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[PMID]:27776448
[Au] Autor:Ye C; Zhang W; Jiang S; Yu Y; Zhou X; Zhu L; Xue D; He R
[Ad] Endereço:a Department of Orthopedic Surgery , the Second Affiliated Hospital, School of Medicine, Zhejiang University , Hangzhou , Zhejiang , China.
[Ti] Título:Platelet-derived growth factor-BB attenuates titanium-particle-induced osteolysis in vivo.
[So] Source:Growth Factors;34(5-6):177-186, 2016 12.
[Is] ISSN:1029-2292
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Inflammation and osteoclastogenesis play critical roles in wear-particle-induced periprosthetic osteolysis (WPO). Platelet-derived growth factor-BB (PDGF-BB) could promote osteogenesis and inhibit inflammatory response. The aim of this study was to investigate the impact of PDGF-BB on WPO. Mice were divided into four groups, namely, sham, vehicle, low-, and high-dose PDGF-BB groups. Mice in the rhPDGF-BB groups were treated with PDGF-BB at 0.25 or 1 mg/ml/kg/day. Mice in the sham and vehicle groups received PBS daily. Two weeks after surgery, calvariae were harvested. Immunohistochemical analysis and µ-CT showed that PDGF-BB significantly reduced osteoclast formation and bone resorption. ELISA showed that rhPDGF-BB decreased the secretion of TNF-α, IL-1ß, and IL-6. Western blotting revealed that rhPDGF-BB stimulated the expression of osteocalcin and osteoprotegerin. Furthermore, more VEGF and CD31 proteins were observed due to PDGF-BB by immunofluorescence. In conclusion, these findings suggest that rhPDGF-BB represents a potential treatment for WPO.
[Mh] Termos MeSH primário: Interface Osso-Implante/patologia
Osteólise/tratamento farmacológico
Proteínas Proto-Oncogênicas c-sis/uso terapêutico
Titânio/efeitos adversos
[Mh] Termos MeSH secundário: Animais
Interleucina-1beta/genética
Interleucina-1beta/metabolismo
Interleucina-6/genética
Interleucina-6/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Osteólise/etiologia
Molécula-1 de Adesão Celular Endotelial de Plaquetas/genética
Molécula-1 de Adesão Celular Endotelial de Plaquetas/metabolismo
Proteínas Proto-Oncogênicas c-sis/administração & dosagem
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
Fator A de Crescimento do Endotélio Vascular/genética
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (Interleukin-6); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (Proto-Oncogene Proteins c-sis); 0 (Tumor Necrosis Factor-alpha); 0 (Vascular Endothelial Growth Factor A); 1B56C968OA (becaplermin); D1JT611TNE (Titanium)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1080/08977194.2016.1240680


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[PMID]:27778377
[Au] Autor:Kyyriäinen J; Ekolle Ndode-Ekane X; Pitkänen A
[Ad] Endereço:Department of Neurobiology, A. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, FI-70211, Finland.
[Ti] Título:Dynamics of PDGFRß expression in different cell types after brain injury.
[So] Source:Glia;65(2):322-341, 2017 02.
[Is] ISSN:1098-1136
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Platelet-derived growth factor receptor ß (PDGFRß) is upregulated after brain injury and its depletion results in the blood-brain barrier (BBB) damage. We investigated the time-window and localization of PDGFRß expression in mice with intrahippocampal kainic acid-induced status epilepticus (SE) and in rats with lateral fluid-percussion-induced traumatic brain injury (TBI). Tissue immunohistochemistry was evaluated at several time-points after SE and TBI. The distribution of PDGFRß was analyzed, and its cell type-specific expression was verified with double/triple-labeling of astrocytes (GFAP), NG2 cells, and endothelial cells (RECA-1). In normal mouse hippocampus, we found evenly distributed PDGFRß+ parenchymal cells. In double-labeling, all NG2+ and 40%-60% GFAP+ cells were PDGFRß+. After SE, PDGFRß+ cells clustered in the ipsilateral hilus (178% of that in controls at fourth day, 225% at seventh day, P < 0.05) and in CA3 (201% at seventh day, P < 0.05), but the total number of PDGFRß+ cells was not altered. As in controls, PDGFRß-immunoreactivity was detected in parenchymal NG2+ and GFAP+ cells. We also observed PDGFRß+ structural pericytes, detached reactive pericytes, and endothelial cells. After TBI, PDGFRß+ cells clustered in the perilesional cortex and thalamus, particularly during the first post-injury week. PDGFRß immunopositivity was observed in NG2+ and GFAP+ cells, structural pericytes, detached reactive pericytes, and endothelial cells. In some animals, PDGFRß vascular staining was observed around the cortical glial scar for up to 3 months. Our data revealed an acute accumulation of PDGFRß+ BBB-related cells in degenerating brain areas, which can be long lasting, suggesting an active role for PDGFRß-signaling in blood vessel and post-injury tissue recovery. GLIA 2017;65:322-341.
