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[PMID]:28468787
[Au] Autor:Chandran S; Watkins J; Abdul-Aziz A; Shafat M; Calvert PA; Bowles KM; Flather MD; Rushworth SA; Ryding AD
[Ad] Endereço:Norfolk and Norwich University Hospital, Norwich, United Kingdom.
[Ti] Título:Inflammatory Differences in Plaque Erosion and Rupture in Patients With ST-Segment Elevation Myocardial Infarction.
[So] Source:J Am Heart Assoc;6(5), 2017 May 03.
[Is] ISSN:2047-9980
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Plaque erosion causes 30% of ST-segment elevation myocardial infarctions, but the underlying cause is unknown. Inflammatory infiltrates are less abundant in erosion compared with rupture in autopsy studies. We hypothesized that erosion and rupture are associated with significant differences in intracoronary cytokines in vivo. METHODS AND RESULTS: Forty ST-segment elevation myocardial infarction patients with <6 hours of chest pain were classified as ruptured fibrous cap (RFC) or intact fibrous cap (IFC) using optical coherence tomography. Plasma samples from the infarct-related artery and a peripheral artery were analyzed for expression of 102 cytokines using arrays; results were confirmed with ELISA. Thrombectomy samples were analyzed for differential mRNA expression using quantitative real-time polymerase chain reaction. Twenty-three lesions were classified as RFC (58%), 15 as IFC (38%), and 2 were undefined (4%). In addition, 12% (12 of 102) of cytokines were differentially expressed in both coronary and peripheral plasma. I-TAC was preferentially expressed in RFC (significance analysis of microarrays adjusted <0.001; ELISA IFC 10.2 versus RFC 10.8 log pg/mL; =0.042). IFC was associated with preferential expression of epidermal growth factor (significance analysis of microarrays adjusted <0.001; ELISA IFC 7.42 versus RFC 6.63 log pg/mL, =0.036) and thrombospondin 1 (significance analysis of microarrays adjusted =0.03; ELISA IFC 10.4 versus RFC 8.65 log ng/mL, =0.0041). Thrombectomy mRNA showed elevated I-TAC in RFC ( =0.0007) epidermal growth factor expression in IFC ( =0.0264) but no differences in expression of thrombospondin 1. CONCLUSIONS: These results demonstrate differential intracoronary cytokine expression in RFC and IFC. Elevated thrombospondin 1 and epidermal growth factor may play an etiological role in erosion.
[Mh] Termos MeSH primário: Doença da Artéria Coronariana/complicações
Citocinas/sangue
Mediadores da Inflamação/sangue
Placa Aterosclerótica
Infarto do Miocárdio com Supradesnível do Segmento ST/etiologia
[Mh] Termos MeSH secundário: Idoso
Biomarcadores/sangue
Angiografia Coronária
Doença da Artéria Coronariana/sangue
Doença da Artéria Coronariana/diagnóstico por imagem
Doença da Artéria Coronariana/terapia
Citocinas/genética
Ensaio de Imunoadsorção Enzimática
Fator de Crescimento Epidérmico/sangue
Feminino
Fibrose
Perfilação da Expressão Gênica/métodos
Seres Humanos
Masculino
Meia-Idade
Análise de Sequência com Séries de Oligonucleotídeos
Intervenção Coronária Percutânea
Estudos Prospectivos
Reação em Cadeia da Polimerase em Tempo Real
Fatores de Risco
Ruptura Espontânea
Infarto do Miocárdio com Supradesnível do Segmento ST/sangue
Infarto do Miocárdio com Supradesnível do Segmento ST/diagnóstico por imagem
Infarto do Miocárdio com Supradesnível do Segmento ST/terapia
Trombectomia
Trombospondina 1/sangue
Tomografia de Coerência Óptica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cytokines); 0 (Inflammation Mediators); 0 (Thrombospondin 1); 0 (thrombospondin-1, human); 62229-50-9 (Epidermal Growth Factor)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


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[PMID]:28747434
[Au] Autor:Sallon C; Callebaut I; Boulay I; Fontaine J; Logeart-Avramoglou D; Henriquet C; Pugnière M; Cayla X; Monget P; Harichaux G; Labas V; Canepa S; Taragnat C
[Ad] Endereço:From the Unité Physiologie de la Reproduction et des Comportements, UMR85, Institut National de la Recherche Agronomique, CNRS, Institut Français du Cheval et de l'Equitation, Université de Tours, F-37380 Nouzilly, France.
