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Pesquisa : D12.776.860.300.250.400.100 [Categoria DeCS]
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[PMID]:28460472
[Au] Autor:Å Urga S; Nanut MP; Kos J; Sabotic J
[Ad] Endereço:Department of Biotechnology, Jožef Stefan Institute, Ljubljana, Slovenia.
[Ti] Título:Fungal lectin MpL enables entry of protein drugs into cancer cells and their subcellular targeting.
[So] Source:Oncotarget;8(16):26896-26910, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lectins have been recognized as promising carrier molecules for targeted drug delivery. They specifically bind carbohydrate moieties on cell membranes and trigger cell internalization. Fungal lectin MpL (Macrolepiota procera lectin) does not provoke cancer cell cytotoxicity but is able to bind aminopeptidase N (CD13) and integrin α3ß1, two glycoproteins that are overexpressed on the membrane of tumor cells. Upon binding, MpL is endocytosed in a clathrin-dependent manner and accumulates initially in the Golgi apparatus and, finally, in the lysosomes. For effective binding and internalization a functional binding site on the α-repeat is needed. To test the potential of MpL as a carrier for delivering protein drugs to cancer cells we constructed fusion proteins consisting of MpL and the cysteine peptidase inhibitors cystatin C and clitocypin. The fused proteins followed the same endocytic route as the unlinked MpL. Peptidase inhibitor-MpL fusions impaired both the intracellular degradation of extracellular matrix and the invasiveness of cancer cells. MpL is thus shown in vitro to be a lectin that can enable protein drugs to enter cancer cells, enhance their internalization and sort them to lysosomes and the Golgi apparatus.
[Mh] Termos MeSH primário: Portadores de Fármacos
Proteínas Fúngicas/metabolismo
Lectinas/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Membrana Celular/metabolismo
Colágeno Tipo IV/metabolismo
Endocitose
Glicoproteínas/metabolismo
Seres Humanos
Espaço Intracelular/metabolismo
Ligação Proteica
Transporte Proteico
Proteólise
Proteínas Recombinantes de Fusão/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type IV); 0 (Drug Carriers); 0 (Fungal Proteins); 0 (Glycoproteins); 0 (Lectins); 0 (Recombinant Fusion Proteins)
[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.15849


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[PMID]:28467828
[Au] Autor:Ooi JD; Petersen J; Tan YH; Huynh M; Willett ZJ; Ramarathinam SH; Eggenhuizen PJ; Loh KL; Watson KA; Gan PY; Alikhan MA; Dudek NL; Handel A; Hudson BG; Fugger L; Power DA; Holt SG; Coates PT; Gregersen JW; Purcell AW; Holdsworth SR; La Gruta NL; Reid HH; Rossjohn J; Kitching AR
[Ad] Endereço:Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, Clayton, Victoria 3168, Australia.
[Ti] Título:Dominant protection from HLA-linked autoimmunity by antigen-specific regulatory T cells.
[So] Source:Nature;545(7653):243-247, 2017 05 11.
[Is] ISSN:1476-4687
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Susceptibility and protection against human autoimmune diseases, including type I diabetes, multiple sclerosis, and Goodpasture disease, is associated with particular human leukocyte antigen (HLA) alleles. However, the mechanisms underpinning such HLA-mediated effects on self-tolerance remain unclear. Here we investigate the molecular mechanism of Goodpasture disease, an HLA-linked autoimmune renal disorder characterized by an immunodominant CD4 T-cell self-epitope derived from the α3 chain of type IV collagen (α3 ). While HLA-DR15 confers a markedly increased disease risk, the protective HLA-DR1 allele is dominantly protective in trans with HLA-DR15 (ref. 2). We show that autoreactive α3 -specific T cells expand in patients with Goodpasture disease and, in α3 -immunized HLA-DR15 transgenic mice, α3 -specific T cells infiltrate the kidney and mice develop Goodpasture disease. HLA-DR15 and HLA-DR1 exhibit distinct peptide repertoires and binding preferences and present the α3 epitope in different binding registers. HLA-DR15-α3 tetramer T cells in HLA-DR15 transgenic mice exhibit a conventional T-cell phenotype (T ) that secretes pro-inflammatory cytokines. In contrast, HLA-DR1-α3 tetramer T cells in HLA-DR1 and HLA-DR15/DR1 transgenic mice are predominantly CD4 Foxp3 regulatory T cells (T cells) expressing tolerogenic cytokines. HLA-DR1-induced T cells confer resistance to disease in HLA-DR15/DR1 transgenic mice. HLA-DR15 and HLA-DR1 healthy human donors display altered α3 -specific T-cell antigen receptor usage, HLA-DR15-α3 tetramer Foxp3 T and HLA-DR1-α3 tetramer Foxp3 CD25 CD127 T dominant phenotypes. Moreover, patients with Goodpasture disease display a clonally expanded α3 -specific CD4 T-cell repertoire. Accordingly, we provide a mechanistic basis for the dominantly protective effect of HLA in autoimmune disease, whereby HLA polymorphism shapes the relative abundance of self-epitope specific T cells that leads to protection or causation of autoimmunity.