[Mh] Termos MeSH primário: Astrócitos/classificação
Astrócitos/metabolismo
Lesões Encefálicas/patologia
Células Endoteliais/metabolismo
Molécula-1 de Adesão Celular Endotelial de Plaquetas/metabolismo
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos/metabolismo
Modelos Animais de Doenças
Proteína Glial Fibrilar Ácida/metabolismo
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Pericitos/metabolismo
Pericitos/patologia
Proteoglicanas/metabolismo
Ratos
Ratos Sprague-Dawley
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/genética
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens); 0 (Glial Fibrillary Acidic Protein); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (Proteoglycans); 0 (chondroitin sulfate proteoglycan 4); 147336-22-9 (Green Fluorescent Proteins); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor alpha)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1002/glia.23094


  3 / 4907 MEDLINE  
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[PMID]:29351334
[Au] Autor:Chang W; Lajko M; Fawzi AA
[Ad] Endereço:Department of Ophthalmology, Northwestern University, Feinberg School of Medicine, Chicago, IL, United States of America.
[Ti] Título:Endothelin-1 is associated with fibrosis in proliferative diabetic retinopathy membranes.
[So] Source:PLoS One;13(1):e0191285, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To characterize the relationship between endothelin-1 and fibrosis in epiretinal membranes in proliferative diabetic retinopathy and explore the role of endothelial-mesenchymal transition in these membranes. METHODS: Membranes were obtained from eyes undergoing pars plana vitrectomy for complicated proliferative diabetic retinopathy or idiopathic epiretinal membrane. Through standard immunohistochemical techniques, we labeled membranes to explore the distribution of endothelin-1 and endothelin receptor B, comparing proliferative diabetic retinopathy and idiopathic epiretinal membranes. In addition, membranes were also labeled with markers for fibroblasts, endothelial, and glial cells and studied with confocal laser scanning microscopy. The intensity of endothelin-1 labeling was quantified using standard image analysis software. RESULTS: Fourteen membranes were included in the analysis, nine from eyes with proliferative diabetic retinopathy and five idiopathic membranes. Flatmount diabetic membranes showed co-localization of endothelin-1 with S100A4 and CD31. Immunohistochemistry and quantitative analysis of cross-sectional membranes showed significantly higher endothelin-1 labeling in proliferative diabetic retinopathy membranes compared to idiopathic membranes (p<0.05). Diabetic membranes showed more elements staining positive for S100A4 compared to idiopathic membranes. CONCLUSION: Epiretinal membrane formation in proliferative diabetic retinopathy involves higher tissue levels of endothelin-1 and fibroblastic activity. Furthermore, endothelin-1, endothelial and fibroblastic staining appear to be correlated, suggestive of endothelial-to-mesenchymal transition in proliferative diabetic retinopathy.
[Mh] Termos MeSH primário: Retinopatia Diabética/metabolismo
Retinopatia Diabética/patologia
Endotelina-1/metabolismo
[Mh] Termos MeSH secundário: Adulto
Proliferação Celular
Feminino
Fibrose
Proteína Glial Fibrilar Ácida/metabolismo
Seres Humanos
Masculino
Membranas/patologia
Meia-Idade
Molécula-1 de Adesão Celular Endotelial de Plaquetas/metabolismo
Retina/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Endothelin-1); 0 (Glial Fibrillary Acidic Protein); 0 (Platelet Endothelial Cell Adhesion Molecule-1)
[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:180120
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191285


  4 / 4907 MEDLINE  
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[PMID]:29253861
[Au] Autor:Eich G; Bartosova M; Tischer C; Wlodkowski TT; Schaefer B; Pichl S; Kraewer N; Ranchin B; Vondrak K; Liebau MC; Hackert T; Schmitt CP
[Ad] Endereço:Center for Pediatric and Adolescent Medicine, University Hospital Heidelberg, Heidelberg, Germany.
