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Pesquisa : D12.776.543.750.705.408.100.950 [Categoria DeCS]
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[PMID]:28542214
[Au] Autor:Naik MU; Naik TU; Summer R; Naik UP
[Ad] Endereço:Cardeza Center for Vascular Biology, Department of Medicine, Thomas Jefferson University, Philadelphia, PA, United States of America.
[Ti] Título:Binding of CIB1 to the αIIb tail of αIIbß3 is required for FAK recruitment and activation in platelets.
[So] Source:PLoS One;12(5):e0176602, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: It is believed that activation of c-Src bound to the integrin ß3 subunit initiates outside-in signaling. The involvement of αIIb in outside-in signaling is poorly understood. OBJECTIVES: We have previously shown that CIB1 specifically interacts with the cytoplasmic domain of αIIb and is required for αIIbß3 outside-in signaling. Here we evaluated the role of CIB1 in regulating outside-in signaling in the absence of inside-out signaling. METHODS: We used αIIb cytoplasmic domain peptide and CIB1-function blocking antibody to inhibit interaction of CIB1 with αIIb subunit as well as Cib1-/- platelets to evaluate the consequence of CIB1 interaction with αIIb on outside-in signaling. RESULTS: Fibrinogen binding to αIIbß3 results in calcium-dependent interaction of CIB1 with αIIb, which is not required for filopodia formation. Dynamic rearrangement of cytoskeleton results in CIB1-dependent recruitment of FAK to the αIIb complex and its activation. Disruption of the association of CIB1 and αIIb by incorporation of αIIb peptide or anti-CIB1 inhibited both FAK association and activation. Furthermore, FAK recruitment to the integrin complex was required for c-Src activation. Inhibition of c-Src had no effect on CIB1 accumulation with the integrin at the filopodia, suggesting that c-Src activity is not required for the formation of CIB1-αIIb-FAK complex. CONCLUSION: Our results suggest that interaction of CIB1 with αIIb is one of the early events occurring during outside-in signaling. Furthermore, CIB1 recruits FAK to the αIIbß3 complex at the filopodia where FAK is activated, which in turn activates c-Src, resulting in propagation of outside-in signaling leading to platelet spreading.
[Mh] Termos MeSH primário: Plaquetas/metabolismo
Proteínas de Ligação ao Cálcio/metabolismo
Quinase 1 de Adesão Focal/metabolismo
Complexo Glicoproteico GPIIb-IIIa de Plaquetas/metabolismo
Glicoproteína IIb da Membrana de Plaquetas/metabolismo
[Mh] Termos MeSH secundário: Animais
Plaquetas/citologia
Western Blotting
Proteínas de Ligação ao Cálcio/genética
Citoesqueleto/metabolismo
Ativação Enzimática
Imunofluorescência
Seres Humanos
Imunoprecipitação
Camundongos Endogâmicos C57BL
Camundongos Knockout
Microscopia de Fluorescência
Ativação Plaquetária
Ligação Proteica
Pseudópodes/metabolismo
Transdução de Sinais
Quinases da Família src/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CIB1 protein, human); 0 (Calcium-Binding Proteins); 0 (Cib1 protein, mouse); 0 (Platelet Glycoprotein GPIIb-IIIa Complex); 0 (Platelet Membrane Glycoprotein IIb); EC 2.7.10.2 (CSK tyrosine-protein kinase); 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); EC 2.7.10.2 (src-Family Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0176602


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[PMID]:28495930
[Au] Autor:Dhanesha N; Doddapattar P; Chorawala MR; Nayak MK; Kokame K; Staber JM; Lentz SR; Chauhan AK
[Ad] Endereço:From the Department of Internal Medicine (N.D., P.D., M.R.C., M.K.N., S.R.L., A.K.C.) and Stead Family Department of Pediatrics (J.M.S.), University of Iowa; and Department of Molecular Pathogenesis, National Cardiovascular Centre Research Institute, Suita, Osaka, Japan (K.K.).
[Ti] Título:ADAMTS13 Retards Progression of Diabetic Nephropathy by Inhibiting Intrarenal Thrombosis in Mice.
