Base de dados : MEDLINE
Pesquisa : D12.644.276.374.480 [Categoria DeCS]
Referências encontradas : 17045 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 1705 ir para página                         

  1 / 17045 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29429180
[Au] Autor:Hu J; Chen ZC; Zhang YZ; Han P; Ma WJ; Zhang Q; Xu M
[Ad] Endereço:Department of Otorhinolaryngology Head and Neck Surgery, Second Affiliated Hospital, Xi'an Jiaotong University School of Medicine, Xi'an 710004, China.
[Ti] Título:[The experimental study on endoplasmic reticulum stress-participated outer hair cell apoptosis in cadherin 23 gene mutant mice].
[So] Source:Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi;53(2):110-117, 2018 Feb 07.
[Is] ISSN:1673-0860
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To test the mechanism and upstream pathway of outer hair cell apoptosis in Cadherin 23 (Cdh23) gene mutant mice. The mutant 23 ( ) 57 /6 ( 6) . 70 . - ( ) . ( ) ( ) . - - ( ) / ( ) . . . 23 . The ABR thresholds in mice were significantly higher than those in B6 mice at the age of 1 and 3 months (both <0.05). The surface preparation with TUNEL staining confirmed OHC apoptosis in mouse cochleae which showed a higher TUNEL positive cell ratio than B6 mouse( =11.291, <0.01). The ER stress marker and mRNA were upregulated in the mouse inner ear, when compared with those in the B6 mouse(both <0.05). The BiP protein extracted from the mouse cochleae was significantly higher than that of B6 mouse measured by Western blot ( =3.66, =0.02). Immunostaining showed that BiP and CHOP were highly detected in the OHC in mouse cochleae, and was mainly detected in the perinuclear region of OHC. However, a bare BiP and CHOP signal were shown in B6 mouse cochleae. The CDH23 protein was specifically localized at the top of the OHC in B6 mice, indicating the localization of the tip links in hair bundle stereocilia. On the contrary, the CDH23 protein was found to be localized from the top to the nuclei of the OHC in mice. Portions of the CDH23 proteins failed to reach the top of the hair bundles and remained in the OHC cytoplasm. As the downstream response of the Cdh23 gene mutation, portions of the mutant CDH23 protein was accumulated in ER lumen resulting in the increase of ER loading and ultimately triggered ER stress and hair cell apoptosis in mouse cochleae.
[Mh] Termos MeSH primário: Apoptose/genética
Caderinas/genética
Estresse do Retículo Endoplasmático/genética
Células Ciliadas Auditivas Externas/patologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Cóclea/patologia
Estresse do Retículo Endoplasmático/fisiologia
Potenciais Evocados Auditivos do Tronco Encefálico
Células Ciliadas Vestibulares
Marcação In Situ das Extremidades Cortadas
Linfocinas/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Mutação
RNA Mensageiro/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fator de Transcrição CHOP/genética
Fator de Transcrição CHOP/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cadherins); 0 (Cdh23 protein, mouse); 0 (Lymphokines); 0 (RNA, Messenger); 0 (immunoglobulin-binding factors); 147336-12-7 (Transcription Factor CHOP)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180213
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1673-0860.2018.02.006


  2 / 17045 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28468281
[Au] Autor:Rubin D; Zhang W; Karch H; Kuczius T
[Ad] Endereço:Institute for Hygiene, Westfälische Wilhelms-University and University Hospital Münster, Robert Koch-Straße 41, 48149 Münster, Germany. dennis.rubin@ukmuenster.de.
[Ti] Título:Distinct Expression of Immunoglobulin-Binding Proteins in Shiga Toxin-Producing Escherichia coli Implicates High Protein Stability and a Characteristic Phenotype.
[So] Source:Toxins (Basel);9(5), 2017 Apr 29.