[Ti] Título:Bicarbonate buffered peritoneal dialysis fluid upregulates angiopoietin-1 and promotes vessel maturation.
[So] Source:PLoS One;12(12):e0189903, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Ultrafiltration decline is a progressive issue for patients on chronic peritoneal dialysis (PD) and can be caused by peritoneal angiogenesis induced by PD fluids. A recent pediatric trial suggests better preservation of ultrafiltration with bicarbonate versus lactate buffered fluid; underlying molecular mechanisms are unknown. METHODS: Angiogenic cytokine profile, tube formation capacity and Receptor Tyrosine Kinase translocation were assessed in primary human umbilical vein endothelial cells following incubation with bicarbonate (BPDF) and lactate buffered (LPDF), pH neutral PD fluid with low glucose degradation product content and lactate buffered, acidic PD fluid with high glucose degradation product content (CPDF). Peritoneal biopsies from age-, PD-vintage- and dialytic glucose exposure matched, peritonitis-free children on chronic PD underwent automated histomorphometry and immunohistochemistry. RESULTS: In endothelial cells angiopoietin-1 mRNA and protein abundance increased 200% upon incubation with BPDF, but decreased by 70% with LPDF as compared to medium control; angiopoietin-2 remained unchanged. Angiopoietin-1/Angiopoietin-2 protein ratio was 15 and 3-fold increased with BPDF compared to LPDF and medium. Time-lapse microscopy with automated network analysis demonstrated less endothelial cell tube formation with BPDF compared to LPDF and CPDF incubation. Receptor Tyrosine Kinase translocated to the cell membrane in BPDF but not in LPDF or CPDF incubated endothelial cells. In children dialyzed with BPDF peritoneal vessels were larger and angiopoietin-1 abundance in CD31 positive endothelium higher compared to children treated with LPDF. CONCLUSION: Bicarbonate buffered PD fluid promotes vessel maturation via upregulation of angiopoietin-1 in vitro and in children on dialysis. Our findings suggest a molecular mechanism for the observed superior preservation of ultrafiltration capacity with bicarbonate buffered PD fluid with low glucose degradation product content.
[Mh] Termos MeSH primário: Angiopoietina-1/metabolismo
Bicarbonatos/química
Tampões (Química)
Diálise Peritoneal
[Mh] Termos MeSH secundário: Adolescente
Angiopoietina-2/metabolismo
Biópsia
Criança
Doença Crônica
Citocinas/metabolismo
Células Endoteliais/metabolismo
Glucose/química
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Concentração de Íons de Hidrogênio
Nefropatias/terapia
Lactatos/química
Peritônio/patologia
Molécula-1 de Adesão Celular Endotelial de Plaquetas/metabolismo
Receptores Proteína Tirosina Quinases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ANGPT1 protein, human); 0 (ANGPT2 protein, human); 0 (Angiopoietin-1); 0 (Angiopoietin-2); 0 (Bicarbonates); 0 (Buffers); 0 (Cytokines); 0 (Lactates); 0 (Platelet Endothelial Cell Adhesion Molecule-1); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189903


  5 / 4907 MEDLINE  
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[PMID]:29244817
[Au] Autor:Montiel-Dávalos A; Silva Sánchez GJ; Huerta-García E; Rueda-Romero C; Soca Chafre G; Mitre-Aguilar IB; Alfaro-Moreno E; Pedraza-Chaverri J; López-Marure R
[Ad] Endereço:Subdirección de Investigación Básica, Instituto Nacional de Cancerología, Ciudad de México, México.
[Ti] Título:Curcumin inhibits activation induced by urban particulate material or titanium dioxide nanoparticles in primary human endothelial cells.
