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[PMID]:29377910
[Au] Autor:Ikezono T; Matsumura T; Matsuda H; Shikaze S; Saitoh S; Shindo S; Hasegawa S; Oh SH; Hagiwara Y; Ogawa Y; Ogawa H; Sato H; Tono T; Araki R; Maeda Y; Usami SI; Kase Y
[Ad] Endereço:Department of Otorhinolaryngology, Saitama Medical University, Saitama, Japan.
[Ti] Título:The diagnostic performance of a novel ELISA for human CTP (Cochlin-tomoprotein) to detect perilymph leakage.
[So] Source:PLoS One;13(1):e0191498, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Perilymphatic fistula is defined as an abnormal communication between the perilymph-filled space and the middle ear, or cranial spaces. The manifestations include a broad spectrum of neuro-otological symptoms such as hearing loss, vertigo/dizziness, disequilibrium, aural fullness, tinnitus, and cognitive dysfunction. By sealing the fistula, perilymphatic fistula is a surgically correctable disease. Also, appropriate recognition and treatment of perilymphatic fistula can improve a patient's condition and hence the quality of life. However, the difficulty in making a definitive diagnosis due to the lack of an appropriate biomarker to detect perilymph leakage has caused a long-standing debate regarding its management. We have reported a clinical test for the diagnosis of perilymphatic fistula by detecting a perilymph specific protein, Cochlin-tomoprotein, as a diagnostic marker using a western blot. The aim of this study is to establish an ELISA-based human Cochlin-tomoprotein detection test and to evaluate its diagnostic accuracy in clinical subjects. The results of ELISA showed good dilution reproducibility. The mean concentration was 49.7±9.4 of 10 perilymph samples. The ROC curve in differentiating the perilymph leakage condition from the normal middle ear was significant (P < 0.001) with an area under the curve (AUC) of 0.918 (95% CI 0.824-0.100). We defined the diagnostic criteria as follows: CTP<0.4 negative; 0.4≦CTP<0.8 intermediate; 0.8≦CTP(ng/ml) positive in the clinical usage of the hCTP ELISA, and sensitivity and specificity were 86.4% and 100%, respectively. We further tested the expression specificity of the Cochlin-tomoprotein by testing blood and CSF samples. The concentration was below the detection limit (0.2 ng/ml) in 38 of the 40 blood, and 14 of the 19 CSF samples. We report the accuracy of this test for the diagnosis of perilymphatic fistula. Using ELISA, we can improve the throughput of the test. Furthermore, it is useful for a large-scale study to characterize the clinical picture and delineate the management of this medical condition.
[Mh] Termos MeSH primário: Ensaio de Imunoadsorção Enzimática/métodos
Proteínas da Matriz Extracelular/metabolismo
Perilinfa/metabolismo
[Mh] Termos MeSH secundário: Western Blotting
Proteínas da Matriz Extracelular/sangue
Proteínas da Matriz Extracelular/líquido cefalorraquidiano
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (COCH protein, human); 0 (Extracellular Matrix Proteins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180130
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191498


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[PMID]:28460475
[Au] Autor:Song JM; Molla K; Anandharaj A; Cornax I; O Sullivan MG; Kirtane AR; Panyam J; Kassie F
[Ad] Endereço:Masonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA.
[Ti] Título:Triptolide suppresses the in vitro and in vivo growth of lung cancer cells by targeting hyaluronan-CD44/RHAMM signaling.