[Ti] Título:Thrombospondin-1 (TSP-1), a new bone morphogenetic protein-2 and -4 (BMP-2/4) antagonist identified in pituitary cells.
[So] Source:J Biol Chem;292(37):15352-15368, 2017 09 15.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bone morphogenetic proteins (BMPs) regulate diverse cellular responses during embryogenesis and in adulthood including cell differentiation, proliferation, and death in various tissues. In the adult pituitary, BMPs participate in the control of hormone secretion and cell proliferation, suggesting a potential endocrine/paracrine role for BMPs, but some of the mechanisms are unclear. Here, using a bioactivity test based on embryonic cells (C3H10T1/2) transfected with a BMP-responsive element, we sought to determine whether pituitary cells secrete BMPs or BMP antagonists. Interestingly, we found that pituitary-conditioned medium contains a factor that inhibits action of BMP-2 and -4. Combining surface plasmon resonance and high-resolution mass spectrometry helped pinpoint this factor as thrombospondin-1 (TSP-1). Surface plasmon resonance and co-immunoprecipitation confirmed that recombinant human TSP-1 can bind BMP-2 and -4 and antagonize their effects on C3H10T1/2 cells. Moreover, TSP-1 inhibited the action of serum BMPs. We also report that the von Willebrand type C domain of TSP-1 is likely responsible for this BMP-2/4-binding activity, an assertion based on sequence similarity that TSP-1 shares with the von Willebrand type C domain of Crossveinless 2 (CV-2), a BMP antagonist and member of the chordin family. In summary, we identified for the first time TSP-1 as a BMP-2/-4 antagonist and presented a structural basis for the physical interaction between TSP-1 and BMP-4. We propose that TSP-1 could regulate bioavailability of BMPs, either produced locally or reaching the pituitary via blood circulation. In conclusion, our findings provide new insights into the involvement of TSP-1 in the BMP-2/-4 mechanisms of action.
[Mh] Termos MeSH primário: Proteína Morfogenética Óssea 2/antagonistas & inibidores
Proteína Morfogenética Óssea 4/antagonistas & inibidores
Modelos Moleculares
Hipófise/secreção
Elementos de Resposta
Trombospondina 1/secreção
[Mh] Termos MeSH secundário: Animais
Animais Endogâmicos
Proteína Morfogenética Óssea 2/sangue
Proteína Morfogenética Óssea 2/genética
Proteína Morfogenética Óssea 2/metabolismo
Proteína Morfogenética Óssea 4/sangue
Proteína Morfogenética Óssea 4/genética
Proteína Morfogenética Óssea 4/metabolismo
Linhagem Celular
Células Cultivadas
Biologia Computacional
Feminino
Genes Reporter
Seres Humanos
Camundongos
Hipófise/citologia
Hipófise/metabolismo
Domínios e Motivos de Interação entre Proteínas
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/isolamento & purificação
Proteínas Recombinantes de Fusão/metabolismo
Proteínas Recombinantes/química
Proteínas Recombinantes/metabolismo
Homologia de Sequência de Aminoácidos
Carneiro Doméstico
Trombospondina 1/química
Trombospondina 1/isolamento & purificação
Trombospondina 1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (BMP2 protein, human); 0 (BMP4 protein, human); 0 (Bone Morphogenetic Protein 2); 0 (Bone Morphogenetic Protein 4); 0 (Recombinant Fusion Proteins); 0 (Recombinant Proteins); 0 (Thrombospondin 1); 0 (thrombospondin-1, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171230
[Lr] Data última revisão:
171230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.736207


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[PMID]:29040286
[Au] Autor:Mousa AA; Roche DB; Terkawi MA; Kameyama K; Kamyingkird K; Vudriko P; Salama A; Cao S; Orabi S; Khalifa H; Ahmed M; Attia M; Elkirdasy A; Nishikawa Y; Xuan X; Cornillot E
[Ad] Endereço:Institut de Biologie Computationnelle (IBC), LIRMM, CNRS, Université de Montpellier, Montpellier, France.
[Ti] Título:Human babesiosis: Indication of a molecular mimicry between thrombospondin domains from a novel Babesia microti BmP53 protein and host platelets molecules.