[So] Source:PLoS One;12(12):e0188169, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Curcumin has protective effects against toxic agents and shows preventive properties for various diseases. Particulate material with an aerodynamic diameter of ≤10 µm (PM10) and titanium dioxide nanoparticles (TiO2-NPs) induce endothelial dysfunction and activation. We explored whether curcumin is able to attenuate different events related to endothelial activation. This includes adhesion, expression of adhesion molecules and oxidative stress induced by PM10 and TiO2-NPs. Human umbilical vein endothelial cells (HUVEC) were treated with 1, 10 and 100 µM curcumin for 1 h and then exposed to PM10 at 3 µg/cm2 or TiO2-NPs at 10 µg/cm2. Cell adhesion was evaluated by co-culture with U937 human myelomonocytic cells. Adhesion molecules expression was measured by flow cytometry after 3 or 24 h of exposure. Oxidative stress was determined by 2,7-dichlorodihydrofluorescein (H2DCF) oxidation. PM10 and TiO2-NPs induced the adhesion of U937 cells and the expression of E- and P-selectins, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and platelet-endothelial cell adhesion molecule-1 (PECAM-1). The expression of E- and P-selectins matched the adhesion of monocytes to HUVEC after 3 h. In HUVEC treated with 1 or 10 µM curcumin, the expression of adhesion molecules and monocytes adhesion was significantly diminished. Curcumin also partially reduced the H2DCF oxidation induced by PM10 and TiO2-NPs. Our results suggest an anti-inflammatory and antioxidant role by curcumin attenuating the activation caused on endothelial cells by exposure to particles. Therefore, curcumin could be useful in the treatment of diseases where an inflammatory process and endothelial activation are involved.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Curcumina/farmacologia
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Nanopartículas/toxicidade
Material Particulado/antagonistas & inibidores
[Mh] Termos MeSH secundário: Biomarcadores/metabolismo
Adesão Celular/efeitos dos fármacos
Cidades
Técnicas de Cocultura
Selectina E/genética
Selectina E/metabolismo
Fluoresceínas/química
Expressão Gênica
Células Endoteliais da Veia Umbilical Humana/citologia
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Molécula 1 de Adesão Intercelular/genética
Molécula 1 de Adesão Intercelular/metabolismo
México
Estresse Oxidativo/efeitos dos fármacos
Selectina-P/genética
Selectina-P/metabolismo
Material Particulado/farmacologia
Molécula-1 de Adesão Celular Endotelial de Plaquetas/genética
Molécula-1 de Adesão Celular Endotelial de Plaquetas/metabolismo
Titânio/farmacologia
Células U937
Molécula 1 de Adesão de Célula Vascular/genética
Molécula 1 de Adesão de Célula Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Biomarkers); 0 (E-Selectin); 0 (Fluoresceins); 0 (ICAM1 protein, human); 0 (P-Selectin); 0 (Particulate Matter); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (SELE protein, human); 0 (Vascular Cell Adhesion Molecule-1); 106070-31-9 (2',7'-dichlorodihydrofluorescein); 126547-89-5 (Intercellular Adhesion Molecule-1); 15FIX9V2JP (titanium dioxide); D1JT611TNE (Titanium); IT942ZTH98 (Curcumin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188169


  6 / 4907 MEDLINE  
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[PMID]:29236794
[Au] Autor:Arruda EGP; Munhoz AM; Matsumoto W; Ueda T; Coudry RA; Gemperli R
[Ad] Endereço:Assistant Professor, Plastic Surgery Division, Department of Surgery, School of Medicine, Universidade de São Paulo (USP), Brazil. Conception and design of the study, acquisition and interpretation of data.
[Ti] Título:Qualitative analysis of the viability of autogenous fat grafts grafted in different environments of interstitial pressure. Preliminary results and description of a new experimental model in mini-pigs.
[So] Source:Acta Cir Bras;32(11):891-902, 2017 Nov.