[So] Source:Oncotarget;8(16):26927-26940, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Higher levels of hyaluronan (HA) and its receptors CD44 and RHAMM have been associated with poor prognosis and metastasis in NSCLC. In the current study, our goal was to define, using cellular and orthotopic lung tumor models, the role of HA-CD44/RHAMM signaling in lung carcinogenesis and to assess the potential of triptolide to block HA-CD44/RHAMM signaling and thereby suppress the development and progression of lung cancer. Triptolide reduced the viability of five non-small cell lung cancer (NSCLC) cells, the proliferation and self-renewal of pulmospheres, and levels of HA synthase 2 (HAS2), HAS3, HA, CD44, RHAMM, EGFR, Akt and ERK, but increased the cleavage of caspase 3 and PARP. Silencing of HAS2, CD44 or RHAMM induced similar effects. Addition of excess HA to the culture media completely abrogated the effects of triptolide and siRNAs targeting HAS2, CD44, or RHAMM. In an orthotopic lung cancer model in nude rats, intranasal administration of liposomal triptolide (400 µg/kg) for 8 weeks significantly reduced lung tumor growth as determined by bioluminescence imaging, lung weight measurements and gross and histopathological analysis of tumor burden. Also, triptolide suppressed expressions of Ki-67, a marker for cell proliferation, HAS2, HAS3, HA, CD44, and RHAMM in lung tumors. Overall, our results provide a strong rationale for mitigating lung cancer by targeting the HA-CD44/RHAMM signaling axis.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/farmacologia
Diterpenos/farmacologia
Proteínas da Matriz Extracelular/metabolismo
Receptores de Hialuronatos/antagonistas & inibidores
Receptores de Hialuronatos/metabolismo
Neoplasias Pulmonares/metabolismo
Fenantrenos/farmacologia
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Modelos Animais de Doenças
Compostos de Epóxi/farmacologia
Inativação Gênica
Seres Humanos
Receptores de Hialuronatos/genética
Hialuronan Sintases/genética
Hialuronan Sintases/metabolismo
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
Masculino
RNA Interferente Pequeno/genética
Ratos
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 0 (CD44 protein, human); 0 (Diterpenes); 0 (Epoxy Compounds); 0 (Extracellular Matrix Proteins); 0 (Hyaluronan Receptors); 0 (Phenanthrenes); 0 (RNA, Small Interfering); 0 (hyaluronan-mediated motility receptor); 19ALD1S53J (triptolide); EC 2.4.1.212 (Hyaluronan Synthases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15879


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[PMID]:29364909
[Au] Autor:de Bruyn JR; Becker MA; Steenkamer J; Wildenberg ME; Meijer SL; Buskens CJ; Bemelman WA; Löwenberg M; Ponsioen CY; van den Brink GR; D'Haens GR
[Ad] Endereço:Department of Gastroenterology and Hepatology, Academic Medical Center, Amsterdam, The Netherlands.
[Ti] Título:Intestinal fibrosis is associated with lack of response to Infliximab therapy in Crohn's disease.
[So] Source:PLoS One;13(1):e0190999, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Overt fibrostenotic disease is a relative contraindication for anti-TNF therapy in Crohn's disease. We hypothesized that subclinical fibrosis may also contribute to an incomplete response to anti-TNF therapy before the onset of symptomatic stenosis. METHODS: In a previous trial, patients with ileocecal Crohn's disease were randomized to either immediate ileocecal resection or medical treatment with Infliximab. In case of insufficient response to Infliximab, the latter underwent secondary ileocecal resection. We compared specimens from those patients undergoing immediate resection (Infliximab naïve, n = 20) to those who failed Infliximab therapy (n = 20). RESULTS: Infliximab naïve and Infliximab failure patients had similar severity of inflammation when assessed by CRP levels (median 14 vs 9 mg/L) and histology (Geboes-D'Haens-score, median 10 vs 11 points). On immunohistochemistry, collagen-III and fibronectin depositions were increased in patients previously exposed to Infliximab compared to patients naïve to Infliximab. On mRNA level, procollagen peptidase showed significantly more mucosal mRNA expression in Crohn's disease patients who failed Infliximab. Infliximab responders showed no increase of this marker after 4 weeks of successful Infliximab treatment. DISCUSSION: Failure to Infliximab therapy is associated with subclinical fibrosis in Crohn's disease.