[So] Source:PLoS One;12(10):e0185372, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human babesiosis is caused by the apicomplexan parasite Babesia microti, which is of major public health concern in the United States and elsewhere, resulting in malaise and fatigue, followed by a fever and hemolytic anemia. In this paper we focus on the characterization of a novel B. microti thrombospondin domain (TSP1)-containing protein (BmP53) from the new annotation of the B. microti genome (locus 'BmR1_04g09041'). This novel protein (BmP53) had a single TSP1 and a transmembrane domain, with a short cytoplasmic tail containing a sub-terminal glutamine residue, but no signal peptide and Von Willebrand factor type A domains (VWA), which are found in classical thrombospondin-related adhesive proteins (TRAP). Co-localization assays of BmP53 and Babesia microti secreted antigen 1 (BmSA1) suggested that BmP53 might be a non-secretory membranous protein. Molecular mimicry between the TSP1 domain from BmP53 and host platelets molecules was indicated through different measures of sequence homology, phylogenetic analysis, 3D structure and shared epitopes. Indeed, hamster isolated platelets cross-reacted with mouse anti-BmP53-TSP1. Molecular mimicry are used to help parasites to escape immune defenses, resulting in immune evasion or autoimmunity. Furthermore, specific host reactivity was also detected against the TSP1-free part of BmP53 in infected hamster sera. In conclusion, the TSP1 domain mimicry might help in studying the mechanisms of parasite-induced thrombocytopenia, with the TSP1-free truncate of the protein representing a potential safe candidate for future vaccine studies.
[Mh] Termos MeSH primário: Antígenos de Protozoários/imunologia
Babesia microti/imunologia
Babesiose/parasitologia
Plaquetas/parasitologia
Evasão da Resposta Imune
Proteínas de Protozoários/imunologia
Trombospondina 1/imunologia
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Antígenos de Protozoários/química
Antígenos de Protozoários/genética
Babesia microti/genética
Babesia microti/isolamento & purificação
Babesiose/imunologia
Sítios de Ligação
Clonagem Molecular
Cricetulus
Eritrócitos/parasitologia
Escherichia coli/genética
Escherichia coli/metabolismo
Expressão Gênica
Glutationa Transferase/genética
Glutationa Transferase/metabolismo
Seres Humanos
Camundongos
Modelos Moleculares
Mimetismo Molecular
Ligação Proteica
Domínios e Motivos de Interação entre Proteínas
Estrutura Secundária de Proteína
Proteínas de Protozoários/química
Proteínas de Protozoários/genética
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/genética
Proteínas Recombinantes de Fusão/imunologia
Alinhamento de Sequência
Homologia de Sequência de Aminoácidos
Trombospondina 1/química
Trombospondina 1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Protozoan); 0 (Protozoan Proteins); 0 (Recombinant Fusion Proteins); 0 (Thrombospondin 1); EC 2.5.1.18 (Glutathione Transferase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171018
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185372


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[PMID]:28913875
[Au] Autor:Santolini I; Celli R; Cannella M; Imbriglio T; Guiducci M; Parisi P; Schubert J; Iacomino M; Zara F; Lerche H; Moyanova S; Ngomba RT; van Luijtelaar G; Battaglia G; Bruno V; Striano P; Nicoletti F; EuroEPINOMICS CoGIE Consortium; Genetic Commission of Italian League Against Epilepsy (LICE)
[Ad] Endereço:I.R.C.C.S. Neuromed, Pozzilli, Italy.
[Ti] Título:Alterations in the α δ ligand, thrombospondin-1, in a rat model of spontaneous absence epilepsy and in patients with idiopathic/genetic generalized epilepsies.
[So] Source:Epilepsia;58(11):1993-2001, 2017 Nov.