[Is] ISSN:1678-2674
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To evaluate the feasibility of an experimental model of autologous fat graft (AFG) in different interstitial pressure (IP) environments. METHODS: Three mini-pigs(Minipig-BR) with age of 8 months (weight: 25-30 kg) were used. AFG were collected from the bucal fat pad, and grafted in the intramuscular pocket (biceps femoralis muscle). IP model was based on a fusiform ressection followed by primary closure "under tension". A blood pressure catheter located in the intramuscular region connected to a pressure module was applied to quantify IP. RESULTS: The mean operative time was 236 min (210 - 272 min). All the AFG and muscular segments were removed successfully. Average interstitial pressure CP and H were 3 and 10.6 mmHg respectively. The AFG were biopsied for histopathological analysis 30 days after graft. Hematoxylin-eosin staining and immunohistochemical analyzes (TNF-alpha, CD31 and Perilipine with monoclonal antibodies) were employed. CONCLUSION: The data show that minipigs model could be used as a recipient site for autologous fat graft techniques and allow the development of studies to explore the AFG intake and pathophysiology response.
[Mh] Termos MeSH primário: Tecido Adiposo/transplante
Modelos Animais de Doenças
Procedimentos Cirúrgicos Reconstrutivos/métodos
Transplante Autólogo/métodos
[Mh] Termos MeSH secundário: Animais
Estudos de Viabilidade
Sobrevivência de Enxerto
Imuno-Histoquímica
Masculino
Perilipinas/análise
Molécula-1 de Adesão Celular Endotelial de Plaquetas/análise
Pressão
Procedimentos Cirúrgicos Reconstrutivos/normas
Suínos
Porco Miniatura
Transplante Autólogo/normas
Fator de Necrose Tumoral alfa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Perilipins); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171220
[Lr] Data última revisão:
171220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE


  7 / 4907 MEDLINE  
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[PMID]:29182510
[Au] Autor:Soe HJ; Khan AM; Manikam R; Samudi Raju C; Vanhoutte P; Sekaran SD
[Ad] Endereço:1​Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
[Ti] Título:High dengue virus load differentially modulates human microvascular endothelial barrier function during early infection.
[So] Source:J Gen Virol;98(12):2993-3007, 2017 Dec.
[Is] ISSN:1465-2099
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Plasma leakage is the main pathophysiological feature in severe dengue, resulting from altered vascular barrier function associated with an inappropriate immune response triggered upon infection. The present study investigated functional changes using an electric cell-substrate impedance sensing system in four (brain, dermal, pulmonary and retinal) human microvascular endothelial cell (MEC) lines infected with purified dengue virus, followed by assessment of cytokine profiles and the expression of inter-endothelial junctional proteins. Modelling of changes in electrical impedance suggests that vascular leakage in dengue-infected MECs is mostly due to the modulation of cell-to-cell interactions, while this loss of vascular barrier function observed in the infected MECs varied between cell lines and DENV serotypes. High levels of inflammatory cytokines (IL-6 and TNF-α), chemokines (CXCL1, CXCL5, CXCL11, CX3CL1, CCL2 and CCL20) and adhesion molecules (VCAM-1) were differentially produced in the four infected MECs. Further, the tight junctional protein, ZO-1, was down-regulated in both the DENV-1-infected brain and pulmonary MECs, while claudin-1, PECAM-1 and VE-cadherin were differentially expressed in these two MECs after infection. Non-purified virus stock was also studied to investigate the impact of virus stock purity on dengue-specific immune responses, and the results suggest that virus stock propagated through cell culture may include factors that mask or alter the DENV-specific immune responses of the MECs. The findings of the present study show that high DENV load differentially modulates human microvascular endothelial barrier function and disrupts the function of inter-endothelial junctional proteins during early infection with organ-specific cytokine production.