[Mh] Termos MeSH primário: Doença de Crohn/tratamento farmacológico
Fármacos Gastrointestinais/uso terapêutico
Infliximab/uso terapêutico
Enteropatias/complicações
[Mh] Termos MeSH secundário: Adulto
Doença de Crohn/complicações
Doença de Crohn/metabolismo
Proteínas da Matriz Extracelular/metabolismo
Feminino
Fibrose
Seres Humanos
Enteropatias/metabolismo
Enteropatias/patologia
Mucosa Intestinal/enzimologia
Masculino
Meia-Idade
Pró-Colágeno N-Endopeptidase/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Extracellular Matrix Proteins); 0 (Gastrointestinal Agents); B72HH48FLU (Infliximab); EC 3.4.24.14 (Procollagen N-Endopeptidase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180125
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190999


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[PMID]:29351342
[Au] Autor:van der Ven AT; Kobbe B; Kohl S; Shril S; Pogoda HM; Imhof T; Ityel H; Vivante A; Chen J; Hwang DY; Connaughton DM; Mann N; Widmeier E; Taglienti M; Schmidt JM; Nakayama M; Senguttuvan P; Kumar S; Tasic V; Kehinde EO; Mane SM; Lifton RP; Soliman N; Lu W; Bauer SB; Hammerschmidt M; Wagener R; Hildebrandt F
[Ad] Endereço:Division of Nephrology, Department of Medicine, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America.
[Ti] Título:A homozygous missense variant in VWA2, encoding an interactor of the Fraser-complex, in a patient with vesicoureteral reflux.
[So] Source:PLoS One;13(1):e0191224, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Congenital anomalies of the kidney and urinary tract (CAKUT) are the most common cause (40-50%) of chronic kidney disease (CKD) in children. About 40 monogenic causes of CAKUT have so far been discovered. To date less than 20% of CAKUT cases can be explained by mutations in these 40 genes. To identify additional monogenic causes of CAKUT, we performed whole exome sequencing (WES) and homozygosity mapping (HM) in a patient with CAKUT from Indian origin and consanguineous descent. We identified a homozygous missense mutation (c.1336C>T, p.Arg446Cys) in the gene Von Willebrand factor A domain containing 2 (VWA2). With immunohistochemistry studies on kidneys of newborn (P1) mice, we show that Vwa2 and Fraser extracellular matrix complex subunit 1 (Fras1) co-localize in the nephrogenic zone of the renal cortex. We identified a pronounced expression of Vwa2 in the basement membrane of the ureteric bud (UB) and derivatives of the metanephric mesenchyme (MM). By applying in vitro assays, we demonstrate that the Arg446Cys mutation decreases translocation of monomeric VWA2 protein and increases translocation of aggregated VWA2 protein into the extracellular space. This is potentially due to the additional, unpaired cysteine residue in the mutated protein that is used for intermolecular disulfide bond formation. VWA2 is a known, direct interactor of FRAS1 of the Fraser-Complex (FC). FC-encoding genes and interacting proteins have previously been implicated in the pathogenesis of syndromic and/or isolated CAKUT phenotypes in humans. VWA2 therefore constitutes a very strong candidate in the search for novel CAKUT-causing genes. Our results from in vitro experiments indicate a dose-dependent neomorphic effect of the Arg446Cys homozygous mutation in VWA2.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/genética
Síndrome de Fraser/genética
Mutação de Sentido Incorreto
Anormalidades Urogenitais/genética
Refluxo Vesicoureteral/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Substituição de Aminoácidos
Animais
Animais Recém-Nascidos
Biomarcadores Tumorais/química
Criança
Consanguinidade
Sequência Conservada
Éxons
Proteínas da Matriz Extracelular/genética
Proteínas da Matriz Extracelular/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Homozigoto
Seres Humanos
Masculino
Camundongos
Modelos Animais
Modelos Moleculares
Linhagem
Homologia de Sequência de Aminoácidos
Sistema Urogenital/crescimento & desenvolvimento
Sistema Urogenital/metabolismo
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Extracellular Matrix Proteins); 0 (Fras1 protein, mouse); 0 (VWA2 protein, human); 0 (Vwa2 protein, mouse)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180120
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191224


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[PMID]:29223396
[Au] Autor:Matsuishi YI; Kato H; Masuda K; Yamaza H; Hirofuji Y; Sato H; Wada H; Kiyoshima T; Nonaka K
[Ad] Endereço:Section of Oral Medicine for Children, Division of Oral Health, Growth and Development, Faculty of Dental Science, Kyushu University, 3-1-1 Maidashi, Higashi-Ku, Fukuoka 812-8582, Japan.
