreático/patologia
Progressão da Doença
Desenho de Drogas
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Imunoterapia/métodos
Camundongos
Terapia de Alvo Molecular
Neoplasias Pancreáticas/genética
Neoplasias Pancreáticas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Mucin-4)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1080/14728222.2017.1323880


  2 / 410 MEDLINE  
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[PMID]:29061782
[Au] Autor:Urey C; Hilmersson KS; Andersson B; Ansari D; Andersson R
[Ad] Endereço:Department of Surgery, Clinical Sciences Lund, Skane University Hospital, Lund University, Lund, Sweden.
[Ti] Título:Development and Characterization of a Gemcitabine-loaded MUC4-targeted Immunoliposome Against Pancreatic Ductal Adenocarcinoma.
[So] Source:Anticancer Res;37(11):6031-6039, 2017 11.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Pancreatic Ductal adeno-carcinoma (PDAC) is a devastating disease. Gemcitabine is the standard chemotherapeutic agent against PDAC but has only limited effectiveness. The aim of the study was to develop and study the targeting affinity and in vitro antiproliferative effect of a MUC4-targeted gemcitabine-loaded immuno-liposome for treatment of PDAC. MATERIALS AND METHODS: Gemcitabine-loaded immunoliposomes were developed by grafting anti-MUC4 antibodies to the liposomal surface. Targeting affinity was compared in vitro between immunoliposomes and non-targeted liposomes and anti-proliferative effect was compared in vitro between free drug, non-targeted liposomal gemcitabine and MUC4-targeted immunoliposomal gemcitabine on a MUC4-positive pancreatic cancer cell line, Capan-1. RESULTS: Development of a MUC4-targeted immunoliposome was confirmed and characterized by immunoblots and size characterization. The MUC4-targeted immunoliposome showed a significantly higher targeting affinity compared to the non-targeted liposomes and also showed an improved antiproliferative effect compared to free and non-targeted liposomal drug. CONCLUSION: Successful development and characterization of a MUC4-targeted immunoliposome shows promising results for a targeted treatment and improved retention of gemcitabine for treatment of PDAC.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/farmacologia
Carcinoma Ductal Pancreático/patologia
Desoxicitidina/análogos & derivados
Lipossomos/administração & dosagem
Mucina-4/antagonistas & inibidores
Neoplasias Pancreáticas/patologia
[Mh] Termos MeSH secundário: Antimetabólitos Antineoplásicos/farmacologia
Apoptose/efeitos dos fármacos
Carcinoma Ductal Pancreático/tratamento farmacológico
Carcinoma Ductal Pancreático/imunologia
Proliferação Celular/efeitos dos fármacos
Desoxicitidina/farmacologia
Sinergismo Farmacológico
Seres Humanos
Técnicas In Vitro
Lipossomos/química
Mucina-4/imunologia
Neoplasias Pancreáticas/tratamento farmacológico
Neoplasias Pancreáticas/imunologia
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antimetabolites, Antineoplastic); 0 (Liposomes); 0 (Mucin-4); 0W860991D6 (Deoxycytidine); B76N6SBZ8R (gemcitabine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171025
[St] Status:MEDLINE


  3 / 410 MEDLINE  
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[PMID]:28866095
[Au] Autor:Sadras T; Heatley SL; Kok CH; Dang P; Galbraith KM; McClure BJ; Muskovic W; Venn NC; Moore S; Osborn M; Revesz T; Moore AS; Hughes TP; Yeung D; Sutton R; White DL
[Ad] Endereço:Cancer Theme, South Australian Health & Medical Research Institute, Adelaide, SA, Australia; Discipline of Medicine, University of Adelaide, Adelaide, SA, Australia.
[Ti] Título:Differential expression of MUC4, GPR110 and IL2RA defines two groups of CRLF2-rearranged acute lymphoblastic leukemia patients with distinct secondary lesions.