[Mh] Termos MeSH primário: Células Endoteliais/virologia
Endotélio Vascular/virologia
Interações Hospedeiro-Patógeno
Carga Viral/imunologia
[Mh] Termos MeSH secundário: Antígenos CD/genética
Antígenos CD/imunologia
Encéfalo/citologia
Encéfalo/imunologia
Encéfalo/virologia
Caderinas/genética
Caderinas/imunologia
Linhagem Celular
Quimiocina CCL2/genética
Quimiocina CCL2/imunologia
Quimiocina CCL20/genética
Quimiocina CCL20/imunologia
Quimiocina CX3CL1/genética
Quimiocina CX3CL1/imunologia
Quimiocinas CXC/genética
Quimiocinas CXC/imunologia
Claudina-1/genética
Claudina-1/imunologia
Vírus da Dengue/genética
Vírus da Dengue/crescimento & desenvolvimento
Vírus da Dengue/imunologia
Derme/citologia
Derme/imunologia
Derme/virologia
Impedância Elétrica
Células Endoteliais/citologia
Células Endoteliais/imunologia
Endotélio Vascular/citologia
Endotélio Vascular/imunologia
Regulação da Expressão Gênica
Seres Humanos
Interleucina-6/genética
Interleucina-6/imunologia
Pulmão/citologia
Pulmão/imunologia
Pulmão/virologia
Especificidade de Órgãos
Permeabilidade
Molécula-1 de Adesão Celular Endotelial de Plaquetas/genética
Molécula-1 de Adesão Celular Endotelial de Plaquetas/imunologia
Retina/citologia
Retina/imunologia
Retina/virologia
Transdução de Sinais
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/imunologia
Molécula 1 de Adesão de Célula Vascular/genética
Molécula 1 de Adesão de Célula Vascular/imunologia
Internalização do Vírus
Proteína da Zônula de Oclusão-1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (CCL2 protein, human); 0 (CCL20 protein, human); 0 (CX3CL1 protein, human); 0 (Cadherins); 0 (Chemokine CCL2); 0 (Chemokine CCL20); 0 (Chemokine CX3CL1); 0 (Chemokines, CXC); 0 (Claudin-1); 0 (IL6 protein, human); 0 (Interleukin-6); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (TJP1 protein, human); 0 (Tumor Necrosis Factor-alpha); 0 (Vascular Cell Adhesion Molecule-1); 0 (Zonula Occludens-1 Protein); 0 (cadherin 5)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171213
[Lr] Data última revisão:
171213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1099/jgv.0.000981


  8 / 4907 MEDLINE  
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[PMID]:29059426
[Au] Autor:Bais C; Mueller B; Brady MF; Mannel RS; Burger RA; Wei W; Marien KM; Kockx MM; Husain A; Birrer MJ; NRG Oncology/Gynecologic Oncology Group
[Ad] Endereço:Genentech Inc., South San Francisco, CA; F Hoffmann-La Roche Ltd, Basel, Switzerland; NRG Statistical and Data Center, Roswell Park Cancer Institute, Buffalo, NY; University of Oklahoma, Oklahoma City, OK; Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, University of Penns
[Ti] Título:Tumor Microvessel Density as a Potential Predictive Marker for Bevacizumab Benefit: GOG-0218 Biomarker Analyses.
[So] Source:J Natl Cancer Inst;109(11), 2017 Nov 01.
[Is] ISSN:1460-2105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Combining bevacizumab with frontline chemotherapy statistically significantly improved progression-free survival (PFS) but not overall survival (OS) in the phase III GOG-0218 trial. Evaluation of candidate biomarkers was an exploratory objective. Methods: Patients with stage III (incompletely resected) or IV ovarian cancer were randomly assigned to receive six chemotherapy cycles with placebo or bevacizumab followed by single-agent placebo or bevacizumab. Five candidate tumor biomarkers were assessed by immunohistochemistry. The biomarker-evaluable population was categorized into high or low biomarker-expressing subgroups using median and quartile cutoffs. Associations between biomarker expression and efficacy were analyzed. All statistical tests were two-sided. Results: The biomarker-evaluable population (n = 980) comprising 78.5% of the intent-to-treat population had representative baseline characteristics and efficacy outcomes. Neither prognostic nor predictive associations were seen for vascular endothelial growth factor (VEGF) receptor-2, neuropilin-1, or MET. Higher microvessel density (MVD; measured by CD31) showed predictive value for PFS (hazard ratio [HR] for bevacizumab vs placebo = 0.40, 95% confidence interval [CI] = 0.29 to 0.54, vs 0.80, 95% CI = 0.59 to 1.07, for high vs low MVD, respectively, P interaction = .003) and OS (HR = 0.67, 95% CI = 0.51 to 0.88, vs 1.10, 95% CI = 0.84 to 1.44, P interaction = .02). Tumor VEGF-A was not predictive for PFS but showed potential predictive value for OS using a third-quartile cutoff for high VEGF-A expression. Conclusions: These retrospective tumor biomarker analyses suggest a positive association between density of vascular endothelial cells (the predominant cell type expressing VEGF receptors) and tumor VEGF-A levels and magnitude of bevacizumab effect in ovarian cancer. The potential predictive value of MVD (CD31) and tumor VEGF-A is consistent with a mechanism of action driven by VEGF-A signaling blockade.