[Ti] Título:Accelerated dentinogenesis by inhibiting the mitochondrial fission factor, dynamin related protein 1.
[So] Source:Biochem Biophys Res Commun;495(2):1655-1660, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Undifferentiated odontogenic epithelium and dental papilla cells differentiate into ameloblasts and odontoblasts, respectively, both of which are essential for tooth development. These differentiation processes involve dramatic functional and morphological changes of the cells. For these changes to occur, activation of mitochondrial functions, including ATP production, is extremely important. In addition, these changes are closely related to mitochondrial fission and fusion, known as mitochondrial dynamics. However, few studies have focused on the role of mitochondrial dynamics in tooth development. The purpose of this study was to clarify this role. We used mouse tooth germ organ cultures and a mouse dental papilla cell line with the ability to differentiate into odontoblasts, in combination with knockdown of the mitochondrial fission factor, dynamin related protein (DRP)1. In organ cultures of the mouse first molar, tooth germ developed to the early bell stage. The amount of dentin formed under DRP1 inhibition was significantly larger than that of the control. In experiments using a mouse dental papilla cell line, differentiation into odontoblasts was enhanced by inhibiting DRP1. This was associated with increased mitochondrial elongation and ATP production compared to the control. These results suggest that DRP1 inhibition accelerates dentin formation through mitochondrial elongation and activation. This raises the possibility that DRP1 might be a therapeutic target for developmental disorders of teeth.
[Mh] Termos MeSH primário: Dentinogênese/fisiologia
Dinaminas/antagonistas & inibidores
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/biossíntese
Ameloblastos/citologia
Ameloblastos/fisiologia
Animais
Diferenciação Celular/genética
Diferenciação Celular/fisiologia
Linhagem Celular
Dinaminas/genética
Dinaminas/fisiologia
Proteínas da Matriz Extracelular/biossíntese
Feminino
Camundongos
Camundongos Endogâmicos C57BL
Dinâmica Mitocondrial/fisiologia
Odontoblastos/citologia
Odontoblastos/fisiologia
Técnicas de Cultura de Órgãos
Fosfoproteínas/biossíntese
Gravidez
RNA Interferente Pequeno/genética
Sialoglicoproteínas/biossíntese
Germe de Dente/citologia
Germe de Dente/embriologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Extracellular Matrix Proteins); 0 (Phosphoproteins); 0 (RNA, Small Interfering); 0 (Sialoglycoproteins); 0 (dentin sialophosphoprotein); 8L70Q75FXE (Adenosine Triphosphate); EC 3.6.5.5 (Dnm1l protein, mouse); EC 3.6.5.5 (Dynamins)
[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:171211
[St] Status:MEDLINE


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[PMID]:29244110
[Au] Autor:Jamaluddin MFB; Ko YA; Kumar M; Brown Y; Bajwa P; Nagendra PB; Skerrett-Byrne DA; Hondermarck H; Baker MA; Dun MD; Scott RJ; Nahar P; Tanwar PS
[Ad] Endereço:School of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan, New South Wales, Australia.
[Ti] Título:Proteomic Profiling of Human Uterine Fibroids Reveals Upregulation of the Extracellular Matrix Protein Periostin.