[So] Source:Cancer Lett;408:92-101, 2017 Nov 01.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:CRLF2-rearrangements (CRLF2-r) occur frequently in Ph-like B-ALL, a high-risk ALL sub-type characterized by a signaling profile similar to Ph + ALL, however accumulating evidence indicates genetic heterogeneity within CRLF2-r ALL. We performed thorough genomic characterization of 35 CRLF2-r cases (P2RY8-CRLF2 n = 18; IGH-CRLF2 n = 17). Activating JAK2 mutations were present in 34% of patients, and a CRLF2-F232C mutation was identified in an additional 17%. IKZF1 deletions were detected in 63% of cases. The majority of patients (26/35) classified as Ph-like, and these were characterized by significantly higher levels of MUC4, GPR110 and IL2RA/CD25. In addition, Ph-like CRLF2-r samples were significantly enriched for IKZF1 deletions, JAK2/CRLF2 mutations and increased expression of JAK/STAT target genes (CISH, SOCS1), suggesting that mutation-driven CRLF2/JAK2 activation is more frequent in this sub-group. Less is known about the genomics of CRLF2-r cases lacking JAK2-pathway mutations, but KRAS/NRAS mutations were identified in 4/9 non-Ph-like samples. This work highlights the heterogeneity of secondary lesions which may arise and influence intracellular-pathway activation in CRLF2-r patients, and importantly presents distinct therapeutic targets within a group of patients harboring identical primary translocations, for whom efficient directed therapies are currently lacking.
[Mh] Termos MeSH primário: Regulação Leucêmica da Expressão Gênica
Rearranjo Gênico
Subunidade alfa de Receptor de Interleucina-2/metabolismo
Mucina-4/metabolismo
Proteínas Oncogênicas/metabolismo
Leucemia-Linfoma Linfoblástico de Células Precursoras/patologia
Receptores de Citocinas/genética
Receptores Acoplados a Proteínas-G/metabolismo
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Subunidade alfa de Receptor de Interleucina-2/genética
Janus Quinase 2/genética
Janus Quinase 2/metabolismo
Mucina-4/genética
Mutação/genética
Proteínas Oncogênicas/genética
Cromossomo Filadélfia
Leucemia-Linfoma Linfoblástico de Células Precursoras/genética
Leucemia-Linfoma Linfoblástico de Células Precursoras/metabolismo
Prognóstico
Receptores Acoplados a Proteínas-G/genética
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CRLF2 protein, human); 0 (GPR110 protein, human); 0 (IL2RA protein, human); 0 (Interleukin-2 Receptor alpha Subunit); 0 (MUC4 protein, human); 0 (Mucin-4); 0 (Oncogene Proteins); 0 (Receptors, Cytokine); 0 (Receptors, G-Protein-Coupled); EC 2.7.10.2 (JAK2 protein, human); EC 2.7.10.2 (Janus Kinase 2)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170904
[St] Status:MEDLINE


  4 / 410 MEDLINE  
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[PMID]:28270046
[Au] Autor:Urey C; Andersson B; Ansari D; Sasor A; Said-Hilmersson K; Nilsson J; Andersson R
[Ad] Endereço:a Department of Surgery , Clinical Sciences Lund, Skåne University Hospital, Lund University , Lund , Sweden.
[Ti] Título:Low MUC4 expression is associated with survival benefit in patients with resectable pancreatic cancer receiving adjuvant gemcitabine.
[So] Source:Scand J Gastroenterol;52(5):595-600, 2017 May.
[Is] ISSN:1502-7708
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Previous in vitro studies have shown that mucin 4 (MUC4) confers resistance toward gemcitabine in pancreatic cancer cells. To date, there are few clinical studies corroborating these findings. The aim of this study was to evaluate the predictive impact of MUC4 expression on survival in patients with resectable pancreatic cancer receiving adjuvant gemcitabine. MATERIALS AND METHODS: MUC4 expression was investigated by immunohistochemistry in 78 tissue sections from patients with pancreatic ductal adenocarcinoma undergoing Whipple resection. The H-score was used to evaluate MUC4 expression. The Kaplan-Meier method and Cox proportional hazards regression analysis were used to assess the predictive role of MUC4 expression. RESULTS: The MUC4 protein was expressed in 93.6% (73/78) of pancreatic cancer tissue specimens. None of the normal control pancreatic tissues had any MUC4 expression. Low MUC4 expression (H-score ≤100) was detectable in 42 (53.8%) of tumors and high MUC4 expression (H-score >100) was detectable in 36 (46.2%) of tumors. Low expression of MUC4 was associated with favorable survival (p = .027), whereas high MUC4 expression did not correlate with survival (p = .87) in patients receiving adjuvant gemcitabine treatment. CONCLUSIONS: This is the first study indicating a predictive role of MUC4 expression for gemcitabine treatment in the clinical setting.