[Is] ISSN:2072-6651
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Several immunoglobulin-binding proteins of (Eib) have been isolated from both non-pathogenic and pathogenic strains. Shiga toxin (Stx)-producing (STEC) contain G either as a single gene or in combination with C, while other strains harbour single or multiple genes. The Eib proteins bind human immunoglobulins in a non-immune manner and contribute to bacterial chain-like adherence to human epithelial cells. In this study, the EibG expression in several STEC strains was analysed under different environmental conditions. STEC produced high levels of EibG in complex media and lower levels in low-grade and minimal media under static growth conditions. This characteristic was independent on the Eib subtypes. Microscopically, EibG-expressing STEC exhibited chain formation and aggregation in all employed media, while aggregates were only visible after growth in complex medium. Once expressed, EibG proteins demonstrate high stability during prolonged incubation. Our findings indicate that the regulation of the expression of Eib proteins is highly complex, although the protein levels vary among STEC strains. However, positive upregulation conditions generally result in distinct phenotypes of the isolates.
[Mh] Termos MeSH primário: Proteínas de Escherichia coli/metabolismo
Linfocinas/metabolismo
Escherichia coli Shiga Toxigênica/metabolismo
[Mh] Termos MeSH secundário: Fenótipo
Estabilidade Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Escherichia coli Proteins); 0 (Lymphokines); 0 (immunoglobulin-binding factors)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


  3 / 17045 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28886061
[Au] Autor:Shah DD; Singh SM; Dzieciatkowska M; Mallela KMG
[Ad] Endereço:Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States of America.
[Ti] Título:Biophysical analysis of the effect of chemical modification by 4-oxononenal on the structure, stability, and function of binding immunoglobulin protein (BiP).
[So] Source:PLoS One;12(9):e0183975, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Binding immunoglobulin protein (BiP) is a molecular chaperone important for the folding of numerous proteins, which include millions of immunoglobulins in human body. It also plays a key role in the unfolded protein response (UPR) in the endoplasmic reticulum. Free radical generation is a common phenomenon that occurs in cells under healthy as well as under stress conditions such as ageing, inflammation, alcohol consumption, and smoking. These free radicals attack the cell membranes and generate highly reactive lipid peroxidation products such as 4-oxononenal (4-ONE). BiP is a key protein that is modified by 4-ONE. In this study, we probed how such chemical modification affects the biophysical properties of BiP. Upon modification, BiP shows significant tertiary structural changes with no changes in its secondary structure. The protein loses its thermodynamic stability, particularly, that of the nucleotide binding domain (NBD) where ATP binds. In terms of function, the modified BiP completely loses its ATPase activity with decreased ATP binding affinity. However, modified BiP retains its immunoglobulin binding function and its chaperone activity of suppressing non-specific protein aggregation. These results indicate that 4-ONE modification can significantly affect the structure-function of key proteins such as BiP involved in cellular pathways, and provide a molecular basis for how chemical modifications can result in the failure of quality control mechanisms inside the cell.
[Mh] Termos MeSH primário: Aldeídos/química
Cetonas/química
Linfocinas/química
Linfocinas/metabolismo
Chaperonas Moleculares/química
Chaperonas Moleculares/metabolismo
Conformação Proteica
[Mh] Termos MeSH secundário: Adenosina Trifosfatases/química
Adenosina Trifosfatases/metabolismo
Hidrólise
Interações Hidrofóbicas e Hidrofílicas
Modelos Moleculares
Peso Molecular
Agregados Proteicos
Ligação Proteica
Domínios e Motivos de Interação entre Proteínas
Estabilidade Proteica
Solubilidade
Resposta a Proteínas não Dobradas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4-oxopentanal); 0 (Aldehydes); 0 (Ketones); 0 (Lymphokines); 0 (Molecular Chaperones); 0 (Protein Aggregates); 0 (immunoglobulin-binding factors); EC 3.6.1.- (Adenosine Triphosphatases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183975


  4 / 17045 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28806447
[Au] Autor:Lee YJ; Chiu CC; Ke CY; Tien N; Lin PK
[Ad] Endereço:School of Medicine, Fu-Jen Catholic University, Hsinchuang, New Taipei City, Taiwan.
[Ti] Título:Homocysteine Facilitates Prominent Polygonal Angiogenetic Networks of a Choroidal Capillary Sprouting Model.