[Mh] Termos MeSH primário: Inibidores da Angiogênese/uso terapêutico
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Bevacizumab/uso terapêutico
Biomarcadores Tumorais/análise
Neoplasias Ovarianas/irrigação sanguínea
Neoplasias Ovarianas/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores Tumorais/metabolismo
Carboplatina/administração & dosagem
Intervalos de Confiança
Intervalo Livre de Doença
Método Duplo-Cego
Esquema de Medicação
Feminino
Seres Humanos
Análise de Intenção de Tratamento
Microvasos
Meia-Idade
Neuropilina-1/metabolismo
Neoplasias Ovarianas/metabolismo
Neoplasias Ovarianas/patologia
Paclitaxel/administração & dosagem
Molécula-1 de Adesão Celular Endotelial de Plaquetas/análise
Proteínas Proto-Oncogênicas c-met/metabolismo
Estudos Retrospectivos
Fator A de Crescimento do Endotélio Vascular/metabolismo
Receptor 2 de Fatores de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Angiogenesis Inhibitors); 0 (Biomarkers, Tumor); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (Vascular Endothelial Growth Factor A); 144713-63-3 (Neuropilin-1); 2S9ZZM9Q9V (Bevacizumab); BG3F62OND5 (Carboplatin); EC 2.7.10.1 (MET protein, human); EC 2.7.10.1 (Proto-Oncogene Proteins c-met); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-2); P88XT4IS4D (Paclitaxel)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171117
[Lr] Data última revisão:
171117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171024
[St] Status:MEDLINE
[do] DOI:10.1093/jnci/djx066


  9 / 4907 MEDLINE  
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[PMID]:28957406
[Au] Autor:Wang W; Li P; Li W; Jiang J; Cui Y; Li S; Wang Z
[Ad] Endereço:Department of Plastic and Aesthetic Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China.
[Ti] Título:Osteopontin activates mesenchymal stem cells to repair skin wound.
[So] Source:PLoS One;12(9):e0185346, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mesenchymal stem cells (MSCs) are promising candidates for skin wound repair due to their capabilities of accumulating at wounds and differentiating into multiple types of skin cells. However, the underlying mechanisms responsible for these processes remain unclear. In this study, we found that osteopontin (OPN) stimulated the migration of MSCs in vitro, and observed the recruitment of endogenous MSCs to a skin wound and their differentiation into keratinocytes and endothelial cells. In OPN knock-out mice, the recruitment of MSCs to the skin wound was significantly inhibited, and wound closure was hampered after an intradermal injection of exogenous MSCs compared to wild-type mice. Consistent with these observations, the expressions of adhesion molecule CD44 and its receptor E-selectin were significantly decreased in the lesions of OPN knock-out mice compared with wild-type mice suggesting that OPN may regulate the migration of MSCs through its interactions with CD44 during skin wound recovery. In summary, our data demonstrated that OPN played a critical role in activating the migration of MSCs to injured sites and their differentiation into specific skin cell types during skin wound healing.