[Mh] Termos MeSH primário: Antimetabólitos Antineoplásicos/uso terapêutico
Carcinoma Ductal Pancreático/tratamento farmacológico
Desoxicitidina/análogos & derivados
Mucina-4/metabolismo
Neoplasias Pancreáticas/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Idoso
Carcinoma Ductal Pancreático/genética
Carcinoma Ductal Pancreático/mortalidade
Desoxicitidina/uso terapêutico
Feminino
Seres Humanos
Imuno-Histoquímica
Masculino
Meia-Idade
Mucina-4/genética
Pâncreas/patologia
Neoplasias Pancreáticas/genética
Neoplasias Pancreáticas/mortalidade
Análise de Sobrevida
Suécia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimetabolites, Antineoplastic); 0 (MUC4 protein, human); 0 (Mucin-4); 0W860991D6 (Deoxycytidine); B76N6SBZ8R (gemcitabine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170309
[St] Status:MEDLINE
[do] DOI:10.1080/00365521.2017.1290134


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[PMID]:27923652
[Au] Autor:Xu D; Liu S; Zhang L; Song L
[Ad] Endereço:Department of Obstetrics & Gynaecology, Cangzhou Central Hospital, Hebei, 061001, China.
[Ti] Título:MiR-211 inhibits invasion and epithelial-to-mesenchymal transition (EMT) of cervical cancer cells via targeting MUC4.
[So] Source:Biochem Biophys Res Commun;485(2):556-562, 2017 Apr 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The dysregulated molecules and their involvement in lymph node metastases of cervical cancer are far from been fully revealed. In this study, by reviewing MUC4 expression in The Human Protein Atlas and retrieving gene microarray data in GEO dataset (No. GDS4664), we found that MUC4 upregulation is associated with lymph node metastasis in cervical cancer. Knockdown of MUC4 in Hela and SiHa cells significantly reduced their invasion and also reduced the mesenchymal properties. By performing bioinformatics analysis, we observed that miR-211 is a potential suppressor of MUC4, which has a predicted highly conserved binding site in the 3'UTR of MUC among mammals. The following assays confirmed that miR-211 can directly target the 3'UTR of MUC4 and inhibit its expression at both mRNA and protein levels. In addition, enforced miR-211 expression phenocopies the effects of MUC4 siRNA in inhibiting cervical cancer cell invasion and reversing EMT properties. Therefore, we infer that miR-211 is a novel miRNA with suppressive effect on MUC4 expression and can inhibit cervical cancer cell invasion and EMT.
[Mh] Termos MeSH primário: Transição Epitelial-Mesenquimal/genética
Regulação Neoplásica da Expressão Gênica
MicroRNAs/genética
Mucina-4/genética
Neoplasias do Colo do Útero/genética
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas/genética
Sequência de Bases
Western Blotting
Linhagem Celular Tumoral
Movimento Celular/genética
Feminino
Perfilação da Expressão Gênica/estatística & dados numéricos
Células HeLa
Seres Humanos
Microscopia de Fluorescência
Mucina-4/metabolismo
Invasividade Neoplásica
Análise de Sequência com Séries de Oligonucleotídeos/estatística & dados numéricos
Interferência de RNA
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Homologia de Sequência do Ácido Nucleico
Neoplasias do Colo do Útero/metabolismo
Neoplasias do Colo do Útero/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (MIRN211 microRNA, human); 0 (MUC4 protein, human); 0 (MicroRNAs); 0 (Mucin-4)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170613
[Lr] Data última revisão:
170613
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161208
[St] Status:MEDLINE


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[PMID]:27872404
[Au] Autor:O'Neil A; Petersen CP; Choi E; Engevik AC; Goldenring JR
[Ad] Endereço:Department of Surgery (AO, EC, ACE, JRG), Vanderbilt University Medical Center, Nashville, Tennessee.
[Ti] Título:Unique Cellular Lineage Composition of the First Gland of the Mouse Gastric Corpus.