[So] Source:Invest Ophthalmol Vis Sci;58(10):4332­4343, 2017 08 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: To investigate the effects of homocysteine on choroidal angiogenesis, we established an ex vivo choroidal sprouting explant model and examined the potential growth factors for angiogenesis. Methods: Choroid fragments with retinal pigment epithelium were isolated from mouse and embedded in Matrigel. Homocysteine at different concentrations were added to the culture mediums. The choroidal explants were observed at different time points, and the total area of choroidal sprouting was measured and analyzed. Results: Homocysteine evoked choroidal capillary sprouting by inducing capillary endothelial cell proliferation with pericyte formation and by facilitating polygonal angiogenetic networks. In some cases, vascular lumens were observed in the newly forming capillaries facilitated by homocysteine. The choroidal sprouting effect of homocysteine can only be observed at a certain range of homocysteine concentration, with 1-mM homocysteine exhibiting the most significantly increased choroidal sprouting areas. Isolectin overexpression was noted in the homocysteine-treated group. Possible growth factors for angiogenesis were detected through immunofluorescent staining, which demonstrated the overexpression of platelet-derived growth factor C and angiopoietin 1 in the homocysteine-treated preparations only. In these preparations, platelet-derived growth factor C was highly expressed in the tip cells of sprouting capillaries. Conclusions: We therefore conclude that platelet-derived growth factor C and angiopoietin 1 may play key roles in the choroid angiogenesis evoked by homocysteine.
[Mh] Termos MeSH primário: Indutores da Angiogênese/farmacologia
Proliferação Celular/fisiologia
Corioide/irrigação sanguínea
Endotélio Vascular/citologia
Homocisteína/farmacologia
Modelos Biológicos
Neovascularização Fisiológica/efeitos dos fármacos
[Mh] Termos MeSH secundário: Angiopoietina-1/metabolismo
Animais
Capilares/fisiologia
Colágeno
Combinação de Medicamentos
Endotélio Vascular/metabolismo
Feminino
Técnica Indireta de Fluorescência para Anticorpo
Laminina
Linfocinas/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Técnicas de Cultura de Órgãos
Fator de Crescimento Derivado de Plaquetas/metabolismo
Proteoglicanas
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inducing Agents); 0 (Angiopoietin-1); 0 (Angpt1 protein, mouse); 0 (Drug Combinations); 0 (Laminin); 0 (Lymphokines); 0 (Platelet-Derived Growth Factor); 0 (Proteoglycans); 0 (Vascular Endothelial Growth Factor A); 0 (platelet-derived growth factor C); 0 (vascular endothelial growth factor A, mouse); 0LVT1QZ0BA (Homocysteine); 119978-18-6 (matrigel); 9007-34-5 (Collagen)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170815
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.17-22308


  5 / 17045 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28686658
[Au] Autor:Ciarlillo D; Celeste C; Carmeliet P; Boerboom D; Theoret C
[Ad] Endereço:Département de biomédecine vétérinaire, Faculté de médecine vétérinaire, Université de Montréal, St-Hyacinthe, Québec, Canada.
[Ti] Título:A hypoxia response element in the Vegfa promoter is required for basal Vegfa expression in skin and for optimal granulation tissue formation during wound healing in mice.
[So] Source:PLoS One;12(7):e0180586, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hypoxia in skin wounds is thought to contribute to healing through the induction of hypoxia inducible factor-1 (HIF-1). Although HIF-1 can regulate the expression of vascular endothelial growth factor A (Vegfa), whether hypoxia and HIF-1 are required to induce Vegfa expression in the context of wound healing is unknown. To test this hypothesis, we evaluated Vegfa expression and wound healing in mutant mice that lack a functional HIF-1 binding site in the Vegfa promoter. Full-thickness excisional wounds were made using a biopsy punch, left to heal by second intention, and granulation tissue isolated on a time course during healing. mRNA levels of Vegfa and its target genes platelet-derived growth factors B (Pdgfb) and stromal cell-derived factor-1 (Sdf1) were measured by RT-qPCR, and HIF-1alpha and VEGFA protein levels measured by immunoblotting. Lower levels of Vegfa, Pdgf1 and Sdf1 mRNA were found in intact skin of mutant mice relative to wild-type controls (n = 6 mice/genotype), whereas levels in granulation tissue during wound healing were unaltered. VEGFA protein levels were also lower in intact skin of the mutant versus the wild-type mice. Decreased Vegfa mRNA levels in skin of mutant mice could not be attributed to decreased HIF-1alpha protein expression, and were therefore a consequence of the loss of HIF-1 responsiveness of the Vegfa promoter. Comparative histologic analyses of healing wounds in mutant and wild-type mice (n = 8 mice/genotype) revealed significant defects in granulation tissue in the mutant mice, both in terms of quantity and capillary density, although epithelialization and healing rates were unaltered. We conclude that HIF-1 is not a major regulator of Vegfa expression during wound healing; rather, it serves to maintain basal levels of expression of Vegfa and its target genes in intact skin, which are required for optimal granulation tissue formation in response to wounding.