[Is] ISSN:1528-1167
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Thrombospondins, which are known to interact with the α δ subunit of voltage-sensitive calcium channels to stimulate the formation of excitatory synapses, have recently been implicated in the process of epileptogenesis. No studies have been so far performed on thrombospondins in models of absence epilepsy. We examined whether expression of the gene encoding for thrombospondin-1 was altered in the brain of WAG/Rij rats, which model absence epilepsy in humans. In addition, we examined the frequency of genetic variants of THBS1 in a large cohort of children affected by idiopathic/genetic generalized epilepsies (IGE/GGEs). METHODS: We measured the transcripts of thrombospondin-1 and α δ subunit, and protein levels of α δ, Rab3A, and the vesicular glutamate transporter, VGLUT1, in the somatosensory cortex and ventrobasal thalamus of presymptomatic and symptomatic WAG/Rij rats and in two control strains by real-time polymerase chain reaction (PCR) and immunoblotting. We examined the genetic variants of THBS1 and CACNA2D1 in two independent cohorts of patients affected by IGE/GGE recruited through the Genetic Commission of the Italian League Against Epilepsy (LICE) and the EuroEPINOMICS-CoGIE Consortium. RESULTS: Thrombospondin-1 messenger RNA (mRNA) levels were largely reduced in the ventrobasal thalamus of both presymptomatic and symptomatic WAG/Rij rats, whereas levels in the somatosensory cortex were unchanged. VGLUT1 protein levels were also reduced in the ventrobasal thalamus of WAG/Rij rats. Genetic variants of THBS1 were significantly more frequent in patients affected by IGE/GGE than in nonepileptic controls, whereas the frequency of CACNA2D1 was unchanged. SIGNIFICANCE: These findings suggest that thrombospondin-1 may have a role in the pathogenesis of IGE/GGEs.
[Mh] Termos MeSH primário: Canais de Cálcio/genética
Modelos Animais de Doenças
Epilepsia Tipo Ausência/genética
Epilepsia Generalizada/genética
Trombospondina 1/genética
[Mh] Termos MeSH secundário: Animais
Canais de Cálcio/biossíntese
Estudos de Coortes
Epilepsia Tipo Ausência/metabolismo
Epilepsia Generalizada/metabolismo
Seres Humanos
Masculino
Ratos
Ratos Wistar
Trombospondina 1/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CACNA2D1 protein, human); 0 (Calcium Channels); 0 (Thrombospondin 1); 0 (thrombospondin-1, human)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE
[do] DOI:10.1111/epi.13898


  5 / 1729 MEDLINE  
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[PMID]:28886036
[Au] Autor:Ishida T; Yoshida T; Shinohara K; Cao K; Nakahama KI; Morita I; Ohno-Matsui K
[Ad] Endereço:Department of Ophthalmology and Visual Science, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
[Ti] Título:Potential role of sirtuin 1 in Müller glial cells in mice choroidal neovascularization.
[So] Source:PLoS One;12(9):e0183775, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study investigated the potential role of sirtuin 1 in Müller glial cells in choroidal neovascularization. In the in vitro study, primary Müller glial cells were cultured and treated with resveratrol, a sirtuin 1 activator. Glial fibrillary acidic protein expression and angiogenesis-related gene expression were examined using quantitative polymerase chain reaction and phagocytosis, as a marker of Müller glial cell function; in addition, a latex bead assay was used to analyze cell function. For the in vivo study, choroidal neovascularization was induced in C57BL/6 mice via laser photocoagulation, and resveratrol was administered intravitreally. Eyecup whole mounts were created to measure choroidal neovascularization volumes on day 7. Immunohistochemical analysis with anti-glial fibrillary acidic protein antibody was used to detect Müller glial cell activation in eyes with choroidal neovascularization on day 1, 3, 5, and 7 after laser surgery. Resveratrol significantly promoted glial fibrillary acidic protein, anti-angiogenic factor, pigment epithelium-derived factor, and thrombospondin-1 expression in the cells as well as the phagocytic activities. Treatment of the choroidal neovascularization model with resveratrol resulted in early activation of Müller glial cells near choroidal neovascularization sites. Resveratrol-activated cells but not the controls migrated to the top of choroidal neovascularization sites and into the lesions from day 3. Resveratrol reduced the choroidal neovascularization size relative to controls. In conclusion, sirtuin 1 activation in Müller glial cells suppressed the development of choroidal neovascularization, and therefore, might be a therapeutic option.