[Mh] Termos MeSH primário: Doença Antimembrana Basal Glomerular/imunologia
Autoimunidade/imunologia
Linfócitos T Reguladores/imunologia
[Mh] Termos MeSH secundário: Animais
Doença Antimembrana Basal Glomerular/patologia
Sequência de Bases
Linfócitos T CD4-Positivos/imunologia
Colágeno Tipo IV/química
Colágeno Tipo IV/imunologia
Citocinas/imunologia
Feminino
Fatores de Transcrição Forkhead/metabolismo
Subtipos Sorológicos de HLA-DR/imunologia
Antígeno HLA-DR1/imunologia
Seres Humanos
Epitopos Imunodominantes
Masculino
Camundongos
Camundongos Transgênicos
Modelos Moleculares
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Collagen Type IV); 0 (Cytokines); 0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (HLA-DR Serological Subtypes); 0 (HLA-DR1 Antigen); 0 (HLA-DR15 antigen); 0 (Immunodominant Epitopes)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1038/nature22329


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[PMID]:28448264
[Au] Autor:Lullove EJ
[Ad] Endereço:West Boca Center for Wound Healing, Boca Raton, FL.
[Ti] Título:Use of Ovine-based Collagen Extracellular Matrix and Gentian Violet/Methylene Blue Antibacterial Foam Dressings to Help Improve Clinical Outcomes in Lower Extremity Wounds: A Retrospective Cohort Study.
[So] Source:Wounds;29(4):107-114, 2017 04.
[Is] ISSN:1943-2704
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dressings that provide broad spectrum metalloprotease reduction along with inherent aspects of an extracellular matrix may contribute to improved wound healing outcomes and shorter treatment times. OBJECTIVE: The author performed a retrospective case series analysis to determine the clinical outcomes of regular debridement with the use of ovine-based collagen extracellular matrix dressings and gentian violet/methylene blue polyurethane antibacterial foam dressings in treating 53 patients with 53 chronic lower extremity wounds (diabetic foot ulcers [DFUs], venous leg ulcers, and heel pressure ulcers). MATERIALS AND METHODS: Patients were treated twice weekly in an outpatient clinic for the first 4 weeks and weekly thereafter until closure. RESULTS: Average body mass index (BMI) for the study population was 28.3, and the average patient age was 75.9 years. Mean percent wound surface area reduction at 4, 8, and 12 weeks was 38.5%, 73.3%, and 91.3%, respectively. Average time to closure for all wounds was 10.6 weeks (range, 5-24 weeks). All wounds were 100% reepithelialized by week 20 except 1 DFU that reepithelialized at week 24. The average cost of care for a single wound episode (from presentation to closure) was $2749.49. CONCLUSION: Results of this analysis showed that the healing of chronic wounds in this series could be achieved at a reasonable cost with regular debridement and a collagen matrix dressing regimen, even in patients of advanced age and above average BMI as well as in wounds that did not achieve > 40% wound surface area reduction at 4 weeks.
[Mh] Termos MeSH primário: Antibacterianos/uso terapêutico
Pé Diabético/terapia
Violeta de Genciana/uso terapêutico
Úlcera da Perna/terapia
Azul de Metileno/uso terapêutico
Lesão por Pressão/terapia
Úlcera Varicosa/terapia
Cicatrização/fisiologia
[Mh] Termos MeSH secundário: Idoso
Assistência Ambulatorial/métodos
Colágeno Tipo IV/farmacologia
Colágeno Tipo IV/uso terapêutico
Desbridamento/métodos
Pé Diabético/patologia
Matriz Extracelular/patologia
Feminino
Violeta de Genciana/farmacologia
Seres Humanos
Úlcera da Perna/patologia
Masculino
Azul de Metileno/farmacologia
Curativos Oclusivos
Lesão por Pressão/patologia
Estudos Retrospectivos
Resultado do Tratamento
Úlcera Varicosa/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Collagen Type IV); J4Z741D6O5 (Gentian Violet); T42P99266K (Methylene Blue)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180103
[Lr] Data última revisão:
180103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE


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[PMID]:28457922
[Au] Autor:Yasuda J; Okada M; Yamawaki H
[Ad] Endereço:Laboratory of Veterinary Pharmacology, School of Veterinary Medicine, Kitasato University, Higashi 23 Bancho 35-1, Towada, Aomori 034-8628, Japan.