[Mh] Termos MeSH primário: Subunidade alfa do Fator 1 Induzível por Hipóxia/genética
Pele/metabolismo
Fator A de Crescimento do Endotélio Vascular/genética
Cicatrização/genética
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação
Quimiocina CXCL12/genética
Proteínas de Ligação a DNA/genética
Modelos Animais de Doenças
Regulação da Expressão Gênica
Tecido de Granulação/metabolismo
Tecido de Granulação/fisiopatologia
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/biossíntese
Linfocinas/genética
Camundongos
Fator de Crescimento Derivado de Plaquetas/genética
Regiões Promotoras Genéticas
Elementos de Resposta/genética
Pele/fisiopatologia
Fator A de Crescimento do Endotélio Vascular/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CXCL12); 0 (Cxcl12 protein, mouse); 0 (DNA-Binding Proteins); 0 (Hif1a protein, mouse); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Lymphokines); 0 (Pdgfd protein, mouse); 0 (Platelet-Derived Growth Factor); 0 (Vascular Endothelial Growth Factor A); 0 (vascular endothelial growth factor A, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180586


  6 / 17045 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28376187
[Au] Autor:Ubink I; Elias SG; Moelans CB; Laclé MM; van Grevenstein WMU; van Diest PJ; Borel Rinkes IHM; Kranenburg O
[Ad] Endereço:Cancer Center, University Medical Center Utrecht, Utrecht, The Netherlands.
[Ti] Título:A Novel Diagnostic Tool for Selecting Patients With Mesenchymal-Type Colon Cancer Reveals Intratumor Subtype Heterogeneity.
[So] Source:J Natl Cancer Inst;109(8), 2017 08 01.
[Is] ISSN:1460-2105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Consensus molecular subtype 4 (CMS4) is a recently identified aggressive colon cancer subtype for which platelet-derived growth factor receptors (PDGFRs) and KIT are potential therapeutic targets. We aimed to develop a clinically applicable CMS4 reverse transcription polymerase chain reaction (RT-qPCR) test to select patients for PDGFR/KIT-targeted therapy. Methods: We used logistic regression to develop a CMS4 prediction rule based on microarray expression values of PDGFRA , PDGFRB , PDGFC , and KIT (566 training and 1259 test samples, using the 273-gene random forest classifier as CMS4 reference standard). We next translated the prediction rule into a single-sample RT-qPCR test, which we independently validated in 29 fresh tumor samples. To study intratumor CMS4 heterogeneity, we used the RT-qPCR test to analyze five random regions of 20 colon tumors. Results: The microarray-based prediction rule diagnosed CMS4-type tumors extremely well in both training and independent test samples (training: area under the curve [AUC] = 0.95, 95% confidence interval [CI] = 0.94 to 0.97; test: AUC = 0.95, 95% CI = 0.94 to 0.96), with excellent calibration and approximately 80% overall net benefit over a large threshold range. Translation into an RT-qPCR test did not affect discrimination (AUC = 0.97, 95% CI = 0.93 to 1.00, independent validation). RT-qPCR analysis of five random tumor regions revealed extensive intratumor CMS4 heterogeneity in nine out of 20 tumors. At least two regions likely have to be analyzed to identify patients that are predominantly CMS4 positive (>50% average CMS4 chance). Conclusion: The CMS4 RT-qPCR test is a promising clinical tool for selecting individual patients for CMS4-subtype-targeted therapy.