[Mh] Termos MeSH primário: Células Ependimogliais/metabolismo
Sirtuína 1/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteínas do Olho/metabolismo
Proteína Glial Fibrilar Ácida/metabolismo
Imuno-Histoquímica
Camundongos
Camundongos Endogâmicos C57BL
Fatores de Crescimento Neural/metabolismo
Neuroglia/metabolismo
Serpinas/metabolismo
Trombospondina 1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Eye Proteins); 0 (Glial Fibrillary Acidic Protein); 0 (Nerve Growth Factors); 0 (Serpins); 0 (Thrombospondin 1); 0 (pigment epithelium-derived factor); 0 (thrombospondin-1, mouse); EC 3.5.1.- (Sirtuin 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183775


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[PMID]:28778947
[Au] Autor:Kim CW; Pokutta-Paskaleva A; Kumar S; Timmins LH; Morris AD; Kang DW; Dalal S; Chadid T; Kuo KM; Raykin J; Li H; Yanagisawa H; Gleason RL; Jo H; Brewster LP
[Ad] Endereço:From Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta (C.W.K., A.P.-P., S.K., D.-W.K., J.R., R.L.G., H.J., L.P.B.); Department of Microbiology, College of Medicine, Inha University, Incheon, Republic of Korea (C.W.K.); Department
[Ti] Título:Disturbed Flow Promotes Arterial Stiffening Through Thrombospondin-1.
[So] Source:Circulation;136(13):1217-1232, 2017 Sep 26.
[Is] ISSN:1524-4539
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Arterial stiffness and wall shear stress are powerful determinants of cardiovascular health, and arterial stiffness is associated with increased cardiovascular mortality. Low and oscillatory wall shear stress, termed disturbed flow (d-flow), promotes atherosclerotic arterial remodeling, but the relationship between d-flow and arterial stiffness is not well understood. The objective of this study was to define the role of d-flow on arterial stiffening and discover the relevant signaling pathways by which d-flow stiffens arteries. METHODS: D-flow was induced in the carotid arteries of young and old mice of both sexes. Arterial stiffness was quantified ex vivo with cylindrical biaxial mechanical testing and in vivo from duplex ultrasound and compared with unmanipulated carotid arteries from 80-week-old mice. Gene expression and pathway analysis was performed on endothelial cell-enriched RNA and validated by immunohistochemistry. In vitro testing of signaling pathways was performed under oscillatory and laminar wall shear stress conditions. Human arteries from regions of d-flow and stable flow were tested ex vivo to validate critical results from the animal model. RESULTS: D-flow induced arterial stiffening through collagen deposition after partial carotid ligation, and the degree of stiffening was similar to that of unmanipulated carotid arteries from 80-week-old mice. Intimal gene pathway analyses identified transforming growth factor-ß pathways as having a prominent role in this stiffened arterial response, but this was attributable to thrombospondin-1 (TSP-1) stimulation of profibrotic genes and not changes to transforming growth factor-ß. In vitro and in vivo testing under d-flow conditions identified a possible role for TSP-1 activation of transforming growth factor-ß in the upregulation of these genes. TSP-1 knockout animals had significantly less arterial stiffening in response to d-flow than wild-type carotid arteries. Human arteries exposed to d-flow had similar increases TSP-1 and collagen gene expression as seen in our model. CONCLUSIONS: TSP-1 has a critical role in shear-mediated arterial stiffening that is mediated in part through TSP-1's activation of the profibrotic signaling pathways of transforming growth factor-ß. Molecular targets in this pathway may lead to novel therapies to limit arterial stiffening and the progression of disease in arteries exposed to d-flow.
[Mh] Termos MeSH primário: Trombospondina 1/metabolismo
Rigidez Vascular/fisiologia
[Mh] Termos MeSH secundário: Envelhecimento
Animais
Remodelamento Atrial
Artérias Carótidas/metabolismo
Artérias Carótidas/fisiopatologia
Linhagem Celular
Colágeno/genética
Colágeno/metabolismo
Modelos Animais de Doenças
Regulação para Baixo
Endotélio Vascular/citologia
Endotélio Vascular/metabolismo
Feminino
Seres Humanos
Imuno-Histoquímica
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Proteínas Serina-Treonina Quinases/genética
Proteínas Serina-Treonina Quinases/metabolismo
RNA Ribossômico 18S/metabolismo
Receptores de Fatores de Crescimento Transformadores beta/genética
Receptores de Fatores de Crescimento Transformadores beta/metabolismo
Resistência ao Cisalhamento
Trombospondina 1/deficiência
Trombospondina 1/genética
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Ribosomal, 18S); 0 (Receptors, Transforming Growth Factor beta); 0 (Thrombospondin 1); 0 (Transforming Growth Factor beta); 9007-34-5 (Collagen); EC 2.7.1.11 (TGF-beta type I receptor); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170806
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCULATIONAHA.116.026361


  7 / 1729 MEDLINE  
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[PMID]:28767721
[Au] Autor:Endt K; Goepfert J; Omlin A; Athanasiou A; Tennstedt P; Guenther A; Rainisio M; Engeler DS; Steuber T; Gillessen S; Joos T; Schiess R
[Ad] Endereço:ProteoMediX Inc., Schlieren, Switzerland.