[Ti] Título:T3 peptide, an active fragment of tumstatin, inhibits H O -induced apoptosis in H9c2 cardiomyoblasts.
[So] Source:Eur J Pharmacol;807:64-70, 2017 Jul 15.
[Is] ISSN:1879-0712
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Tumstatin, a cleaved fragment of α3 chain of type IV collagen, is an endogenous anti-angiogenetic peptide. Although the expression level of tumstatin changes in the heart tissues of certain experimental cardiac disease models, its effect on cardiomyocytes has not been clarified. In this study, we examined the effects of T3 peptide, an active subfragment of tumstatin, on hydrogen peroxide (H O )-induced cell death in H9c2 cardiomyoblasts. Cell viability was examined by a cell counting assay. Staining using 4', 6-diamidino-2-phenylindole was performed to observe nuclear morphology. Western blotting was performed to examine cleaved caspase-3 expression. Mitochondrial membrane potential and morphology were detected by a Mito Tracker Red staining. Intracellular reactive oxygen species production was examined by 2', 7'-dichlorodihydrofluorescein diacetate staining. T3 peptide (300, 1000ng/ml) suppressed H O (1mM)-induced cell death, apoptotic changes of nuclei and cleaved caspas-3 expression in a concentration-dependent manner. T3 peptide also inhibited H O -induced loss of mitochondrial membrane potential, mitochondrial fission and reactive oxygen species production. Cilengitide, an integrin α ß /α ß inhibitor, prevents the inhibitory effect of T3 peptide on H O -induced reactive oxygen species production. In conclusion, T3 peptide inhibits H O -induced apoptosis at least partly via the inhibition of intracellular reactive oxygen species production through the action on integrin.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Autoantígenos/química
Colágeno Tipo IV/química
Peróxido de Hidrogênio/farmacologia
Miócitos Cardíacos/citologia
Miócitos Cardíacos/efeitos dos fármacos
Fragmentos de Peptídeos/farmacologia
[Mh] Termos MeSH secundário: Animais
Caspase 3/metabolismo
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Peróxido de Hidrogênio/antagonistas & inibidores
Espaço Intracelular/efeitos dos fármacos
Espaço Intracelular/metabolismo
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Dinâmica Mitocondrial/efeitos dos fármacos
Miócitos Cardíacos/metabolismo
Proteólise/efeitos dos fármacos
Ratos
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantigens); 0 (Collagen Type IV); 0 (Peptide Fragments); 0 (Reactive Oxygen Species); 0 (type IV collagen alpha3 chain); BBX060AN9V (Hydrogen Peroxide); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171205
[Lr] Data última revisão:
171205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


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[PMID]:28745689
[Au] Autor:Bulanov NM; Serova AG; Kuznetsova EI; Bulanova ML; Novikov PI; Kozlovskaya LV; Moiseev SV
[Ad] Endereço:I.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia, Moscow, Russia.
[Ti] Título:[Kidney injury molecules (KIM-1, MCP-1) and type IV collagen in the assessment of activity of antineutrophil cytoplasmic antibody-associated glomerulonephritis].
[Ti] Título:Molekuly povrezhdeniia pochechnoi tkani (KIM-1, MCP-1) i kollagen IV tipa v otsenke aktivnosti assotsiirovannogo s antineitrofil'nymi tsitoplazmaticheskimi antitelami glomerulonefrita..
[So] Source:Ter Arkh;89(6):48-55, 2017.