[Mh] Termos MeSH primário: Neoplasias do Colo/diagnóstico
Neoplasias do Colo/genética
Heterogeneidade Genética
Seleção de Pacientes
[Mh] Termos MeSH secundário: Área Sob a Curva
Biópsia/métodos
Colo/patologia
Neoplasias do Colo/classificação
Neoplasias do Colo/patologia
Intervalo Livre de Doença
Perfilação da Expressão Gênica
Seres Humanos
Linfocinas/genética
Análise em Microsséries
Técnicas de Diagnóstico Molecular
Terapia de Alvo Molecular
Estadiamento de Neoplasias
Fator de Crescimento Derivado de Plaquetas/genética
Valor Preditivo dos Testes
Proteínas Proto-Oncogênicas c-kit/genética
Curva ROC
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/genética
Receptor beta de Fator de Crescimento Derivado de Plaquetas/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Taxa de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Lymphokines); 0 (Platelet-Derived Growth Factor); 0 (platelet-derived growth factor C); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor alpha); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor beta)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170405
[St] Status:MEDLINE
[do] DOI:10.1093/jnci/djw303


  7 / 17045 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28346846
[Au] Autor:Zhou S; Gao X; Sun J; Lin Z; Huang Y
[Ad] Endereço:Department of Neurosurgery, Ningbo First Hospital, Ningbo Hospital of Zhejiang University , Ningbo, China .
[Ti] Título:DNA Methylation of the PDGFD Gene Promoter Increases the Risk for Intracranial Aneurysms and Brain Arteriovenous Malformations.
[So] Source:DNA Cell Biol;36(6):436-442, 2017 Jun.
[Is] ISSN:1557-7430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to determine the role of DNA methylation of the platelet-derived growth factor-D (PDGFD) gene promoter in the development of intracranial aneurysms (IAs) and brain arteriovenous malformations (BAVMs). A total of 70 patients with IAs or BAVMs and 26 control individuals were enrolled for this study. The PDGFD level in the plasma was determined using enzyme-linked immunosorbent assay. DNA methylation levels of seven cytosine-phosphate-guanine (CpG) dinucleotides present in the PDGFD gene promoter were measured using bisulfite pyrosequencing technology. The plasma PDGFD levels in IA and BAVM were significantly lower than those in the control group (p = 0.0008 and 0.002, respectively). CpG1 methylation levels of the PDGFD gene promoter were significantly higher in IA patients (4.63 ± 0.35, p = 0.017) than in the control group (3.36 ± 0.35). CpG1 methylation of the PDGFD gene promoter in BAVM patients (6.00 ± 0.86, p = 0.003) was also significantly higher than that in the control group, although these differences were seen in both male and female patients (p = 2.81E-04 and p = 0.017, respectively). In addition, CpG1 methylation of the PDGFD promoter was associated with apolipoprotein E (APOE) levels in IA patients (p = 0.013). In conclusion, our study has demonstrated significant correlations between DNA methylation of the PDGFD gene promoter and the risk of developing either IA or BAVM. Furthermore, PDGFD gene promoter CpG1 methylation shows a significant correlation with APOE in IAs. Further functional studies on these relationships and correlations are warranted.
[Mh] Termos MeSH primário: Fístula Arteriovenosa/genética
Metilação de DNA
Predisposição Genética para Doença/genética
Aneurisma Intracraniano/genética
Malformações Arteriovenosas Intracranianas/genética
Linfocinas/genética
Fator de Crescimento Derivado de Plaquetas/genética
Regiões Promotoras Genéticas/genética
[Mh] Termos MeSH secundário: Sequência de Bases
Ilhas de CpG/genética
Feminino
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lymphokines); 0 (PDGFD protein, human); 0 (Platelet-Derived Growth Factor)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170328
[St] Status:MEDLINE
[do] DOI:10.1089/dna.2016.3499


  8 / 17045 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28338461
[Au] Autor:Li F; Cao J; Zhao Z; Li C; Qi F; Liu T
[Ad] Endereço:Department of General Surgery, Tianjin Medical University General Hospital, Tianjin, China.
[Ti] Título:Mesenchymal Stem Cells Suppress Chronic Rejection in Heterotopic Small Intestine Transplant Rat Models Via Inhibition of CD68, Transforming Growth Factor- ß1, and Platelet-Derived Growth Factor Expression.