[Ti] Título:Development and clinical testing of individual immunoassays for the quantification of serum glycoproteins to diagnose prostate cancer.
[So] Source:PLoS One;12(8):e0181557, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Prostate Cancer (PCa) diagnosis is currently hampered by the high false-positive rate of PSA evaluations, which consequently may lead to overtreatment. Non-invasive methods with increased specificity and sensitivity are needed to improve diagnosis of significant PCa. We developed and technically validated four individual immunoassays for cathepsin D (CTSD), intercellular adhesion molecule 1 (ICAM1), olfactomedin 4 (OLFM4), and thrombospondin 1 (THBS1). These glycoproteins, previously identified by mass spectrometry using a Pten mouse model, were measured in clinical serum samples for testing the capability of discriminating PCa positive and negative samples. The development yielded 4 individual immunoassays with inter and intra-variability (CV) <15% and linearity on dilution of the analytes. In serum, ex vivo protein stability (<15% loss of analyte) was achieved for a duration of at least 24 hours at room temperature and 2 days at 4°C. The measurement of 359 serum samples from PCa positive (n = 167) and negative (n = 192) patients with elevated PSA (2-10 ng/ml) revealed a significantly improved accuracy (P <0.001) when two of the glycoproteins (CTSD and THBS1) were combined with %fPSA and age (AUC = 0.8109; P <0.0001; 95% CI = 0.7673-0.8545). Conclusively, the use of CTSD and THBS1 together with commonly used parameters for PCa diagnosis such as %fPSA and age has the potential to improve the diagnosis of PCa.
[Mh] Termos MeSH primário: Catepsina D/sangue
Antígeno Prostático Específico/sangue
Neoplasias da Próstata/diagnóstico
Trombospondina 1/sangue
[Mh] Termos MeSH secundário: Idoso
Biomarcadores Tumorais/sangue
Fator Estimulador de Colônias de Granulócitos/sangue
Seres Humanos
Imunoensaio
Molécula 1 de Adesão Intercelular/sangue
Masculino
Meia-Idade
Curva ROC
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (ICAM1 protein, human); 0 (OLFM4 protein, human); 0 (Thrombospondin 1); 0 (thrombospondin-1, human); 126547-89-5 (Intercellular Adhesion Molecule-1); 143011-72-7 (Granulocyte Colony-Stimulating Factor); EC 3.4.21.77 (Prostate-Specific Antigen); EC 3.4.23.5 (CTSD protein, human); EC 3.4.23.5 (Cathepsin D)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170803
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181557


  8 / 1729 MEDLINE  
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[PMID]:28737660
[Au] Autor:Xu X; Song N; Zhang X; Jiao X; Hu J; Liang M; Teng J; Ding X
[Ad] Endereço:1 Department of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, P. R. China. 2 Shanghai Institute of Kidney Disease and Dialysis, Shanghai, P. R. China. 3 Shanghai key Laboratory of, Kidney and Blood Purification, Shanghai, P. R. China. 4 Institute of Biochemistry and Cell Biology, SIBS, CAS, Shanghai, P. R. China. 5 Department of Physiology and Center of Systems Molecular Medicine, Medical College of Wisconsin, Milwaukee, WI.
[Ti] Título:Renal Protection Mediated by Hypoxia Inducible Factor-1α Depends on Proangiogenesis Function of miR-21 by Targeting Thrombospondin 1.
[So] Source:Transplantation;101(8):1811-1819, 2017 Aug.