[Is] ISSN:0040-3660
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:AIM: To assess the significance of determining the serum and urinary concentrations of monocyte chemotactic protein-1 (MCP-1), kidney injury molecule-1 (KIM-1), and type IV collagen in patients with antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) to estimate the activity of renal involvement in AAV. SUBJECTS AND METHODS: 78 patients (32 men and 46 women) (median age 55 (45; 61) years) with AAV were examined. The patients were divided into 3 groups according to the AAV activity estimated using the Birmingham vasculitis activity Score (BVAS): 1) 25 patients with active ANCA-associated glomerulonephritis (GN); 2) 26 patients with active AAV without renal involvement; 3) 27 patients in sustained AAV remission. The serum and urinary concentrations of the markers were measured by enzyme immunoassay. RESULTS: The urinary concentration of all 3 biomarkers was higher in patients with renal involvement (Group 1); the differences in the levels of MCP-1 and type IV collagen were statistically significant as compared to Groups 2 and 3 (p<0.01), while that in KIM-1 level was only in Group 2. There were statistically significant correlations between the urinary concentration of these biomarkers and the traditional GN activity indices (erythrocyturia, daily proteinuria (DPU), total BVAS scores that reflect renal involvement, as well as serum creatinine levels and estimated glomerular filtration rate (p<0.05). ROC curve analysis showed that the urinary MCP-1 excretion of ≥159 pg/ml had the highest (92%) sensitivity and urinary type IV collagen excretion of ≥3.09 µg/l had the highest (86%) specificity in assessing the activity of ANCA-associated GN. At the same time, their diagnostic value increased in terms of a combination of DPU and ESR (96% sensitivity, 84.9% specificity). CONCLUSION: The urinary excretion of MCP-1, KIM-1, and type IV collagen reflects the severity of local renal inflammation in AAV patients and a study of these indicators is a promising diagnostic tool for assessing the activity of ANCA-associated GN.
[Mh] Termos MeSH primário: Vasculite Associada a Anticorpo Anticitoplasma de Neutrófilos
Anticorpos Anticitoplasma de Neutrófilos/imunologia
Quimiocina CCL2
Colágeno Tipo IV
Glomerulonefrite
Receptor Celular 1 do Vírus da Hepatite A
[Mh] Termos MeSH secundário: Vasculite Associada a Anticorpo Anticitoplasma de Neutrófilos/sangue
Vasculite Associada a Anticorpo Anticitoplasma de Neutrófilos/imunologia
Vasculite Associada a Anticorpo Anticitoplasma de Neutrófilos/urina
Biomarcadores/sangue
Biomarcadores/urina
Quimiocina CCL2/sangue
Quimiocina CCL2/imunologia
Quimiocina CCL2/urina
Colágeno Tipo IV/sangue
Colágeno Tipo IV/imunologia
Colágeno Tipo IV/urina
Feminino
Glomerulonefrite/sangue
Glomerulonefrite/imunologia
Glomerulonefrite/urina
Receptor Celular 1 do Vírus da Hepatite A/sangue
Receptor Celular 1 do Vírus da Hepatite A/imunologia
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Antineutrophil Cytoplasmic); 0 (Biomarkers); 0 (CCL2 protein, human); 0 (Chemokine CCL2); 0 (Collagen Type IV); 0 (HAVCR1 protein, human); 0 (Hepatitis A Virus Cellular Receptor 1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171129
[Lr] Data última revisão:
171129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.17116/terarkh201789648-55


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[PMID]:28982537
[Au] Autor:Chioran A; Duncan S; Catalano A; Brown TJ; Ringuette MJ
[Ad] Endereço:Department of Cell and Systems Biology, University of Toronto, Toronto, ON, Canada M5S 3G5.
[Ti] Título:Collagen IV trafficking: The inside-out and beyond story.
[So] Source:Dev Biol;431(2):124-133, 2017 11 15.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Collagen IV networks endow basement membranes (BMs) with remarkable tensile strength and function as morphoregulatory substrata for diverse tissue-specific developmental events. A complex repertoire of intracellular and extracellular molecular interactions are required for collagen IV secretion and supramolecular assembly into BMs. These include intracellular chaperones such as Heat shock protein 47 (Hsp47) and the chaperone-binding trafficking protein Transport and Golgi organization protein 1 (Tango1). Mutations in these proteins lead to compromised collagen IV protomer stability and secretion, leading to defective BM assembly and function. In addition to intracellular chaperones, a role for extracellular chaperones orchestrating the transport, supramolecular assembly, and architecture of collagen IV in BM is emerging. We present evidence derived from evolutionarily distant model organisms that supports an extracellular collagen IV chaperone-like activity for the matricellular protein SPARC (Secreted Protein, Acidic, Rich in Cysteine). Loss of SPARC disrupts BM homeostasis and compromises tissue biomechanics and physiological function. Thus, the combined contributions of intracellular and extracellular collagen IV-associated chaperones and chaperone-like proteins are critical to ensure proper secretion and stereotypic assembly of collagen IV networks in BMs.