[So] Source:Endocrinology;159(2):1106-1118, 2018 02 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The central characteristic of uterine fibroids is excessive deposition of extracellular matrix (ECM), which contributes to fibroid growth and bulk-type symptoms. Despite this, very little is known about patterns of ECM protein expression in fibroids and whether these are influenced by the most common genetic anomalies, which relate to MED12. We performed extensive genetic and proteomic analyses of clinically annotated fibroids and adjacent normal myometrium to identify the composition and expression patterns of ECM proteins in MED12 mutation-positive and mutation-negative uterine fibroids. Genetic sequencing of tissue samples revealed MED12 alterations in 39 of 65 fibroids (60%) from 14 patients. Using isobaric tagged-based quantitative mass spectrometry on three selected patients (n = 9 fibroids), we observed a common set of upregulated (>1.5-fold) and downregulated (<0.66-fold) proteins in small, medium, and large fibroid samples of annotated MED12 status. These two sets of upregulated and downregulated proteins were the same in all patients, regardless of variations in fibroid size and MED12 status. We then focused on one of the significant upregulated ECM proteins and confirmed the differential expression of periostin using western blotting and immunohistochemical analysis. Our study defined the proteome of uterine fibroids and identified that increased ECM protein expression, in particular periostin, is a hallmark of uterine fibroids regardless of MED12 mutation status. This study sets the foundation for further investigations to analyze the mechanisms regulating ECM overexpression and the functional role of upregulated ECM proteins in leiomyogenesis.
[Mh] Termos MeSH primário: Moléculas de Adesão Celular/metabolismo
Leiomioma/metabolismo
Proteoma/análise
Neoplasias Uterinas/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Moléculas de Adesão Celular/genética
Transformação Celular Neoplásica/genética
Transformação Celular Neoplásica/metabolismo
Proteínas da Matriz Extracelular/genética
Proteínas da Matriz Extracelular/metabolismo
Feminino
Perfilação da Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Leiomioma/genética
Meia-Idade
Miométrio/metabolismo
Proteoma/metabolismo
Proteômica
Neoplasias Uterinas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cell Adhesion Molecules); 0 (Extracellular Matrix Proteins); 0 (POSTN protein, human); 0 (Proteome)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-03018


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[PMID]:29278708
[Au] Autor:Suzuki S; Hoshino H; Yoshida K; Nakanishi J; Tsuchiya-Hirata S; Kobuke S; Haruyama N; Nishimura F; Shiba H
[Ad] Endereço:Department of Biological Endodontics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, 734-8553, Japan. Electronic address: suzukis@hiroshima-u.ac.jp.
[Ti] Título:Genome-wide identification of chromatin-enriched RNA reveals that unspliced dentin matrix protein-1 mRNA regulates cell proliferation in squamous cell carcinoma.
[So] Source:Biochem Biophys Res Commun;495(3):2303-2309, 2018 01 15.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chromatin-enriched noncoding RNAs (ncRNAs) have emerged as key molecules in epigenetic processes by interacting with chromatin-associated proteins. Recently, protein-coding mRNA genes have been reported to be chromatin-tethered, similar with ncRNA. However, very little is known about whether chromatin-enriched mRNA is involved in the chromatin modification process. Here, we comprehensively examined chromatin-enriched RNA in squamous cell carcinoma (SQCC) cells by RNA subcellular localization analysis, which was a combination of RNA fractionation and RNA-seq. We identified 11 mRNAs as highly chromatin-enriched RNAs. Among these, we focused on the dentin matrix protein-1 (DMP-1) gene because its expression in SQCC cells has not been reported. Furthermore, we clarified that DMP-1 mRNA was retained in chromatin in its unspliced form in SQCC in vitro and in vivo. As the inhibition of the unspliced DMP-1 mRNA (unspDMP-1) expression resulted in decreased cellular proliferation in SQCC cells, we performed ChIP-qPCR to identify cell