[Is] ISSN:1534-6080
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Angiogenesis contributes to the repair process after renal ischemia/reperfusion (I/R) injury. In the present study, we tested the role of miR-21 in the angiogenesis induced by hypoxia inducible factor (HIF)-1α through inhibiting a predicted target gene thrombospondin 1 (TSP-1). METHODS: To stabilize HIF-1α, hypoxia (1% O2 for 24 hours) was performed in human umbilical vein endothelial cells and cobalt chloride (CoCl2) was pretreated intraperitoneally 24 hours before renal I/R in mice. Locked nucleic acid modified anti-miR-21 and scrambled control was transfected with hypoxic cells or delivered into the mice via tail vein 1 hour before CoCl2 injection. The kidneys and blood were collected at 24 hours after reperfusion. RESULTS: HIF-1α induced by hypoxia and CoCl2 upregulated vascular endothelial growth factor and miR-21, and increased angiogenesis. It was found that expression of TSP-1 was inversely related with miR-21 in vitro and in vivo. Targeting of TSP-1 by miR-21 was further confirmed in vitro. Furthermore, HIF-1α improved renal function, accompanied with increased angiogenesis after I/R injury in mice. The protective effect of HIF-1α was attenuated by inhibition of miR-21. CONCLUSIONS: HIF-1α induced angiogenesis by upregulating not only vascular endothelial growth factor but also miR-21 via inhibiting a novel target gene TSP-1. Both of them may contribute to the protective effect of HIF-1α on renal I/R injury.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica
Subunidade alfa do Fator 1 Induzível por Hipóxia/genética
Rim/irrigação sanguínea
MicroRNAs/genética
RNA/genética
Traumatismo por Reperfusão/genética
Trombospondina 1/genética
[Mh] Termos MeSH secundário: Animais
Apoptose
Western Blotting
Células Cultivadas
Modelos Animais de Doenças
Seguimentos
Células Endoteliais da Veia Umbilical Humana/metabolismo
Células Endoteliais da Veia Umbilical Humana/patologia
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/biossíntese
Imuno-Histoquímica
Hibridização In Situ
Rim/metabolismo
Rim/patologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
MicroRNAs/biossíntese
Neovascularização Patológica/genética
Neovascularização Patológica/metabolismo
Neovascularização Patológica/patologia
Reação em Cadeia da Polimerase em Tempo Real
Traumatismo por Reperfusão/metabolismo
Traumatismo por Reperfusão/patologia
Transdução de Sinais
Trombospondina 1/biossíntese
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (MIRN21 microRNA, mouse); 0 (MicroRNAs); 0 (Thrombospondin 1); 63231-63-0 (RNA)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170913
[Lr] Data última revisão:
170913
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170725
[St] Status:MEDLINE
[do] DOI:10.1097/TP.0000000000001501


  9 / 1729 MEDLINE  
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[PMID]:28729362
[Au] Autor:Regano D; Visintin A; Clapero F; Bussolino F; Valdembri D; Maione F; Serini G; Giraudo E
[Ad] Endereço:From the Candiolo Cancer Institute, Fondazione del Piemonte per l'Oncologia, Istituto di Ricovero e Cura a Carattere Scientifico, Candiolo, Torino, Italy (D.R., A.V., F.C., F.B., D.V., F.M., G.S., E.G.); Department of Science and Drug Technology, University of Torino, Italy (D.R., A.V., F.M., E.G.);
[Ti] Título:Sema3F (Semaphorin 3F) Selectively Drives an Extraembryonic Proangiogenic Program.
[So] Source:Arterioscler Thromb Vasc Biol;37(9):1710-1721, 2017 Sep.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Molecular pathways governing blood vessel patterning are vital to vertebrate development. Because of their ability to counteract proangiogenic factors, antiangiogenic secreted Sema3 (class 3 semaphorins) control embryonic vascular morphogenesis. However, if and how Sema3 may play a role in the control of extraembryonic vascular development is presently unknown. APPROACH AND RESULTS: By characterizing genetically modified mice, here, we show that surprisingly Sema3F acts instead as a selective extraembryonic, but not intraembryonic proangiogenic cue. Both in vivo and in vitro, in visceral yolk sac epithelial cells, Sema3F signals to inhibit the phosphorylation-dependent degradation of Myc, a transcription factor that drives the expression of proangiogenic genes, such as the microRNA cluster 17/92. In -null yolk sacs, the transcription of Myc-regulated microRNA 17/92 cluster members is impaired, and the synthesis of Myc and microRNA 17/92 foremost antiangiogenic target Thbs1 (thrombospondin 1) is increased, whereas Vegf (vascular endothelial growth factor) signaling is inhibited in yolk sac endothelial cells. Consistently, exogenous recombinant Sema3F inhibits the phosphorylation-dependent degradation of Myc and the synthesis of Thbs1 in mouse F9 teratocarcinoma stem cells that were in vitro differentiated in visceral yolk sac epithelial cells. mice placentas are also highly anemic and abnormally vascularized. CONCLUSIONS: Sema3F functions as an unconventional Sema3 that promotes extraembryonic angiogenesis by inhibiting the Myc-regulated synthesis of Thbs1 in visceral yolk sac epithelial cells.