[Mh] Termos MeSH primário: Colágeno Tipo IV/metabolismo
[Mh] Termos MeSH secundário: Animais
Membrana Basal/metabolismo
Evolução Molecular
Seres Humanos
Osteonectina/metabolismo
Dobramento de Proteína
Transporte Proteico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Collagen Type IV); 0 (Osteonectin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171007
[St] Status:MEDLINE


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[PMID]:28973331
[Au] Autor:Shiode Y; Morizane Y; Matoba R; Hirano M; Doi S; Toshima S; Takahashi K; Araki R; Kanzaki Y; Hosogi M; Yonezawa T; Yoshida A; Shiraga F
[Ad] Endereço:Department of Ophthalmology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan.
[Ti] Título:The Role of Inverted Internal Limiting Membrane Flap in Macular Hole Closure.
[So] Source:Invest Ophthalmol Vis Sci;58(11):4847-4855, 2017 Sep 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: To investigate the mechanism of macular hole (MH) closure following the inverted internal limiting membrane (ILM) technique. Methods: We performed the inverted ILM flap surgical technique as an experimental MH model in monkeys, and investigated the process of MH closure immunohistochemically. We then investigated the effects of type IV collagen, fibronectin, and laminin, which are constituent proteins of the ILM, on the proliferation and migration of cultivated Müller cells (MIO-M1). We also investigated the expression of neurotrophic factors and basic fibroblast growth factor (bFGF) in human ILM and MIO-M1 cells, and the effect of MIO-M1 migration on the expression of these factors, via immunohistochemical staining and the real-time reverse transcription polymerase chain reaction. Results: Ten days after inverted ILM flap surgery, the MH had closed and proliferating glial fibrillary acidic protein (GFAP)-positive cells surrounded the ILM. Type IV collagen, fibronectin, and laminin all enhanced the proliferation of MIO-M1 cells, and type IV collagen and fibronectin enhanced the migration of MIO-M1 cells. Neurotrophic factors and bFGF were present on the surface of the human ILM, and MIO-M1 cells produced these factors. Neurotrophic factors and bFGF were expressed to a significantly greater extent by migrating MIO-M1 cells than by these cells in their static state. Conclusions: During MH closure, the ILM functioned as a scaffold for the proliferation and migration of Müller cells, and may promote Müller cell activation. Neurotrophic factors and bFGF produced by activated Müller cells and present on the surface of the ILM may contribute to MH closure.
[Mh] Termos MeSH primário: Membrana Epirretiniana/cirurgia
Perfurações Retinianas/cirurgia
Retalhos Cirúrgicos
Vitrectomia/métodos
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Membrana Basal/cirurgia
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Colágeno Tipo IV/farmacologia
Modelos Animais de Doenças
Células Ependimogliais/efeitos dos fármacos
Células Ependimogliais/metabolismo
Membrana Epirretiniana/metabolismo
Fator 2 de Crescimento de Fibroblastos/metabolismo
Fibronectinas/farmacologia
Laminina/farmacologia
Macaca fascicularis
Masculino
Fatores de Crescimento Neural/metabolismo
Fatores de Crescimento Neural/farmacologia
Perfurações Retinianas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type IV); 0 (Fibronectins); 0 (Laminin); 0 (Nerve Growth Factors); 103107-01-3 (Fibroblast Growth Factor 2)
[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:171004
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.17-21756


  8 / 3270 MEDLINE  
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[PMID]:28954878
[Au] Autor:Rannikmäe K; Sivakumaran V; Millar H; Malik R; Anderson CD; Chong M; Dave T; Falcone GJ; Fernandez-Cadenas I; Jimenez-Conde J; Lindgren A; Montaner J; O'Donnell M; Paré G; Radmanesh F; Rost NS; Slowik A; Söderholm M; Traylor M; Pulit SL; Seshadri S; Worrall BB; Woo D; Markus HS; Mitchell BD; Dichgans M; Rosand J; Sudlow CLM; Stroke Genetics Network (SiGN), METASTROKE Collaboration, and International Stroke Genetics Consortium (ISGC)
[Ad] Endereço:From the Centre for Clinical Brain Sciences (K.R., C.L.M.S.), College of Medicine and Veterinary Medicine (V.S., H.M.), and Institute for Genetics and Molecular Medicine (C.L.M.S.), University of Edinburgh, UK; Institute for Stroke and Dementia Research (R.M., M.D.), Klinikum der Universität München
[Ti] Título: is associated with lacunar ischemic stroke and deep ICH: Meta-analyses among 21,500 cases and 40,600 controls.