[So] Source:J Histochem Cytochem;65(1):47-58, 2017 01.
[Is] ISSN:1551-5044
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The glandular stomach has two major zones: the acid secreting corpus and the gastrin cell-containing antrum. Nevertheless, a single gland lies at the transition between the forestomach and corpus in the mouse stomach. We have sought to define the lineages that make up this gland unit at the squamocolumnar junction. The first gland in mice showed a notable absence of characteristic corpus lineages, including parietal cells and chief cells. In contrast, the gland showed strong staining of Griffonia simplicifolia-II (GSII)-lectin-positive mucous cells at the bases of glands, which were also positive for CD44 variant 9 and Clusterin. Prominent numbers of doublecortin-like kinase 1 (DCLK1) positive tuft cells were present in the first gland. The first gland contained Lgr5-expressing putative progenitor cells, and a large proportion of the cells were positive for Sox2. The cells of the first gland stained strongly for MUC4 and EpCAM, but both were absent in the normal corpus mucosa. The present studies indicate that the first gland in the corpus represents a unique anatomic entity. The presence of a concentration of progenitor cells and sensory tuft cells in this gland suggests that it may represent a source of reserve reparative cells for adapting to severe mucosal damage.
[Mh] Termos MeSH primário: Mucosa Gástrica/citologia
Células-Tronco/citologia
Estômago/citologia
[Mh] Termos MeSH secundário: Animais
Clusterina/análise
Mucosa Gástrica/ultraestrutura
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Mucina-4/análise
Células Parietais Gástricas/citologia
Lectinas de Plantas/análise
Proteínas Serina-Treonina Quinases/análise
Receptores Acoplados a Proteínas-G/análise
Fatores de Transcrição SOXB1/análise
Células-Tronco/ultraestrutura
Estômago/ultraestrutura
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Clusterin); 0 (Griffonia simplicifolia lectins); 0 (Lgr5 protein, mouse); 0 (Muc4 protein, mouse); 0 (Mucin-4); 0 (Plant Lectins); 0 (Receptors, G-Protein-Coupled); 0 (SOXB1 Transcription Factors); 0 (Sox2 protein, mouse); EC 2.7.1.- (Dcamkl1 protein, mouse); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161123
[St] Status:MEDLINE
[do] DOI:10.1369/0022155416678182


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[PMID]:27829225
[Au] Autor:Xia P; Choi AH; Deng Z; Yang Y; Zhao J; Wang Y; Hardwidge PR; Zhu G
[Ad] Endereço:College of Veterinary Medicine, Yangzhou University, Yangzhou, China.
[Ti] Título:Cell membrane-anchored MUC4 promotes tumorigenicity in epithelial carcinomas.
[So] Source:Oncotarget;8(8):14147-14157, 2017 Feb 21.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cell surface membrane-bound mucin protein MUC4 promotes tumorigenicity, aggressive behavior, and poor outcomes in various types of epithelial carcinomas, including pancreatic, breast, colon, ovarian, and prostate cancer. This review summarizes the theories and findings regarding MUC4 function, and its role in epithelial carcinogenesis. Based on these insights, we developed an outline of the processes and mechanisms by which MUC4 critically supports the propagation and survival of cancer cells in various epithelial organs. MUC4 may therefore be a useful prognostic and diagnostic tool that improves our ability to eradicate various forms of cancer.
[Mh] Termos MeSH primário: Carcinoma/patologia
Transformação Celular Neoplásica/metabolismo
Mucina-4/metabolismo
Neoplasias Epiteliais e Glandulares/patologia
[Mh] Termos MeSH secundário: Animais
Carcinoma/metabolismo
Membrana Celular/metabolismo
Transformação Celular Neoplásica/patologia
Seres Humanos
Neoplasias Epiteliais e Glandulares/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Mucin-4)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161110
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.13122


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[PMID]:27639937
[Au] Autor:Milara J; Morell A; Ballester B; Armengot M; Morcillo E; Cortijo J
[Ad] Endereço:Department of Pharmacy, University Hospital Consortium, Valencia, Spain; Department of Pharmacology, Faculty of Medicine, Jaume I University, Castellon, Spain; Department of Pharmacology, Faculty of Medicine, University of Valencia, Valencia, Spain; CIBERES, Health Institute Carlos III, Valencia, Sp
[Ti] Título:MUC4 impairs the anti-inflammatory effects of corticosteroids in patients with chronic rhinosinusitis with nasal polyps.