[So] Source:Arterioscler Thromb Vasc Biol;37(7):1332-1338, 2017 Jul.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: ADAMTS13 (a disintegrin and metalloprotease with thrombospondin type I repeats-13) prevents microvascular thrombosis by cleaving prothrombogenic ultralarge von Willebrand factor (VWF) multimers. Clinical studies have found association between reduced ADAMTS13-specific activity, ultralarge VWF multimers, and thrombotic angiopathy in patients with diabetic nephropathy. It remains unknown, however, whether ADAMTS13 deficiency or ultralarge VWF multimers have a causative effect in diabetic nephropathy. APPROACH AND RESULTS: The extent of renal injury was evaluated in wild-type (WT), 13 and 13 mice after 26 weeks of streptozotocin-induced diabetic nephropathy. We found that WT diabetic mice exhibited low plasma ADAMTS13-specific activity and increased VWF levels ( <0.05 versus WT nondiabetic mice). 13 diabetic mice exhibited deterioration of kidney function (increased albuminuria, plasma creatinine, and urea; <0.05 versus WT diabetic mice), independent of hyperglycemia and hypertension. Deterioration of kidney function in 13 diabetic mice was concomitant with aggravated intrarenal thrombosis (assessed by plasminogen activator inhibitor, VWF, fibrin(ogen), and CD41-positive microthrombi), increased mesangial cell expansion, and extracellular matrix deposition ( <0.05 versus WT diabetic mice). Genetic deletion of VWF in 13 diabetic mice improved kidney function, inhibited intrarenal thrombosis, and alleviated histological changes in glomeruli, suggesting that exacerbation of diabetic nephropathy in the setting of ADAMTS13 deficiency is VWF dependent. CONCLUSIONS: ADAMTS13 retards progression of diabetic nephropathy, most likely by inhibiting VWF-dependent intrarenal thrombosis. Alteration in ADAMTS13-VWF balance may be one of the key pathophysiological mechanisms of thrombotic angiopathy in diabetes mellitus.
[Mh] Termos MeSH primário: Proteína ADAMTS13/metabolismo
Nefropatias Diabéticas/prevenção & controle
Glomérulos Renais/enzimologia
Trombose/prevenção & controle
[Mh] Termos MeSH secundário: Proteína ADAMTS13/deficiência
Proteína ADAMTS13/genética
Albuminúria/enzimologia
Albuminúria/prevenção & controle
Animais
Proliferação Celular
Creatinina/sangue
Diabetes Mellitus Experimental/induzido quimicamente
Nefropatias Diabéticas/enzimologia
Nefropatias Diabéticas/genética
Nefropatias Diabéticas/patologia
Progressão da Doença
Matriz Extracelular/metabolismo
Matriz Extracelular/patologia
Fibrinogênio/metabolismo
Predisposição Genética para Doença
Glomérulos Renais/patologia
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fenótipo
Inibidor 1 de Ativador de Plasminogênio/metabolismo
Glicoproteína IIb da Membrana de Plaquetas/metabolismo
Estreptozocina
Trombose/enzimologia
Trombose/genética
Trombose/patologia
Ureia/sangue
Fator de von Willebrand/genética
Fator de von Willebrand/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Plasminogen Activator Inhibitor 1); 0 (Platelet Membrane Glycoprotein IIb); 0 (von Willebrand Factor); 5W494URQ81 (Streptozocin); 8W8T17847W (Urea); 9001-32-5 (Fibrinogen); AYI8EX34EU (Creatinine); EC 3.4.24.- (ADAMTS13 protein, mouse); EC 3.4.24.87 (ADAMTS13 Protein)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170513
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309539


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[PMID]:28336526
[Au] Autor:Miyawaki K; Iwasaki H; Jiromaru T; Kusumoto H; Yurino A; Sugio T; Uehara Y; Odawara J; Daitoku S; Kunisaki Y; Mori Y; Arinobu Y; Tsuzuki H; Kikushige Y; Iino T; Kato K; Takenaka K; Miyamoto T; Maeda T; Akashi K
[Ad] Endereço:Department of Medicine and Biosystemic Science, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan; and.
[Ti] Título:Identification of unipotent megakaryocyte progenitors in human hematopoiesis.