[So] Source:Neurology;89(17):1829-1839, 2017 Oct 24.
[Is] ISSN:1526-632X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To determine whether common variants in familial cerebral small vessel disease (SVD) genes confer risk of sporadic cerebral SVD. METHODS: We meta-analyzed genotype data from individuals of European ancestry to determine associations of common single nucleotide polymorphisms (SNPs) in 6 familial cerebral SVD genes ( , , , , , and ) with intracerebral hemorrhage (ICH) (deep, lobar, all; 1,878 cases, 2,830 controls) and ischemic stroke (IS) (lacunar, cardioembolic, large vessel disease, all; 19,569 cases, 37,853 controls). We applied data quality filters and set statistical significance thresholds accounting for linkage disequilibrium and multiple testing. RESULTS: A locus in was associated (significance threshold < 3.5 × 10 ) with both lacunar IS (lead SNP rs9515201: odds ratio [OR] 1.17, 95% confidence interval [CI] 1.11-1.24, = 6.62 × 10 ) and deep ICH (lead SNP rs4771674: OR 1.28, 95% CI 1.13-1.44, = 5.76 × 10 ). A SNP in was associated (significance threshold < 5.5 × 10 ) with lacunar IS (rs79043147: OR 1.23, 95% CI 1.10-1.37, = 1.90 × 10 ) and less robustly with deep ICH. There was no clear evidence for association of common variants in either or with non-SVD strokes or in any of the other genes with any stroke phenotype. CONCLUSIONS: These results provide evidence of shared genetic determinants and suggest common pathophysiologic mechanisms of distinct ischemic and hemorrhagic cerebral SVD stroke phenotypes, offering new insights into the causal mechanisms of cerebral SVD.
[Mh] Termos MeSH primário: Hemorragia Cerebral/genética
Colágeno Tipo IV/genética
Polimorfismo de Nucleotídeo Único/genética
Acidente Vascular Cerebral Lacunar/genética
[Mh] Termos MeSH secundário: Hemorragia Cerebral/epidemiologia
Europa (Continente)/epidemiologia
Estudos de Associação Genética
Seres Humanos
Acidente Vascular Cerebral Lacunar/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (COL4A2 protein, human); 0 (Collagen Type IV)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171105
[Lr] Data última revisão:
171105
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170929
[St] Status:MEDLINE
[do] DOI:10.1212/WNL.0000000000004560


  9 / 3270 MEDLINE  
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[PMID]:28886586
[Au] Autor:Clark AG; Worni-Schudel IM; Korte FM; Foster MH
[Ad] Endereço:Department of Medicine, Duke University Health System, Durham, NC, USA; Durham VA Medical Center, Durham, NC, USA. Electronic address: amy.clark@duke.edu.
[Ti] Título:A murine Ig light chain transgene reveals IGKV3 gene contributions to anti-collagen types IV and II specificities.