cycle-related genes whose expression was epigenetically modified by unspDMP-1, and found that the CDKN1B promoter became active in SQCC cells by inhibiting unspDMP-1 expression. This result was further validated by the increased CDKN1B gene expression in the cells treated with siRNA for unspDMP-1 and by restoration of the decreased cellular proliferation rate by simultaneously inhibiting CDKN1B expression in SQCC cells. Further, to examine whether unspDMP-1 was able to associate with the CDKN1B promoter region, SQCC cells stably expressing PP7-mCherry fusion protein were transiently transfected with the unspDMP-1 fused to 24 repeats of the PP7 RNA stem loop (unspDMP-1-24xPP7) and we found that unspDMP-1-24xPP7 was efficiently precipitated with the antibody against mCherry and was significantly enriched in the CDKN1B promoter region. Thus, unspDMP-1 is a novel chromatin-enriched RNA that epigenetically regulates cellular proliferation of SQCC.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/genética
Carcinoma de Células Escamosas/patologia
Proliferação Celular/genética
Cromatina/genética
Proteínas da Matriz Extracelular/genética
Fosfoproteínas/genética
RNA Neoplásico/genética
RNA não Traduzido/genética
[Mh] Termos MeSH secundário: Carcinoma de Células Escamosas/metabolismo
Linhagem Celular Tumoral
Mapeamento Cromossômico/métodos
Seres Humanos
MicroRNAs/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chromatin); 0 (DMP1 protein, human); 0 (Extracellular Matrix Proteins); 0 (MicroRNAs); 0 (Phosphoproteins); 0 (RNA, Neoplasm); 0 (RNA, Untranslated)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


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[PMID]:29277616
[Au] Autor:Bae CJ; Hong CS; Saint-Jeannet JP
[Ad] Endereço:Department of Basic Science & Craniofacial Biology, College of Dentistry, New York University, New York, USA.
[Ti] Título:Anosmin-1 is essential for neural crest and cranial placodes formation in Xenopus.
[So] Source:Biochem Biophys Res Commun;495(3):2257-2263, 2018 01 15.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:During embryogenesis vertebrates develop a complex craniofacial skeleton associated with sensory organs. These structures are primarily derived from two embryonic cell populations the neural crest and cranial placodes, respectively. Neural crest cells and cranial placodes are specified through the integrated action of several families of signaling molecules, and the subsequent activation of a complex network of transcription factors. Here we describe the expression and function of Anosmin-1 (Anos1), an extracellular matrix protein, during neural crest and cranial placodes development in Xenopus laevis. Anos1 was identified as a target of Pax3 and Zic1, two transcription factors necessary and sufficient to generate neural crest and cranial placodes. Anos1 is expressed in cranial neural crest progenitors at early neurula stage and in cranial placode derivatives later in development. We show that Anos1 function is required for neural crest and sensory organs development in Xenopus, consistent with the defects observed in Kallmann syndrome patients carrying a mutation in ANOS1. These findings indicate that anos1 has a conserved function in the development of craniofacial structures, and indicate that anos1-depleted Xenopus embryos represent a useful model to analyze the pathogenesis of Kallmann syndrome.
[Mh] Termos MeSH primário: Desenvolvimento Embrionário/fisiologia
Proteínas da Matriz Extracelular/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Crista Neural/embriologia
Crista Neural/metabolismo
Neurogênese/fisiologia
Crânio/embriologia
Crânio/metabolismo
Proteínas de Xenopus/metabolismo
[Mh] Termos MeSH secundário: Animais
Xenopus
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Extracellular Matrix Proteins); 0 (Nerve Tissue Proteins); 0 (Xenopus Proteins); 0 (anosmin-1 protein, Xenopus)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


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[PMID]:28452178
[Au] Autor:Matsusaki M; Komeda M; Mura S; Tanaka HY; Kano MR; Couvreur P; Akashi M
[Ad] Endereço:Department of Applied Chemistry, Graduate School of Engineering, Osaka University, 2-1 Yamadaoka, Suita, Osaka, 565-0871, Japan.