[So] Source:Blood;129(25):3332-3343, 2017 Jun 22.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The developmental pathway for human megakaryocytes remains unclear, and the definition of pure unipotent megakaryocyte progenitor is still controversial. Using single-cell transcriptome analysis, we have identified a cluster of cells within immature hematopoietic stem- and progenitor-cell populations that specifically expresses genes related to the megakaryocyte lineage. We used CD41 as a positive marker to identify these cells within the CD34 CD38 IL-3Rα CD45RA common myeloid progenitor (CMP) population. These cells lacked erythroid and granulocyte-macrophage potential but exhibited robust differentiation into the megakaryocyte lineage at a high frequency, both in vivo and in vitro. The efficiency and expansion potential of these cells exceeded those of conventional bipotent megakaryocyte/erythrocyte progenitors. Accordingly, the CD41 CMP was defined as a unipotent megakaryocyte progenitor (MegP) that is likely to represent the major pathway for human megakaryopoiesis, independent of canonical megakaryocyte-erythroid lineage bifurcation. In the bone marrow of patients with essential thrombocythemia, the MegP population was significantly expanded in the context of a high burden of Janus kinase 2 mutations. Thus, the prospectively isolatable and functionally homogeneous human MegP will be useful for the elucidation of the mechanisms underlying normal and malignant human hematopoiesis.
[Mh] Termos MeSH primário: Hematopoese
Células Progenitoras de Megacariócitos/citologia
Células Progenitoras de Megacariócitos/metabolismo
Megacariócitos/citologia
[Mh] Termos MeSH secundário: Adulto
Animais
Antígenos CD/análise
Linhagem da Célula
Células Cultivadas
Seres Humanos
Células Progenitoras de Megacariócitos/patologia
Megacariócitos/metabolismo
Camundongos Endogâmicos C57BL
Transtornos Mieloproliferativos/genética
Transtornos Mieloproliferativos/patologia
Glicoproteína IIb da Membrana de Plaquetas/análise
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Platelet Membrane Glycoprotein IIb)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170325
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2016-09-741611


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[PMID]:28276730
[Au] Autor:Biolik G; Kokot M; Sznapka M; Swieszek A; Ziaja D; Pawlicki K; Ziaja K
[Ad] Endereço:a Department of General Vascular Surgery, Faculty of Medicine in Katowice , School of Health Science, Medical University of Silesia , Katowice , Poland.
[Ti] Título:Platelet reactivity in thromboelastometry. Revision of the FIBTEM test: a basic study.
[So] Source:Scand J Clin Lab Invest;77(3):216-222, 2017 May.
[Is] ISSN:1502-7686
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:This study aimed to investigate modifications to the FIBTEM test to better assess fibrinogen levels and the quality of fibrin polymerization in citrated blood using Multiplate impedance aggregometry to verify platelet inhibition. Blood samples from 26 healthy volunteers were subjected to thromboelastometry studies (EXTEM/FIBTEM tests) in accordance with the standard study protocol (cytochalasin D) and according to a modified protocol (synthetic IIbIIIa receptor antagonist vs. acetylsalicylic acid [ASA] + synthetic IIbIIIa receptor antagonist instead of cytochalasin D). Independent of thromboelastometry, Multiplate impedance aggregometry was used to assess the degree of restriction by the platelet blocked with the following treatments: (1) cytochalasin D, (2) synthetic IIbIIIa antagonist or (3) ASA + synthetic IIbIIIa antagonist to assess the aggregation response to activation with an agonist (ADP, collagen, thrombin receptor activating peptide-6 [TRAP-6], and arachidonic acid). Via aggregometry, cytochalasin D more weakly inhibited platelet aggregation than simultaneous administration of the -IIbIIIa receptor antagonist with ASA. However, total platelet aggregation inhibition was observed after simultaneous administration of cytochalasin D combined with a synthetic IIbIIIa receptor antagonist. In the thromboelastometry, a significant decrease of the A10, A20 and MCF parameters were observed in the EXTEM/FIBTEM tests after they were modified by the addition of a synthetic IIbIIIa receptor antagonist alone or in combination with ASA. In conclusion, in this Multiplate- and ROTEM-based laboratory approach, a two-way blockade (IIbIIIa-antagonist + cytochalasine D) was sufficient to completely inhibit procoagulant platelet function as observed by aggregometry and thromboelastometry.