[Mh] Termos MeSH primário: Células Epiteliais/metabolismo
Proteínas de Membrana/metabolismo
Neovascularização Fisiológica
Proteínas do Tecido Nervoso/metabolismo
Placenta/irrigação sanguínea
Saco Vitelino/irrigação sanguínea
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Células-Tronco de Carcinoma Embrionário/metabolismo
Células Endoteliais/metabolismo
Feminino
Regulação da Expressão Gênica no Desenvolvimento
Genótipo
Idade Gestacional
Proteínas de Membrana/deficiência
Proteínas de Membrana/genética
Camundongos Endogâmicos C57BL
Camundongos Knockout
MicroRNAs/genética
MicroRNAs/metabolismo
Proteínas do Tecido Nervoso/deficiência
Proteínas do Tecido Nervoso/genética
Fenótipo
Fosforilação
Gravidez
Proteólise
Proteínas Proto-Oncogênicas c-myc/metabolismo
Transdução de Sinais
Trombospondina 1/genética
Trombospondina 1/metabolismo
Fator A de Crescimento do Endotélio Vascular/genética
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN17-92 microRNA, mouse); 0 (Membrane Proteins); 0 (MicroRNAs); 0 (Myc protein, mouse); 0 (Nerve Tissue Proteins); 0 (Proto-Oncogene Proteins c-myc); 0 (Sema3f protein, mouse); 0 (Thrombospondin 1); 0 (Vascular Endothelial Growth Factor A); 0 (thrombospondin-1, mouse); 0 (vascular endothelial growth factor A, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170722
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.308226


  10 / 1729 MEDLINE  
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[PMID]:28698383
[Au] Autor:Cunha DA; Cito M; Grieco FA; Cosentino C; Danilova T; Ladrière L; Lindahl M; Domanskyi A; Bugliani M; Marchetti P; Eizirik DL; Cnop M
[Ad] Endereço:From the Université Libre de Bruxelles Center for Diabetes Research, Faculty of Medicine, Université Libre de Bruxelles, 1070 Brussels, Belgium.
[Ti] Título:Pancreatic ß-cell protection from inflammatory stress by the endoplasmic reticulum proteins thrombospondin 1 and mesencephalic astrocyte-derived neutrotrophic factor (MANF).
[So] Source:J Biol Chem;292(36):14977-14988, 2017 Sep 08.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cytokine-induced endoplasmic reticulum (ER) stress is one of the molecular mechanisms underlying pancreatic ß-cell demise in type 1 diabetes. Thrombospondin 1 (THBS1) was recently shown to promote ß-cell survival during lipotoxic stress. Here we show that ER-localized THBS1 is cytoprotective to rat, mouse, and human ß-cells exposed to cytokines or thapsigargin-induced ER stress. THBS1 confers cytoprotection by maintaining expression of mesencephalic astrocyte-derived neutrotrophic factor (MANF) in ß-cells and thereby prevents the BH3-only protein BIM (BCL2-interacting mediator of cell death)-dependent triggering of the mitochondrial pathway of apoptosis. Prolonged exposure of ß-cells to cytokines or thapsigargin leads to THBS1 and MANF degradation and loss of this prosurvival mechanism. Approaches that sustain intracellular THBS1 and MANF expression in ß-cells should be explored as a cytoprotective strategy in type 1 diabetes.
[Mh] Termos MeSH primário: Inflamação/metabolismo
Células Secretoras de Insulina/metabolismo
Fatores de Crescimento Neural/metabolismo
Trombospondina 1/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Citocinas/metabolismo
Retículo Endoplasmático/metabolismo
Seres Humanos
Células Secretoras de Insulina/efeitos dos fármacos
Camundongos
Fatores de Crescimento Neural/antagonistas & inibidores
Estresse Oxidativo
Tapsigargina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (MANF protein, human); 0 (MANF protein, mouse); 0 (Nerve Growth Factors); 0 (Thrombospondin 1); 67526-95-8 (Thapsigargin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170713
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.769877



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