[Mh] Termos MeSH primário: Células Mesenquimais Estromais/citologia
Células Mesenquimais Estromais/metabolismo
Osteopontina/metabolismo
Pele/patologia
Cicatrização
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/efeitos dos fármacos
Movimento Celular/efeitos dos fármacos
Separação Celular
Regulação para Baixo/efeitos dos fármacos
Selectina E/metabolismo
Células Endoteliais/citologia
Células Endoteliais/efeitos dos fármacos
Células Endoteliais/metabolismo
Imunofluorescência
Proteínas de Fluorescência Verde/metabolismo
Receptores de Hialuronatos/metabolismo
Queratina-14/metabolismo
Queratinócitos/citologia
Queratinócitos/efeitos dos fármacos
Masculino
Células Mesenquimais Estromais/efeitos dos fármacos
Camundongos Endogâmicos C57BL
Osteopontina/deficiência
Molécula-1 de Adesão Celular Endotelial de Plaquetas/metabolismo
Proteínas Recombinantes/farmacologia
Pele/lesões
Cicatrização/efeitos dos fármacos
Fator de von Willebrand/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (E-Selectin); 0 (Hyaluronan Receptors); 0 (Keratin-14); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (Recombinant Proteins); 0 (von Willebrand Factor); 106441-73-0 (Osteopontin); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170929
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185346


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[PMID]:28922851
[Au] Autor:Mehta RI; Tsymbalyuk N; Ivanova S; Stokum JA; Woo K; Gerzanich V; Simard JM
[Ad] Endereço:Department of Pathology and Laboratory Medicine; Center for Neurotherapeutics Discovery, Department of Neuroscience; Center for Translational Neuromedicine, University of Rochester, Rochester, New York; Department of Pathology; Department of Neurosurgery; Department of Physiology, University of Mary
[Ti] Título:α-Endosulfine (ARPP-19e) Expression in a Rat Model of Stroke.
[So] Source:J Neuropathol Exp Neurol;76(10):898-907, 2017 10 01.
[Is] ISSN:1554-6578
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In nutrient restricted environments, the yeast endosulfines Igo1/2 are activated via TORC1 inhibition and function critically to initiate and coordinate the cellular stress response that promotes survival. We examined expression of αEnsa, the mammalian homolog of yeast endosulfines, in rat stroke. Prominent neuronal upregulation of αEnsa was identified in 3 patterns within the ischemic gradient: (1) neurons in GFAP-/HSF1+ cortex showed upregulation and near-complete nuclear translocation of αEnsa protein within hours of ischemic onset; (2) neurons in GFAP+/HSF1+ cortex showed upregulation in cytoplasm and nuclei that persisted for days; (3) neurons in GFAP+/HSF1- cortex showed delayed cytosolic-only upregulation that persisted for days. Findings were corroborated using in situ hybridization for ENSA mRNA. Rapamycin treatment was found to reduce infarct size and behavioral deficits and, in GFAP+/HSF1+ zones, enhance αEnsa neuronal nuclear translocation and mitigate cell death, relative to controls. Based on the conservation of TOR signaling across species, and on the finding that the Rim15-Igo1/2-PP2A module is triggered by substrate deprivation in eukaryotic yeast, we speculate that αEnsa is activated by substrate deprivation, functioning through the homologous MASTL-αEnsa/ARPP19-PP2A module to promote neuronal survival. In conjunction with recent studies suggesting a neuroprotective role, our data highlight a potential function for αEnsa within ischemic brain.
[Mh] Termos MeSH primário: Encéfalo/patologia
Regulação da Expressão Gênica/fisiologia
Neurônios/metabolismo
Peptídeos/metabolismo
Acidente Vascular Cerebral/patologia
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Infarto Encefálico/tratamento farmacológico
Infarto Encefálico/patologia
Moléculas de Adesão Celular/metabolismo
Chaperonina 60/metabolismo
Modelos Animais de Doenças
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Imunossupressores/farmacologia
Masculino
Proteínas Mitocondriais/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Neurônios/efeitos dos fármacos
Peptídeos/genética
Molécula-1 de Adesão Celular Endotelial de Plaquetas/metabolismo
Ratos
Ratos Wistar
Sirolimo/farmacologia
Somatostatina/metabolismo
Acidente Vascular Cerebral/tratamento farmacológico
Acidente Vascular Cerebral/fisiopatologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Adhesion Molecules); 0 (Chaperonin 60); 0 (Esam protein, rat); 0 (Hspd1 protein, rat); 0 (Immunosuppressive Agents); 0 (Mitochondrial Proteins); 0 (Nerve Tissue Proteins); 0 (Peptides); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (endosulfine); 51110-01-1 (Somatostatin); W36ZG6FT64 (Sirolimus)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170920
[St] Status:MEDLINE
[do] DOI:10.1093/jnen/nlx074



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