[Mh] Termos MeSH primário: Aspirina/farmacologia
Plaquetas/efeitos dos fármacos
Citocalasina D/farmacologia
Ativação Plaquetária/efeitos dos fármacos
Agregação Plaquetária/efeitos dos fármacos
Tromboelastografia/normas
[Mh] Termos MeSH secundário: Difosfato de Adenosina/farmacologia
Adulto
Ácido Araquidônico/farmacologia
Testes de Coagulação Sanguínea
Plaquetas/citologia
Plaquetas/metabolismo
Colágeno/farmacologia
Feminino
Fibrina/metabolismo
Fibrinogênio/metabolismo
Seres Humanos
Integrina beta3/metabolismo
Masculino
Oligopeptídeos/farmacologia
Glicoproteína IIb da Membrana de Plaquetas/metabolismo
Cultura Primária de Células
Tromboelastografia/instrumentação
Tromboelastografia/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Integrin beta3); 0 (Oligopeptides); 0 (Platelet Membrane Glycoprotein IIb); 0 (Ser-Phe-Phe-Leu-Arg-Asn); 22144-77-0 (Cytochalasin D); 27YG812J1I (Arachidonic Acid); 61D2G4IYVH (Adenosine Diphosphate); 9001-31-4 (Fibrin); 9001-32-5 (Fibrinogen); 9007-34-5 (Collagen); R16CO5Y76E (Aspirin)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170421
[Lr] Data última revisão:
170421
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE
[do] DOI:10.1080/00365513.2017.1292538


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[PMID]:28253287
[Au] Autor:Echtler K; Konrad I; Lorenz M; Schneider S; Hofmaier S; Plenagl F; Stark K; Czermak T; Tirniceriu A; Eichhorn M; Walch A; Enders G; Massberg S; Schulz C
[Ad] Endereço:Medizinische Klinik und Poliklinik I, Klinikum der Universität, Ludwig-Maximilians-Universität, Munich, Germany.
[Ti] Título:Platelet GPIIb supports initial pulmonary retention but inhibits subsequent proliferation of melanoma cells during hematogenic metastasis.
[So] Source:PLoS One;12(3):e0172788, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Platelets modulate the process of cancer metastasis. However, current knowledge on the direct interaction of platelets and tumor cells is mostly based on findings obtained in vitro. We addressed the role of the platelet fibrinogen receptor glycoprotein IIb (integrin αIIb) for experimental melanoma metastasis in vivo. Highly metastatic B16-D5 melanoma cells were injected intravenously into GPIIb-deficient (GPIIb-/-) or wildtype (WT) mice. Acute accumulation of tumor cells in the pulmonary vasculature was assessed in real-time by confocal videofluorescence microscopy. Arrest of tumor cells was dramatically reduced in GPIIb-/- mice as compared to WT. Importantly, we found that mainly multicellular aggregates accumulated in the pulmonary circulation of WT, instead B16-D5 aggregates were significantly smaller in GPIIb-/- mice. While pulmonary arrest of melanoma was clearly dependent on GPIIb in this early phase of metastasis, we also addressed tumor progression 10 days after injection. Inversely, and unexpectedly, we found that melanoma metastasis was now increased in GPIIb-/- mice. In contrast, GPIIb did not regulate local melanoma proliferation in a subcutaneous tumor model. Our data suggest that the platelet fibrinogen receptor has a differential role in the modulation of hematogenic melanoma metastasis. While platelets clearly support early steps in pulmonary metastasis via GPIIb-dependent formation of platelet-tumor-aggregates, at a later stage its absence is associated with an accelerated development of melanoma metastases.
[Mh] Termos MeSH primário: Plaquetas/metabolismo
Neoplasias Pulmonares/secundário
Pulmão/patologia
Melanoma Experimental/patologia
Glicoproteína IIb da Membrana de Plaquetas/metabolismo
[Mh] Termos MeSH secundário: Animais
Plaquetas/fisiologia
Agregação Celular
Linhagem Celular Tumoral
Proliferação Celular
Pulmão/irrigação sanguínea
Neoplasias Pulmonares/sangue
Neoplasias Pulmonares/irrigação sanguínea
Neoplasias Pulmonares/patologia
Camundongos
Microcirculação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Platelet Membrane Glycoprotein IIb)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170825
[Lr] Data última revisão:
170825
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170303
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0172788


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[PMID]:28179275
[Au] Autor:Bernitz JM; Daniel MG; Fstkchyan YS; Moore K
[Ad] Endereço:Department of Cell, Developmental and Regenerative Biology, Black Family Stem Cell Institute, and The Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY.
[Ti] Título:Granulocyte colony-stimulating factor mobilizes dormant hematopoietic stem cells without proliferation in mice.