[So] Source:J Allergy Clin Immunol;139(3):855-862.e13, 2017 Mar.
[Is] ISSN:1097-6825
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Current evidence suggests that membrane-tethered mucins could mediate corticosteroid efficacy, interacting with glucocorticoid receptor (GR) in patients with chronic rhinosinusitis with nasal polyps (CRSwNP). Mucin 4 (MUC4)-tethered mucin is expressed in nasal polyp (NP) epithelial cells and upregulated under inflammatory conditions. Moreover, MUC4ß has the capacity to interact with other intracellular proteins. We hypothesized that MUC4 modulates corticosteroid efficacy of patients with CRSwNP. OBJECTIVE: We sought to analyze the role of MUC4 in corticosteroid effectiveness in different cohorts of patients with CRSwNP and elucidate the possible mechanisms involved. METHODS: Eighty-one patients with CRSwNP took oral corticosteroids for 15 days. Corticosteroid resistance was evaluated by using nasal endoscopy. Expression of MUC4 and MUC4ß was evaluated by means of real-time PCR, Western blotting, and immunohistochemistry. BEAS-2B knockdown with RNA interference for MUC4 (small interfering RNA [siRNA]-MUC4) was used to analyze the role of MUC4 in the anti-inflammatory effects of dexamethasone. RESULTS: Twenty-two patients had NPs resistant to oral corticosteroids. MUC4 expression was upregulated in these patients. In siRNA-MUC4 BEAS-2B airway epithelial cells dexamethasone produced higher anti-inflammatory effects, increased inhibition of phospho-extracellular signal-regulated kinase 1/2, increased mitogen-activated protein kinase phosphatase 1 expression, and increased glucocorticoid response element activation. Immunoprecipitation and immunofluorescence experiments revealed that MUC4ß forms a complex with GRα in the nuclei of NP epithelial cells from corticosteroid-resistant patients. CONCLUSION: MUC4ß participates in the corticosteroid resistance process, inhibiting normal GRα nuclear function. The high expression of MUC4 in patients with CRSwNP might participate in corticosteroid resistance.
[Mh] Termos MeSH primário: Anti-Inflamatórios/uso terapêutico
Resistência a Medicamentos
Mucina-4/imunologia
Pólipos Nasais/tratamento farmacológico
Pregnenodionas/uso terapêutico
Rinite/tratamento farmacológico
Sinusite/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Idoso
Anti-Inflamatórios/farmacologia
Linhagem Celular
Células Cultivadas
Doença Crônica
Dexametasona/farmacologia
Células Epiteliais/efeitos dos fármacos
Células Epiteliais/metabolismo
Feminino
Células HEK293
Seres Humanos
Masculino
Meia-Idade
Mucina-4/genética
Adulto Jovem
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (MUC4 protein, human); 0 (Mucin-4); 0 (Pregnenediones); 7S5I7G3JQL (Dexamethasone); KR5YZ6AE4B (deflazacort)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170721
[Lr] Data última revisão:
170721
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160919
[St] Status:MEDLINE


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[PMID]:28049186
[Au] Autor:Park IH; Kang JH; Kim JA; Shin JM; Lee HM
[Ad] Endereço:Department of Otorhinolaryngology, Head and Neck Surgery, Guro Hospital, Korea University College of Medicine, Seoul, South Korea.
[Ti] Título:Diesel Exhaust Particles Enhance MUC4 Expression in NCI-H292 Cells and Nasal Epithelial Cells via the p38/CREB Pathway.
[So] Source:Int Arch Allergy Immunol;171(3-4):209-216, 2016.