[So] Source:Exp Clin Transplant;15(2):213-221, 2017 Apr.
[Is] ISSN:2146-8427
[Cp] País de publicação:Turkey
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Mesenchymal stem cells are easy to obtain and expand, with characteristics of low immunogenicity and strong tissue repair capacity. In this study, our aim was to investigate the role of mesenchymal stem cells in chronic immune rejection of heterotopic small intestine transplant in rats. MATERIALS AND METHODS: After successfully constructing a rat chronic immune rejection model of heterotopic small intestine transplant, we infused mesenchymal stem cells into the animal recipients. We observed mesenchymal stem cell location in the recipients, recipient survival, pathology changes, and the expression of CD68, transforming growth factor ß1, and platelet-derived growth factor C in the donor intestine. RESULTS: Mesenchymal stem cells inhibited the lymphocyte proliferation caused by concanavalin A in vitro. After stem cells were infused into recipients, they were mainly located in the donor intestine, as well as in the spleen and thymus. Recovery after transplant and pathology changes of the donor intestine in rats with stem cell infusion were better than in the control group; however, we observed no differences in survival time, accompanied by downregulated expression of CD68, transforming growth factor ß1, and platelet-derived growth factor C. CONCLUSIONS: Mesenchymal stem cells, to a certain extent, could inhibit the process of chronic rejection. The mechanisms may include the inhibited function of these cells on lymphocyte proliferation, reduced infiltration of macrophages, and reduced expression of transforming growth factor ß1 and platelet-derived growth factor C.
[Mh] Termos MeSH primário: Antígenos CD/metabolismo
Antígenos de Diferenciação Mielomonocítica/metabolismo
Rejeição de Enxerto/prevenção & controle
Sobrevivência de Enxerto
Intestino Delgado/transplante
Linfocinas/metabolismo
Transplante de Células-Tronco Mesenquimais
Células Mesenquimais Estromais/metabolismo
Fator de Crescimento Derivado de Plaquetas/metabolismo
Fator de Crescimento Transformador beta1/metabolismo
[Mh] Termos MeSH secundário: Animais
Proliferação Celular
Células Cultivadas
Doença Crônica
Técnicas de Cocultura
Modelos Animais de Doenças
Regulação para Baixo
Rejeição de Enxerto/imunologia
Rejeição de Enxerto/metabolismo
Rejeição de Enxerto/patologia
Intestino Delgado/imunologia
Intestino Delgado/metabolismo
Intestino Delgado/patologia
Ativação Linfocitária
Linfócitos/imunologia
Linfócitos/metabolismo
Macrófagos/imunologia
Macrófagos/metabolismo
Masculino
Ratos Endogâmicos F344
Ratos Endogâmicos Lew
Transdução de Sinais
Fatores de Tempo
Transplante Heterotópico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (CD68 protein, rat); 0 (Lymphokines); 0 (Platelet-Derived Growth Factor); 0 (Tgfb1 protein, rat); 0 (Transforming Growth Factor beta1); 0 (platelet-derived growth factor C)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170325
[St] Status:MEDLINE
[do] DOI:10.6002/ect.2016.0067


  9 / 17045 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28254885
[Au] Autor:Muhl L; Folestad EB; Gladh H; Wang Y; Moessinger C; Jakobsson L; Eriksson U
[Ad] Endereço:Department of Medical Biochemistry and Biophysics, Division of Vascular Biology, Karolinska Institutet, Scheeles väg 2, A3:P4, Stockholm S-17177, Sweden lars.muhl@ki.se.
[Ti] Título:Neuropilin 1 binds PDGF-D and is a co-receptor in PDGF-D-PDGFRß signaling.
[So] Source:J Cell Sci;130(8):1365-1378, 2017 Apr 15.