[So] Source:Blood;129(14):1901-1912, 2017 Apr 06.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Granulocyte colony-stimulating factor (G-CSF) is used clinically to treat leukopenia and to enforce hematopoietic stem cell (HSC) mobilization to the peripheral blood (PB). However, G-CSF is also produced in response to infection, and excessive exposure reduces HSC repopulation capacity. Previous work has shown that dormant HSCs contain all the long-term repopulation potential in the bone marrow (BM), and that as HSCs accumulate a divisional history, they progressively lose regenerative potential. As G-CSF treatment also induces HSC proliferation, we sought to examine whether G-CSF-mediated repopulation defects are a result of increased proliferative history. To do so, we used an established H2BGFP label retaining system to track HSC divisions in response to G-CSF. Our results show that dormant HSCs are preferentially mobilized to the PB on G-CSF treatment. We find that this mobilization does not result in H2BGFP label dilution of dormant HSCs, suggesting that G-CSF does not stimulate dormant HSC proliferation. Instead, we find that proliferation within the HSC compartment is restricted to CD41-expressing cells that function with short-term, and primarily myeloid, regenerative potential. Finally, we show CD41 expression is up-regulated within the BM HSC compartment in response to G-CSF treatment. This emergent CD41 HSC fraction demonstrates no observable engraftment potential, but directly matures into megakaryocytes when placed in culture. Together, our results demonstrate that dormant HSCs mobilize in response to G-CSF treatment without dividing, and that G-CSF-mediated proliferation is restricted to cells with limited regenerative potential found within the HSC compartment.
[Mh] Termos MeSH primário: Proliferação Celular/efeitos dos fármacos
Regulação da Expressão Gênica/efeitos dos fármacos
Fator Estimulador de Colônias de Granulócitos/farmacologia
Mobilização de Células-Tronco Hematopoéticas
Células-Tronco Hematopoéticas/metabolismo
Glicoproteína IIb da Membrana de Plaquetas/biossíntese
[Mh] Termos MeSH secundário: Animais
Proliferação Celular/genética
Regulação da Expressão Gênica/genética
Células-Tronco Hematopoéticas/citologia
Camundongos
Camundongos Transgênicos
Glicoproteína IIb da Membrana de Plaquetas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Platelet Membrane Glycoprotein IIb); 143011-72-7 (Granulocyte Colony-Stimulating Factor)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170810
[Lr] Data última revisão:
170810
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170210
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2016-11-752923


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[PMID]:28101696
[Au] Autor:Li A; Guo Q; Wei A; Zhou Y; Hu W
[Ad] Endereço:Department of Pancreatic Surgery, West China Hospital, Sichuan University, 37 Guoxue Rd, Chengdu, Sichuan Province, China.
[Ti] Título:Role of the Helix in Talin F3 Domain (F3 Helix) in Talin-Mediated Integrin Activation.
[So] Source:Cell Biochem Biophys;75(1):79-86, 2017 Mar.
[Is] ISSN:1559-0283
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Increases in ligand binding to cellular integrins (activation) play an important role in platelet and leukocyte function. Talin is necessary in vivo and sufficient in vitro for integrin αIIbß3 activation. The precise mechanisms by which talin activates integrin are still being elucidated. In particular, talin undergoes conformational changes (around the F3 helix) and inserts the F3 helix into lipid bilayer; however, the connection between this lipid-inserting mechanism of talin and talin's capacity to activate integrin has never been explored before. In this work, we used rational mutagenesis, modeled cell systems, and structural modeling to study the potential role of membrane-induced talin conformational changes in talin-mediated integrin activation. Mutations of the residues critical for talin F3 helix to insert into membrane completely abolished talin-mediated integrin activation without affecting the binding of talin to integrins. Furthermore, mutations of the lipid-binding sequences in talin F3 helix significantly reduced the capacity of talin to activate integrin. Our results suggest that the F3 helix may contribute to talin-mediated integrin activation.
[Mh] Termos MeSH primário: Integrina beta3/metabolismo
Glicoproteína IIb da Membrana de Plaquetas/metabolismo
Talina/química
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Células CHO
Cricetinae
Cricetulus
Modelos Moleculares
Glicoproteína IIb da Membrana de Plaquetas/química
Conformação Proteica em alfa-Hélice
Domínios e Motivos de Interação entre Proteínas
Talina/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Integrin beta3); 0 (Platelet Membrane Glycoprotein IIb); 0 (Talin)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170306
[Lr] Data última revisão:
170306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170120
[St] Status:MEDLINE
[do] DOI:10.1007/s12013-017-0781-x


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[PMID]:28004990
[Au] Autor:Liu H; Wang Y; Zheng J; Li G; Chen T; Lei J; Mao Y; Wang J; Liu W; Zhao G; Tacey M; Yan B
[Ad] Endereço:1 Department of Neurology, the Second Clinical Medical College of North Sichuan Medical College & Nanchong Central Hospital, Nanchong, P R China.