[Is] ISSN:1423-0097
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Diesel exhaust particles (DEPs), the major contributors to air pollution, induce inflammatory responses in the nasal epithelium. Overproduction of airway mucins is an important pathogenic finding in inflammatory airway diseases. OBJECTIVE: The aims of the present study were to determine the effect of DEPs on the expression of the mucin gene MUC4 and to investigate the underlying mechanism of DEP-induced MUC4 expression in NCI-H292 cells and primary nasal epithelial cells (PNECs). METHODS: NCI-H292 cells were stimulated for 24 h with DEPs. Messenger RNA (mRNA) and protein expression of MUC4 was determined by real-time reverse transcription (RT) polymerase chain reaction (PCR) and Western blotting. NCI-H292 cells were exposed to 3 mitogen-activated protein kinase inhibitors (U0126, SB203580, and SP600125) and a CREB (cAMP response element-binding protein) inhibitor prior to stimulation with DEPs, and MUC4 expression was examined by RT-PCR and Western blotting. PNECs were pretreated with a p38 inhibitor and CREB inhibitor prior to stimulation with DEPs, and MUC4 expression was then determined by RT-PCR and/or Western blotting. RESULTS: DEPs significantly increased the expression of MUC4 mRNA and protein. MUC4 mRNA and protein expression was inhibited by pretreatment with p38 and CREB inhibitors in NCI-H292 stimulated with DEPs. p38 and CREB inhibitors also blocked the expression of MUC4 mRNA and protein in DEP-stimulated PNECs. CONCLUSIONS: We demonstrated that DEPs stimulated the expression of MUC4 via the p38/CREB pathway in NCI-H292 cells and PNECs. The results of the present study pave the way for further studies on the role of MUC4 in DEP-induced hypersecretion in airway epithelium.
[Mh] Termos MeSH primário: Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo
Mucina-4/genética
Mucosa Nasal/metabolismo
Material Particulado/efeitos adversos
Transdução de Sinais
Emissões de Veículos
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular
Células Epiteliais
Expressão Gênica
Seres Humanos
Mucina-4/metabolismo
Emissões de Veículos/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclic AMP Response Element-Binding Protein); 0 (MUC4 protein, human); 0 (Mucin-4); 0 (Particulate Matter); 0 (Vehicle Emissions); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170104
[St] Status:MEDLINE
[do] DOI:10.1159/000453033


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[PMID]:27886047
[Au] Autor:Kim CS; Jo K; Lee IS; Kim J
[Ad] Endereço:Korean Medicine Convergence Research Division, Korea Institute of Oriental Medicine, Daejeon 34054, Korea. chskim@kiom.re.kr.
[Ti] Título:Topical Application of Apricot Kernel Extract Improves Dry Eye Symptoms in a Unilateral Exorbital Lacrimal Gland Excision Mouse.
[So] Source:Nutrients;8(11), 2016 Nov 23.
[Is] ISSN:2072-6643
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The purpose of this study was to investigate the therapeutic effects of topical application of apricot kernel extract (AKE) in a unilateral exorbital lacrimal gland excision mouse model of experimental dry eye. Dry eye was induced by surgical removal of the lacrimal gland. Eye drops containing 0.5 or 1 mg/mL AKE were administered twice a day from day 3 to day 7 after surgery. Tear fluid volume and corneal irregularity scores were determined. In addition, we examined the immunohistochemical expression level of Muc4. The topical administration of AKE dose-dependently improved all clinical dry eye symptoms by promoting the secretion of tear fluid and mucin. Thus, the results of this study indicate that AKE may be an efficacious topical agent for treating dry eye disease.
[Mh] Termos MeSH primário: Córnea/efeitos dos fármacos
Aparelho Lacrimal/cirurgia
Extratos Vegetais/farmacologia
Prunus armeniaca/química
Sementes/química
Lágrimas/secreção
Xeroftalmia/tratamento farmacológico
[Mh] Termos MeSH secundário: Administração Oftálmica
Animais
Córnea/metabolismo
Córnea/patologia
Córnea/fisiopatologia
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Feminino
Camundongos Endogâmicos C57BL
Mucina-4/metabolismo
Soluções Oftálmicas
Fitoterapia
Extratos Vegetais/administração & dosagem
Extratos Vegetais/isolamento & purificação
Plantas Medicinais
Fatores de Tempo
Fator de Necrose Tumoral alfa/metabolismo
Xeroftalmia/metabolismo
Xeroftalmia/patologia
Xeroftalmia/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Muc4 protein, mouse); 0 (Mucin-4); 0 (Ophthalmic Solutions); 0 (Plant Extracts); 0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170410
[Lr] Data última revisão:
170410
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161126
[St] Status:MEDLINE



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