[So] Source:Mol Immunol;91:49-56, 2017 11.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A subset of autoimmune diseases result from autoantibodies targeting epitopes on matrix collagen. The most extensively studied are anti-glomerular basement membrane glomerulonephritis (or its systemic counterpart Goodpasture's disease) that destroys kidneys and lungs, and rheumatoid arthritis that leads to disabling arthritis. Autoantibodies in these disorders bind evolutionarily conserved conformational epitopes on the noncollagenous domain 1 (NC1) of the alpha3 chain of type IV [alpha3(IV)NC1] collagen in glomerular and alveolar basement membranes, and on native or citrullinated type II collagen (CII) in joint cartilage, respectively. The genetic origins of pathogenic anti-collagen B cells in these diseases is unknown, but observations from murine models raise the possibility that they overlap despite distinct in vivo immunopathologies. Monoclonal autoantibodies isolated from mice immunized with alpha3(IV)NC1 collagen or CII show a biased use of Ig light chains (LC) encoded by genes of the IGKV3 subgroup (previously Vk21 family), paired with diverse Ig heavy chains. To further explore this relationship and determine if a single murine IGKV3 LC independently predisposes to both anti-collagen responses, we generated a novel transgenic (Tg) C57BL/6 mouse that expresses a productively rearranged IGKV3-encoded LC, termed mLCV3-Tg, in conjunction with endogenously rearranged Ig heavy chains. Tg mice are also genetically deficient in endogenous kappa chains to permit tracking of the mLCV3 transgene. We show that mLCV3-Tg mice are susceptible to humoral autoimmunity against both collagen chains. Anti-alpha3(IV)NC1 collagen, but not anti-CII, mLCV3-encoded Ig are detected in serum of unmanipulated Tg mice, while Toll-like receptor ligands induce secretion of mLCV3-Tg autoantibodies of both collagen specificities from splenocytes ex vivo. This indicates developmental survival of mLCV3-Tg B cells reactive with each antigen, and is consistent with production of the two anti-collagen autoIg from distinct B cell populations. Reduced B cell numbers, low serum Ig kappa levels, low cell surface Ig kappa density, and abundant endogenous lambda chain expression suggest that subsets of IGKV3-encoded B cells are regulated in vivo by mechanisms that include deletion, anergy, and LC editing. These results support the notion that murine IGKV3 LCs contribute structural fitness to antigen binding sites that support diverse anti-collagen autoimmune responses, that these responses are regulated in vivo, and that these cells can nonetheless readily escape immune regulation.
[Mh] Termos MeSH primário: Doença Antimembrana Basal Glomerular/imunologia
Autoanticorpos/imunologia
Colágeno Tipo II/imunologia
Colágeno Tipo IV/imunologia
Cadeias kappa de Imunoglobulina/imunologia
[Mh] Termos MeSH secundário: Animais
Doença Antimembrana Basal Glomerular/genética
Doença Antimembrana Basal Glomerular/patologia
Autoanticorpos/genética
Colágeno Tipo II/genética
Colágeno Tipo IV/genética
Cadeias kappa de Imunoglobulina/genética
Camundongos
Camundongos Endogâmicos NOD
Camundongos SCID
Camundongos Transgênicos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Collagen Type II); 0 (Collagen Type IV); 0 (Immunoglobulin kappa-Chains)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE


  10 / 3270 MEDLINE  
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[PMID]:28864775
[Au] Autor:López-Jiménez AJ; Basak T; Vanacore RM
[Ad] Endereço:From the Department of Medicine, Division of Nephrology and Hypertension and.
[Ti] Título:Proteolytic processing of lysyl oxidase-like-2 in the extracellular matrix is required for crosslinking of basement membrane collagen IV.
[So] Source:J Biol Chem;292(41):16970-16982, 2017 Oct 13.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lysyl oxidase-like-2 (LOXL2) is an enzyme secreted into the extracellular matrix that crosslinks collagens by mediating oxidative deamination of lysine residues. Our previous work demonstrated that this enzyme crosslinks the 7S domain, a structural domain that stabilizes collagen IV scaffolds in the basement membrane. Despite its relevant role in extracellular matrix biosynthesis, little is known about the structural requirements of LOXL2 that enable collagen IV crosslinking. In this study, we demonstrate that LOXL2 is processed extracellularly by serine proteases, generating a 65-kDa form lacking the first two scavenger receptor cysteine-rich domains. Site-specific mutagenesis to prevent proteolytic processing generated a full-length enzyme that is active toward a soluble substrate, but fails to crosslink insoluble collagen IV within the extracellular matrix. In contrast, the processed form of LOXL2 binds to collagen IV and crosslinks the 7S domain. Together, our data demonstrate that proteolytic processing is an important event that allows LOXL2-mediated crosslinking of basement membrane collagen IV.
[Mh] Termos MeSH primário: Aminoácido Oxirredutases/secreção
Membrana Basal/metabolismo
Colágeno Tipo IV/metabolismo
Matriz Extracelular/metabolismo
Processamento de Proteína Pós-Traducional/fisiologia
Proteólise
[Mh] Termos MeSH secundário: Aminoácido Oxirredutases/genética
Colágeno Tipo IV/genética
Matriz Extracelular/genética
Células HEK293
Seres Humanos
Mutagênese Sítio-Dirigida
Domínios Proteicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type IV); EC 1.4.- (Amino Acid Oxidoreductases); EC 1.4.3.- (LOXL2 protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170903
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.798603



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