[Is] ISSN:1477-9137
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Platelet-derived growth factor (PDGF)-D is a PDGF receptor ß (PDGFRß)-specific ligand implicated in a number of pathological conditions, such as cardiovascular disease and cancer, but its biological function remains incompletely understood. In this study, we demonstrate that PDGF-D binds directly to neuropilin 1 (NRP1), in a manner that requires the PDGF-D C-terminal Arg residue. Stimulation with PDGF-D, but not PDGF-B, induced PDGFRß-NRP1 complex formation in fibroblasts. Additionally, PDGF-D induced translocation of NRP1 to cell-cell junctions in endothelial cells, independently of PDGFRß, altering the availability of NRP1 for VEGF-A-VEGFR2 signaling. PDGF-D showed differential effects on pericyte behavior in sprouting assays compared to PDGF-B. Furthermore, PDGF-D-induced PDGFRß-NRP1 interaction can occur in between molecules located in different cells (endothelial cells and pericytes). In summary, we show that NRP1 can act as a co-receptor for PDGF-D-PDGFRß signaling and is possibly implicated in intercellular communication in the vascular wall.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/metabolismo
Endotélio Vascular/metabolismo
Fibroblastos/metabolismo
Junções Intercelulares/metabolismo
Neoplasias/metabolismo
Neuropilina-1/metabolismo
Pericitos/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Transformada
Seres Humanos
Linfocinas/metabolismo
Neovascularização Fisiológica
Fator de Crescimento Derivado de Plaquetas/metabolismo
Ligação Proteica
Receptor beta de Fator de Crescimento Derivado de Plaquetas/metabolismo
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lymphokines); 0 (PDGFD protein, human); 0 (Platelet-Derived Growth Factor); 144713-63-3 (Neuropilin-1); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor beta)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170505
[Lr] Data última revisão:
170505
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170304
[St] Status:MEDLINE
[do] DOI:10.1242/jcs.200493


  10 / 17045 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28163397
[Au] Autor:Manzat Saplacan RM; Balacescu L; Gherman C; Chira RI; Craiu A; Mircea PA; Lisencu C; Balacescu O
[Ad] Endereço:First Medical Clinic, University of Medicine and Pharmacy "Iuliu Hatieganu" Cluj-Napoca, 3-5 Clinicilor Street, 400006 Cluj-Napoca, Romania.
[Ti] Título:The Role of PDGFs and PDGFRs in Colorectal Cancer.
[So] Source:Mediators Inflamm;2017:4708076, 2017.
[Is] ISSN:1466-1861
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Colorectal cancer (CRC) is an important cause of morbidity and mortality worldwide. Angiogenesis was reported as one important mechanism activated in colorectal carcinogenesis. Tumor microenvironment associated angiogenesis involves a large spectrum of signaling molecules and deciphering their role in colorectal carcinogenesis still represents a major challenge. The aim of our study is to point out the diagnosis and prediction role of PDGF family and their receptors in colorectal carcinogenesis. A systematic search in Medline and PubMed for studies reporting the role of platelet-derived growth factors (PDGFs) and their receptors (PDGFRs) in tumor biology related to CRC was made. PDGFs are important growth factors for normal tissue growth and division, with an important role in blood vessel formation. PDGFs/PDGFRs signaling pathway has been demonstrated to be involved in angiogenesis mainly by targeting pericytes and vascular smooth muscle cells. High levels of PDGF-BB were reported in CRC patients compared to those with adenomas, while elevated levels of PDGFR / in the stroma of CRC patients were correlated with invasion and metastasis. Moreover, PDGF-AB and PDGF-C were correlated with early diagnosis, cancer grading, and metastatic disease. Both PDGFs and PDGFRs families play an important role in colorectal carcinogenesis and could be considered to be investigated as useful biomarkers both for diagnosis and treatment of CRC.
[Mh] Termos MeSH primário: Neoplasias Colorretais/metabolismo
Neoplasias Colorretais/patologia
Fator de Crescimento Derivado de Plaquetas/metabolismo
Receptores do Fator de Crescimento Derivado de Plaquetas/metabolismo
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Linfocinas/metabolismo
Neovascularização Patológica/metabolismo
Neovascularização Patológica/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Lymphokines); 0 (Platelet-Derived Growth Factor); 0 (platelet-derived growth factor AB); 0 (platelet-derived growth factor C); EC 2.7.10.1 (Receptors, Platelet-Derived Growth Factor)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170207
[St] Status:MEDLINE
[do] DOI:10.1155/2017/4708076



página 1 de 1705 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde