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[PMID]:27776018
[Au] Autor:Vartanian A; Baryshnikova M; Burova O; Afanasyeva D; Misyurin V; Belyаvsky A; Shprakh Z
[Ad] Endereço:Department of Experimental Diagnosis and Therapy of Tumors, N.N. Blokhin Russian Cancer Research Center, Moscow, Russia.
[Ti] Título:Inhibitor of vasculogenic mimicry restores sensitivity of resistant melanoma cells to DNA-damaging agents.
[So] Source:Melanoma Res;27(1):8-16, 2017 Feb.
[Is] ISSN:1473-5636
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The increasing incidence of melanoma makes this cancer an important public health problem. Therapeutic resistance is still a major obstacle to the therapy of patients with metastatic melanomas. The aim of this study was to develop the melanoma cell line resistant to DNA-alkylating agents and to elucidate the mechanisms involved in acquired drug resistance. We established a unique melanoma subline Mel MeR resistant to DNA-alkylating drug aranoza by continuous stepwise selection of the Mel Me/WT cell line with increasing concentrations of this drug. Mel MeR cells were also cross-resistant to streptozotocin or cisplatin. Here, we show that aranoza-resistant melanoma cells modulate the ABC transporter activity, upregulate the expression of PRAME, adopt a vascular-related phenotype and engage in vasculogenic mimicry. LCS1269, a vasculogenic mimicry low-molecular-weight inhibitor, reverses the sensitivity of resistant melanoma cells to DNA-damaging agents. In this study, we provide experimental evidence that LCS1269 might be considered as a new potential anticancer agent capable of overcoming multidrug resistance for DNA-damaging agents in melanoma.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/farmacologia
Carbazóis/farmacologia
Linhagem Celular Tumoral
Resistência a Medicamentos Antineoplásicos
Glicosídeos/farmacologia
Melanoma/tratamento farmacológico
Melanoma/metabolismo
Metilnitrosoureia/análogos & derivados
Neovascularização Patológica/prevenção & controle
[Mh] Termos MeSH secundário: Membro 1 da Subfamília B de Cassetes de Ligação de ATP/metabolismo
Antígenos de Neoplasias/genética
Apoptose/efeitos dos fármacos
Antígeno CD24/metabolismo
Resistência a Medicamentos Antineoplásicos/genética
Endoglina/metabolismo
Corantes Fluorescentes/metabolismo
Expressão Gênica/efeitos dos fármacos
Seres Humanos
Receptores de Hialuronatos/metabolismo
Molécula 1 de Adesão Intercelular/metabolismo
Masculino
Melanoma/irrigação sanguínea
Melanoma/genética
Metilnitrosoureia/farmacologia
Meia-Idade
Proteínas de Neoplasias/genética
Células-Tronco Neoplásicas/metabolismo
Proteínas Nucleares/genética
Fenótipo
Fosfoproteínas Fosfatases/genética
Proteínas Proto-Oncogênicas c-kit/metabolismo
Rodamina 123/metabolismo
Tetraspanina 30/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ABCB5 protein, human); 0 (ATP-Binding Cassette, Sub-Family B, Member 1); 0 (Antigens, Neoplasm); 0 (Antineoplastic Agents, Alkylating); 0 (CD24 Antigen); 0 (CD24 protein, human); 0 (CD44 protein, human); 0 (CD63 protein, human); 0 (Carbazoles); 0 (ENG protein, human); 0 (Endoglin); 0 (Fluorescent Dyes); 0 (GAGE1 protein, human); 0 (Glycosides); 0 (Hyaluronan Receptors); 0 (LCS1269); 0 (Neoplasm Proteins); 0 (Nuclear Proteins); 0 (PRAME protein, human); 0 (Tetraspanin 30); 0 (aranoza); 126547-89-5 (Intercellular Adhesion Molecule-1); 1N3CZ14C5O (Rhodamine 123); 684-93-5 (Methylnitrosourea); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit); EC 3.1.3.16 (CTDSP1 protein, human); EC 3.1.3.16 (Phosphoprotein Phosphatases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1097/CMR.0000000000000308


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[PMID]:29254293
[Au] Autor:Di Spigna G; Iannone M; Ladogana P; Salzano S; Ventre M; Covelli B; De Marinis E; Postiglione L
[Ad] Endereço:Department of Translational Medical Sciences, University of Naples “Federico II”, Naples, Italy.
[Ti] Título:Human cardiac multipotent adult stem cells in 3D matrix: new approach of tissue engineering in cardiac regeneration post-infarction.
[So] Source:J Biol Regul Homeost Agents;31(4):911-921, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Myocardial infarction is the leading cause of morbidity and mortality in developed countries. It causes a left ventricular dysfunction, mainly due to the loss of functional tissue, resulting in heart failure. New therapies are being developed, using a tissue engineering approach, with the ultimate goal of restoring cardiac function by regenerating and repairing the damaged myocardium. In the present study we investigated the behaviour of a specific population of c-kit positive human cardiac stem cells, called Multipotent Adult Stem Cells (MASCs), grown within three-dimensional collagen scaffolds (3D), to establish whether they could be used in post-infarction cardiac regeneration. We also evaluated the expression levels of the Granulocyte Macrophage-Colony Stimulating Factor Receptor (GM-CSFR) and endoglin, a component of the Transforming Growth Factor beta (TGF-ß) receptor complex. Finally, we also evaluated the expression of the α2ß1integrin. MASCs cultured within 3D collagen matrices are able to proliferate and migrate even in the absence of chemotactic agents and express high levels of factors involved in cell proliferation and migration, such as GM-CSFRα chain and integrins. They therefore represent a promising approach to tissue engineering aimed to restore cardiac function. Our results also suggest a role of GM-CSF in cell proliferation, while TGF-ß does not seem to be relevant.
[Mh] Termos MeSH primário: Células-Tronco Adultas/citologia
Células-Tronco Multipotentes/citologia
Engenharia Tecidual/métodos
Tecidos Suporte
[Mh] Termos MeSH secundário: Células-Tronco Adultas/metabolismo
Técnicas de Cultura de Células
Movimento Celular
Proliferação Celular
Separação Celular
Colágeno/química
Endoglina/genética
Endoglina/metabolismo
Expressão Gênica
Seres Humanos
Integrina alfa2beta1/genética
Integrina alfa2beta1/metabolismo
Células-Tronco Multipotentes/metabolismo
Infarto do Miocárdio
Receptores de Fator Estimulador das Colônias de Granulócitos e Macrófagos/genética
Receptores de Fator Estimulador das Colônias de Granulócitos e Macrófagos/metabolismo
Fator de Crescimento Transformador beta/genética
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ENG protein, human); 0 (Endoglin); 0 (Integrin alpha2beta1); 0 (Receptors, Granulocyte-Macrophage Colony-Stimulating Factor); 0 (Transforming Growth Factor beta); 9007-34-5 (Collagen)
[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:171220
[St] Status:MEDLINE


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[PMID]:28450296
[Au] Autor:Tian H; Ketova T; Hardy D; Xu X; Gao X; Zijlstra A; Blobe GC
[Ad] Endereço:From the Division of Medical Oncology, Department of Medicine (H.T., D.H., G.C.B.) and Department of Pharmacology and Cancer Biology (G.C.B.), Duke University Medical Center, Durham, NC; Department of Pathology, Microbiology, and Immunology (T.K., A.Z.) and Department of Cancer Biology (A.Z.), Vande
[Ti] Título:Endoglin Mediates Vascular Maturation by Promoting Vascular Smooth Muscle Cell Migration and Spreading.
[So] Source:Arterioscler Thromb Vasc Biol;37(6):1115-1126, 2017 Jun.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Endoglin, a transforming growth factor-ß superfamily coreceptor, is predominantly expressed in endothelial cells and has essential roles in vascular development. However, whether endoglin is also expressed in vascular smooth muscle cells (VSMCs), especially in vivo, remains controversial. Furthermore, the roles of endoglin in VSMC biology remain largely unknown. Our objective was to examine the expression and determine the function of endoglin in VSMCs during angiogenesis. APPROACH AND RESULTS: Here, we determine that endoglin is robustly expressed in VSMCs. Using CRISPR/CAS9 knockout and short hairpin RNA knockdown in the VSMC/endothelial coculture model system, we determine that endoglin in VSMCs, but not in endothelial cells, promotes VSMCs recruitment by the endothelial cells both in vitro and in vivo. Using an unbiased bioinformatics analysis of RNA sequencing data and further study, we determine that, mechanistically, endoglin mediates VSMC recruitment by promoting VSMC migration and spreading on endothelial cells via increasing integrin/FAK pathway signaling, whereas endoglin has minimal effects on VSMC adhesion to endothelial cells. In addition, we further determine that loss of endoglin in VSMCs inhibits VSMC recruitment in vivo. CONCLUSIONS: These studies demonstrate that endoglin has an important role in VSMC recruitment and blood vessel maturation during angiogenesis and also provide novel insights into how discordant endoglin function in endothelial and VSMCs may regulate vascular maturation and angiogenesis.
[Mh] Termos MeSH primário: Movimento Celular
Forma Celular
Endoglina/metabolismo
Músculo Liso Vascular/metabolismo
Miócitos de Músculo Liso/metabolismo
[Mh] Termos MeSH secundário: Animais
Sistemas CRISPR-Cas
Células Cultivadas
Técnicas de Cocultura
Endoglina/genética
Células Endoteliais/metabolismo
Quinase 1 de Adesão Focal/metabolismo
Regulação da Expressão Gênica
Seres Humanos
Integrinas/metabolismo
Camundongos Endogâmicos C57BL
Fenótipo
Interferência de RNA
Transdução de Sinais
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ENG protein, human); 0 (Endoglin); 0 (Eng protein, mouse); 0 (Integrins); EC 2.7.10.2 (Focal Adhesion Kinase 1); EC 2.7.10.2 (PTK2 protein, human); EC 2.7.10.2 (Ptk2 protein, mouse)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.116.308859


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[PMID]:28455450
[Au] Autor:Ghosh A; Freestone NS; Anim-Nyame N; Arrigoni FIF
[Ad] Endereço:School of Life Sciences, Pharmacy and Chemistry, Kingston University London, Kingston upon Thames, UK.
[Ti] Título:Microvascular function in pre-eclampsia is influenced by insulin resistance and an imbalance of angiogenic mediators.
[So] Source:Physiol Rep;5(8), 2017 Apr.
[Is] ISSN:2051-817X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In preeclampsia, maternal microvascular function is disrupted and angiogenesis is dysfunctional. Insulin resistance that occurs in some pregnancies also pathologically affects microvascular function. We wished to examine the relationship of angiogenic mediators and insulin resistance on microvascular health in pregnancy. We performed a nested, case-control study of 16 women who developed preeclampsia with 17 normal pregnant controls. We hypothesized that the impaired microvascular blood flow in preeclamptic women associated with an increased ratio of the antiangiogenic factors; (s-endoglin [sEng] and soluble fms-like tyrosine kinase-1 [sFlt-1]) and proangiogenic molecule (placental growth factor [PlGF]) could be influenced by insulin resistance. Serum samples taken after 28 weeks of gestation were measured for the angiogenic factors, insulin, and glucose alongside the inflammatory marker; tumor necrosis factor-α and endothelial activation, namely; soluble vascular cell adhesion molecule 1, intercellular adhesion molecule-1, and e-selectin. Maternal microvascular blood flow, measured by strain gauge plethysmography, correlated with ratios of pro- and antiangiogenic mediators independently of preeclampsia. Decreased microvascular function measured in preeclampsia strongly correlated with both the antiangiogenic factor (sFlt-1 + sEng): PlGF ratio and high levels of insulin resistance, and combining insulin resistance with antiangiogenic factor ratios further strengthened this relationship. In pregnancy, microvascular blood flow is strongly associated with perturbations in pro- and antiangiogenic mediators. In preeclampsia, the relationship of maternal microvascular dysfunction with antiangiogenic mediators is strengthened when combined with insulin resistance.
[Mh] Termos MeSH primário: Indutores da Angiogênese/sangue
Resistência à Insulina/fisiologia
Microcirculação/fisiologia
Pré-Eclâmpsia/fisiopatologia
[Mh] Termos MeSH secundário: Adulto
Inibidores da Angiogênese/fisiologia
Glicemia/metabolismo
Estudos de Casos e Controles
Endoglina/sangue
Feminino
Seres Humanos
Mediadores da Inflamação/metabolismo
Insulina/sangue
Proteínas de Membrana/sangue
Proteínas de Membrana/fisiologia
Microvasos/fisiopatologia
Pré-Eclâmpsia/sangue
Gravidez
Estudos Prospectivos
Receptor 1 de Fatores de Crescimento do Endotélio Vascular/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inducing Agents); 0 (Angiogenesis Inhibitors); 0 (Blood Glucose); 0 (ENG protein, human); 0 (Endoglin); 0 (Inflammation Mediators); 0 (Insulin); 0 (Membrane Proteins); 0 (PIGF protein, human); EC 2.7.10.1 (FLT1 protein, human); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


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[PMID]:29305977
[Au] Autor:Plumitallo S; Ruiz-Llorente L; Langa C; Morini J; Babini G; Cappelletti D; Scelsi L; Greco A; Danesino C; Bernabeu C; Olivieri C
[Ad] Endereço:Molecular Medicine Department, General Biology and Medical Genetics Unit, University of Pavia, Via Forlanini 14, 27100 Pavia, Italy. Electronic address: sara.plumitallo01@univerisitadipavia.it.
[Ti] Título:Functional analysis of a novel ENG variant in a patient with hereditary hemorrhagic telangiectasia (HHT) identifies a new Sp1 binding-site.
[So] Source:Gene;647:85-92, 2018 Mar 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Hereditary Hemorrhagic Telangiectasia (HHT) is a rare disease, with an autosomal dominant inheritance and a worldwide incidence of about 1: 5000 individuals. In >80% of patients, HHT is caused by mutations in either ENG or ACVRL1, which code for ENDOGLIN and Activin A Receptor Type II-Like Kinase 1 (ALK1), belonging to the TGF-ß/BMP signalling pathway. Typical HHT clinical features are mucocutaneous telangiectases, arteriovenous malformations, spontaneous and recurrent epistaxis, as well as gastrointestinal bleedings. An additional, but less frequent, clinical manifestation in some HHT patients is the presence of Pulmonary Arterial Hypertension (PAH). The aim of this work is to describe the functional role of a novel ENG intronic variant found in a patient affected by both HHT and PAH, in order to assess whether it has a pathogenic role. We proved that the variant lies in a novel binding-site for the transcription factor Sp1, known to be involved in the regulation of ENG and ACVRL1 transcription. We confirmed a pathogenic role for this intronic variant, as it significantly reduces ENG transcription by affecting this novel Sp1 binding-site.
[Mh] Termos MeSH primário: Sítios de Ligação/genética
Endoglina/genética
Variação Genética/genética
Fator de Transcrição Sp1/genética
Telangiectasia Hemorrágica Hereditária/genética
[Mh] Termos MeSH secundário: Receptores de Activinas Tipo II/genética
Feminino
Regulação da Expressão Gênica/genética
Seres Humanos
Masculino
Meia-Idade
Ligação Proteica/genética
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ENG protein, human); 0 (Endoglin); 0 (Sp1 Transcription Factor); 0 (Sp1 protein, human); EC 2.7.11.30 (Activin Receptors, Type II)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180107
[St] Status:MEDLINE


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[PMID]:29253907
[Au] Autor:Dingenouts CKE; Bakker W; Lodder K; Wiesmeijer KC; Moerkamp AT; Maring JA; Arthur HM; Smits AM; Goumans MJ
[Ad] Endereço:Department of Molecular Cell Biology, Leiden University Medical Center, Leiden, the Netherlands.
[Ti] Título:Inhibiting DPP4 in a mouse model of HHT1 results in a shift towards regenerative macrophages and reduces fibrosis after myocardial infarction.
[So] Source:PLoS One;12(12):e0189805, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIMS: Hereditary Hemorrhagic Telangiectasia type-1 (HHT1) is a genetic vascular disorder caused by haploinsufficiency of the TGFß co-receptor endoglin. Dysfunctional homing of HHT1 mononuclear cells (MNCs) towards the infarcted myocardium hampers cardiac recovery. HHT1-MNCs have elevated expression of dipeptidyl peptidase-4 (DPP4/CD26), which inhibits recruitment of CXCR4-expressing MNCs by inactivation of stromal cell-derived factor 1 (SDF1). We hypothesize that inhibiting DPP4 will restore homing of HHT1-MNCs to the infarcted heart and improve cardiac recovery. METHODS AND RESULTS: After inducing myocardial infarction (MI), wild type (WT) and endoglin heterozygous (Eng+/-) mice were treated for 5 days with the DPP4 inhibitor Diprotin A (DipA). DipA increased the number of CXCR4+ MNCs residing in the infarcted Eng+/- hearts (Eng+/- 73.17±12.67 vs. Eng+/- treated 157.00±11.61, P = 0.0003) and significantly reduced infarct size (Eng+/- 46.60±9.33% vs. Eng+/- treated 27.02±3.04%, P = 0.03). Echocardiography demonstrated that DipA treatment slightly deteriorated heart function in Eng+/- mice. An increased number of capillaries (Eng+/- 61.63±1.43 vs. Eng+/- treated 74.30±1.74, P = 0.001) were detected in the infarct border zone whereas the number of arteries was reduced (Eng+/- 11.88±0.63 vs. Eng+/- treated 6.38±0.97, P = 0.003). Interestingly, while less M2 regenerative macrophages were present in Eng+/- hearts prior to DipA treatment, (WT 29.88±1.52% vs. Eng+/- 12.34±1.64%, P<0.0001), DPP4 inhibition restored the number of M2 macrophages to wild type levels. CONCLUSIONS: In this study, we demonstrate that systemic DPP4 inhibition restores the impaired MNC homing in Eng+/- animals post-MI, and enhances cardiac repair, which might be explained by restoring the balance between the inflammatory and regenerative macrophages present in the heart.
[Mh] Termos MeSH primário: Dipeptidil Peptidase 4/química
Inibidores da Dipeptidil Peptidase IV/química
Macrófagos/metabolismo
Infarto do Miocárdio/metabolismo
Telangiectasia Hemorrágica Hereditária/genética
[Mh] Termos MeSH secundário: Animais
Quimiocina CXCL12/metabolismo
Modelos Animais de Doenças
Endoglina/metabolismo
Fibrose/metabolismo
Haploinsuficiência
Ventrículos do Coração/patologia
Heterozigoto
Seres Humanos
Masculino
Camundongos
Camundongos Transgênicos
Infarto do Miocárdio/complicações
Miocárdio/metabolismo
Miocárdio/patologia
Regeneração
Telangiectasia Hemorrágica Hereditária/patologia
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CXCL12); 0 (Cxcl12 protein, mouse); 0 (Dipeptidyl-Peptidase IV Inhibitors); 0 (Endoglin); 0 (Transforming Growth Factor beta); EC 3.4.14.5 (Dipeptidyl Peptidase 4); EC 3.4.14.5 (Dpp4 protein, mouse)
[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.0189805


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[PMID]:29190645
[Au] Autor:Fernandez-Pernas P; Rodríguez-Lesende I; de la Fuente A; Mateos J; Fuentes I; De Toro J; Blanco FJ; Arufe MC
[Ad] Endereço:Grupo de Terapia Celular y Medicina Regenerativa (TCMR-CHUAC), CIBER BBN/ISCIII, Instituto de Investigación Biomédica de A Coruña (INIBIC), Complexo Hospitalario Universitario de A Coruña (CHUAC), SERGAS, Departamento de Ciencias Biomédicas, Medicina y Fisioterapia, Facultade de Oza, Universidade da
[Ti] Título:CD105+-mesenchymal stem cells migrate into osteoarthritis joint: An animal model.
[So] Source:PLoS One;12(11):e0188072, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mesenchymal stem cells are being the focus of connective tissue technology and regenerative medicine, presenting a good choice cell source for improving old and well recognized techniques of cartilage defect repair. For instance, the autologous chondrocyte transplantation using new concepts of regenerative medicine. The present study investigated the risk of xenogenicity of human synovial membrane-derived MSCs, injected into the monkeys using intravenous and intra-articular administration. The animal models used were adult monkeys Rhesus which had been injured into the left knee to create an Osteoarthritis (OA) animal model. CD105+-MSCs were injected twice into the OA monkeys with an interval of one week between them. The animals were euthanized one month after treatment. Immunohistochemistry analysis of different organs: spleen, heart, fat, liver, gut, pancreas, lung, skeletal muscle and kidney from the animals revealed that CD105+-MSCs migrated towards the injured knee joint. MSCs naive were found statistically significant increased in the injured knee in front of healthy one. CD105+-MSCs were negatives for CD68 and the area where CD105+-MSCs were found presented SDF-1 increased levels in front of healthy knee. We concluded that a characterized MSCs subset could be a safe alternative for cell therapy in clearly localized pathologies.
[Mh] Termos MeSH primário: Endoglina/imunologia
Células Mesenquimais Estromais/patologia
Osteoartrite/patologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Macaca fascicularis
Masculino
Osteoartrite/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endoglin)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188072


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[PMID]:28456661
[Au] Autor:Hasby Saad MA; Hasby EA
[Ad] Endereço:Medical Parasitology Department, Tanta Faculty of Medicine, Egypt. Electronic address: m.hasby@yahoo.com.
[Ti] Título:Trichinella Spiralis Impact on Mesenchymal Stem Cells: Immunohistochemical Study by Image Analyzer in Murine Model.
[So] Source:Exp Mol Pathol;102(3):396-407, 2017 06.
[Is] ISSN:1096-0945
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:This study aims to elucidate whether Trichinella spiralis infection or its crude antigen administration can stimulate recruitment of CD105 /CD45 cells that could represent MSCs in intestine and skeletal muscle of experimental BALB/c albino mice compared to healthy control mice. Studied mice were divided into: 20 healthy control, 20 with orally induced T. spiralis infection, 20 received adult worm crude antigen orally and 20 received larval crude antigen intramuscular. According to specific timing schedule, mice were sacrificed and tissue sections were examined for CD105 and CD45 immunohistochemical expression using image J image analyzing software, to compare different study groups. T. spiralis infection induced a significant increase in density of CD105 /CD45 cells that could represent MSCs in both intestinal and muscle sections, similarly the intramuscular injected larval crude antigen caused more infiltration of such cells in muscles compared to muscle sections from healthy control mice. However, no significant difference was noticed in intestinal sections after oral adult crude antigen administration compared to healthy control mice. So, injected T. spiralis crude antigen might be a successful stimulant to MSCs attraction and recruitment in tissues nearby injection site. This could be beneficial for cell regeneration and tissue repair in case of presence of a disease induced damage.
[Mh] Termos MeSH primário: Intestinos/parasitologia
Células Mesenquimais Estromais/citologia
Triquinelose/imunologia
[Mh] Termos MeSH secundário: Animais
Antígenos de Helmintos/administração & dosagem
Movimento Celular
Endoglina/metabolismo
Feminino
Imuno-Histoquímica
Intestinos/imunologia
Larva
Antígenos Comuns de Leucócito/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
Músculo Esquelético/imunologia
Músculo Esquelético/parasitologia
Trichinella spiralis
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Helminth); 0 (Endoglin); EC 3.1.3.48 (Leukocyte Common Antigens)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171214
[Lr] Data última revisão:
171214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


  9 / 1669 MEDLINE  
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[PMID]:28947613
[Au] Autor:Kaitu'u-Lino TJ; Brownfoot FC; Hastie R; Chand A; Cannon P; Deo M; Tuohey L; Whitehead C; Hannan NJ; Tong S
[Ad] Endereço:From the Translational Obstetrics Group, Department of Obstetrics and Gynaecology, University of Melbourne, Victoria, Australia (T.J.K.-L., F.C.B., R.H., P.C., M.D., L.T., C.W., N.J.H., S.T.); Mercy Perinatal, Mercy Hospital for Women, Victoria, Australia (T.J.K.-L., F.C.B., R.H., P.C., M.D., L.T.,
[Ti] Título:Activating Transcription Factor 3 Is Reduced in Preeclamptic Placentas and Negatively Regulates sFlt-1 (Soluble fms-Like Tyrosine Kinase 1), Soluble Endoglin, and Proinflammatory Cytokines in Placenta.
[So] Source:Hypertension;70(5):1014-1024, 2017 Nov.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Preeclampsia is a major pregnancy complication associated with poor placental perfusion and placental hypoxia. Systemic and placental inflammation and elevated placental secretion of the antiangiogenic factors sFlt-1 (soluble fms-like tyrosine kinase 1) and sEng (soluble endoglin) are hallmarks of preeclampsia, causing endothelial dysfunction and multiorgan injury. A molecule that links placental hypoxia, inflammation, and antiangiogenic factor release has not been described. ATF3 (activating transcription factor 3) is highly expressed in placenta. We assessed whether placental ATF3 is dysregulated in preterm preeclampsia, is altered by hypoxia, and regulates proinflammatory cytokine and antiangiogenic factor production. ATF3 mRNA and protein expression was significantly reduced in preterm preeclamptic placentas compared with gestation-matched controls. Hypoxia reduced ATF3 expression in primary cytotrophoblast and placental explants. Silencing ATF3 in primary cytotrophoblast increased proinflammatory cytokine (IL-6 [interleukin 6], TNF-α [tumor necrosis factor α]) and NF-κB (nuclear factor κB) expression. In silico analysis identified an ATF3-binding site in the promoter of Flt-1 (the transcript from which sFlt-1 is produced). Silencing ATF3 increased sFlt-1 and sEng secretion from primary cytotrophoblast possibly by increasing Rab11a and Arf1, cargo proteins that facilitate exosomal release of sFlt-1. ATF3 knockout mice did not have a preeclampsia phenotype, suggesting that these pathways may be specific to humans (preeclampsia is a uniquely human condition). To conclude, we have shown that ATF3 is decreased in preeclamptic placentas and that this decrease is likely to occur after prolonged hypoxia. We show that ATF3 is a regulator of placental proinflammatory cytokines and antiangiogenic factors sFlt-1 and sEng. Therefore, reduced ATF3 may be centrally involved in the pathology of preeclampsia.
[Mh] Termos MeSH primário: Fator 3 Ativador da Transcrição/metabolismo
Hipóxia/metabolismo
Inflamação/metabolismo
Doenças Placentárias
Placenta
Pré-Eclâmpsia
[Mh] Termos MeSH secundário: Adulto
Animais
Endoglina/sangue
Feminino
Expressão Gênica
Seres Humanos
Camundongos
Placenta/irrigação sanguínea
Placenta/metabolismo
Placenta/secreção
Doenças Placentárias/diagnóstico
Doenças Placentárias/metabolismo
Doenças Placentárias/fisiopatologia
Pré-Eclâmpsia/diagnóstico
Pré-Eclâmpsia/metabolismo
Pré-Eclâmpsia/fisiopatologia
Gravidez
Estatística como Assunto
Receptor 1 de Fatores de Crescimento do Endotélio Vascular/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Activating Transcription Factor 3); 0 (Endoglin); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-1)
[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:170927
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.117.09548


  10 / 1669 MEDLINE  
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[PMID]:28863727
[Au] Autor:Litwiniuk M; Niemczyk K; Niderla-Bielinska J; Lukawska-Popieluch I; Grzela T
[Ad] Endereço:1 Otolaryngology, Head and Neck Surgery Department, Medical University of Warsaw, Poland.
[Ti] Título:Soluble Endoglin (CD105) Serum Level as a Potential Marker in the Management of Head and Neck Paragangliomas.
[So] Source:Ann Otol Rhinol Laryngol;126(10):717-721, 2017 Oct.
[Is] ISSN:1943-572X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To assess the expression of endoglin in head and neck paragangliomas and the soluble endoglin level in serum of paraganglioma patients. METHODS: Seven tumor samples of patients operated for cervical paraganglioma were assessed, as well as serum samples collected preoperatively, on days 4 and 28 postoperation. Serum level of endoglin in healthy controls was also determined. Tumor samples were subjected to immunofluorescent staining and examined with confocal microscope. The level of soluble endoglin in serum samples was examined using the immunoenzymatic assay (ELISA). RESULTS: Endoglin was highly expressed in all tumor samples. The level of soluble endoglin was significantly higher in paraganglioma patients compared to healthy controls and correlated with the tumor size. The serum level of s-endoglin was reduced after surgical excision of the tumor and remained stable after 4 weeks in all patients with complete resection of the tumor. CONCLUSION: Endoglin is an important factor in the pathophysiology of head and neck paragangliomas and may be a potential diagnostic and prognostic marker in these types of tumors.
[Mh] Termos MeSH primário: Endoglina/sangue
Neoplasias de Cabeça e Pescoço/sangue
Paraganglioma/sangue
[Mh] Termos MeSH secundário: Adulto
Idoso
Biomarcadores Tumorais/sangue
Estudos de Casos e Controles
Ensaio de Imunoadsorção Enzimática
Feminino
Neoplasias de Cabeça e Pescoço/patologia
Neoplasias de Cabeça e Pescoço/cirurgia
Seres Humanos
Masculino
Meia-Idade
Paraganglioma/patologia
Paraganglioma/cirurgia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Endoglin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170903
[St] Status:MEDLINE
[do] DOI:10.1177/0003489417727548



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