[Ti] Título:Desmoplastic Reaction in 3D-Pancreatic Cancer Tissues Suppresses Molecular Permeability.
[So] Source:Adv Healthc Mater;6(15), 2017 Aug.
[Is] ISSN:2192-2659
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The survival rate of pancreatic ductal adenocarcinoma is still the lowest among all types of cancers, primarily as a consequence of an important desmoplastic reaction. Although the presence of thick stromal tissues in pancreatic tumors has been reported, in vivo animal studies do not enable a clear understanding of the crosstalk between cancer cells and fibroblasts. Accordingly, this paper reports the design and characterization of an in vitro pancreatic cancer-stromal 3D-tissue model, which enhances the understanding of the interactions between cancer cells and fibroblasts and their influence on the secretion of extracellular matrix (ECM). 3D-tissue models comprising fibroblasts and pancreatic cancer cells (MiaPaCa-2 cell line) or colon cancer cells (HT29 cell line, used as a control) show decreased molecular permeability with increased cancer cell ratios. The 3D-MiaPaCa-2 tissues display an increase in the secretion of collagen as a function of the cancer cell ratio, whereas 3D-HT29 tissues do not show a significant difference. Notably, the secretion of ECM proteins from single fibroblasts in 3D-tissue models containing 90% MiaPaCa-2 cells is ten times higher than that under 10% cancer cell conditions. In vitro pancreatic cancer 3D-tissues will be a valuable tool to obtain information on the interactions between cancer and stromal cells.
[Mh] Termos MeSH primário: Comunicação Celular
Permeabilidade da Membrana Celular
Proteínas da Matriz Extracelular/metabolismo
Neoplasias Pancreáticas/metabolismo
Esferoides Celulares/metabolismo
Células Estromais/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Células HT29
Seres Humanos
Neoplasias Pancreáticas/patologia
Esferoides Celulares/patologia
Células Estromais/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Extracellular Matrix Proteins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180131
[Lr] Data última revisão:
180131
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1002/adhm.201700057


  10 / 17783 MEDLINE  
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[PMID]:29298336
[Au] Autor:Moeller J; Denisin AK; Sim JY; Wilson RE; Ribeiro AJS; Pruitt BL
[Ad] Endereço:Department of Mechanical Engineering, Stanford University, Stanford, California, United States of America.
[Ti] Título:Controlling cell shape on hydrogels using lift-off protein patterning.
[So] Source:PLoS One;13(1):e0189901, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Polyacrylamide gels functionalized with extracellular matrix proteins are commonly used as cell culture platforms to evaluate the combined effects of extracellular matrix composition, cell geometry and substrate rigidity on cell physiology. For this purpose, protein transfer onto the surface of polyacrylamide hydrogels must result in geometrically well-resolved micropatterns with homogeneous protein distribution. Yet the outcomes of micropatterning methods have not been pairwise evaluated against these criteria. We report a high-fidelity photoresist lift-off patterning method to pattern ECM proteins on polyacrylamide hydrogels with elastic moduli ranging from 5 to 25 kPa. We directly compare the protein transfer efficiency and pattern geometrical accuracy of this protocol to the widely used microcontact printing method. Lift-off patterning achieves higher protein transfer efficiency, increases pattern accuracy, increases pattern yield, and reduces variability of these factors within arrays of patterns as it bypasses the drying and transfer steps of microcontact printing. We demonstrate that lift-off patterned hydrogels successfully control cell size and shape and enable long-term imaging of actin intracellular structure and lamellipodia dynamics when we culture epithelial cells on these substrates.
[Mh] Termos MeSH primário: Forma Celular
Proteínas da Matriz Extracelular/metabolismo
Hidrogéis
[Mh] Termos MeSH secundário: Animais
Cães
Eletroforese em Gel de Poliacrilamida
Células Madin Darby de Rim Canino
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Extracellular Matrix Proteins); 0 (Hydrogels)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189901



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