[Ti] Título:Platelet glycoprotein gene Ia C807T, HPA-3, and Ibα VNTR polymorphisms are associated with increased ischemic stroke risk: Evidence from a comprehensive meta-analysis.
[So] Source:Int J Stroke;12(1):46-70, 2017 Jan.
[Is] ISSN:1747-4949
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background/aims Platelet glycoproteins play a crucial role in the initial stage of thrombus formation and may contribute to the pathophysiology of atherosclerosis. Polymorphisms in glycoprotein genes alter the function of the protein, possibly leading to increased risk of ischemic stroke. However, previous genetic association studies that examined the relationship between glycoprotein genes polymorphisms and ischemic stroke have yielded inconsistent results. This study aimed to evaluate the association between glycoprotein genes and ischemic stroke by the application of meta-analysis. Methods Relevant studies were identified by an extensive search through databases. The quality of included studies was assessed independently using the Newcastle-Ottawa Scale. Allele and genotype frequencies for each included study were extracted. The odds ratio (OR) with 95% confidence interval (95%CI) was calculated using a random-effects or fixed-effects model. Q statistic was used to evaluate homogeneity, and a meta-regression model was used to explore the study-level variables and to describe the heterogeneity in included studies. Egger's test and funnel plot were used to assess publication bias. Results A total of 60 studies (9 polymorphisms) were included and identified in the current meta-analysis. The Newcastle-Ottawa Scale scores ranged from 7 to 9 except for two studies with Newcastle-Ottawa Scale scores of 6. The T allele or TT genotype of the glycoprotein Ia C807T polymorphism were associated with an increased susceptibility to ischemic stroke in combined population (807T allele: OR, 95%CI: 1.24, 1.03-1.50, p = 0.02) or Asian populations (807T allele: OR, 95%CI: 1.31, 1.10-1.54, p = 0.002 and 807TT genotype: OR, 95%CI: 1.53, 1.13-2.08, p = 0.006, respectively), and the Ser allele of HPA-3 was associated with increased risk of ischemic stroke in combined population or in Asians (OR, 95%CI: 1.21, 1.04-1.40, p = 0.01 or 1.54, 1.18-2.01, p = 0.001). Of note, the Ser/Ser genotype was more common in Asians (OR, 95%CI: 2.09, 1.40-3.13, p < 0.001). For glycoprotein Ibα variable number tandem repeat, only B allele showed a mild significant association with ischemic stroke risk in combined population or in Caucasians (OR, 95%CI: 2.17, 1.04-4.55, p = 0.04 or 1.79, 1.02-3.13, p = 0.04). There was no significant association between HPA-1, HPA-2, HPA-4, HPA-5, glycoprotein Ibα-5 T/C as well as Ia G873A polymorphisms and increased risk of ischemic stroke. Conclusions We found that glycoprotein Ia C807T T allele or the TT genotype, the Ser-allele of HPA-3 and B allele of glycoprotein Ibα variable number tandem repeat polymorphisms were associated with increased risk for ischemic stroke. Future studies with larger sample sizes will be necessary to confirm the results. In addition, analyses of ischemic stroke subtypes and gene-gene and gene-environment interactions are warranted.
[Mh] Termos MeSH primário: Isquemia Encefálica/genética
Predisposição Genética para Doença
Integrina alfa2beta1/genética
Repetições Minissatélites
Complexo Glicoproteico GPIb-IX de Plaquetas/genética
Glicoproteína IIb da Membrana de Plaquetas/genética
Acidente Vascular Cerebral/genética
[Mh] Termos MeSH secundário: Seres Humanos
Polimorfismo Genético
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Integrin alpha2beta1); 0 (Platelet Glycoprotein GPIb-IX Complex); 0 (Platelet Membrane Glycoprotein IIb)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161223
[St] Status:MEDLINE
[do] DOI:10.1177/1747493016672085


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[PMID]:27870830
[Au] Autor:Henninger J; Santoso B; Hans S; Durand E; Moore J; Mosimann C; Brand M; Traver D; Zon L
[Ad] Endereço:Stem Cell Program and Division of Hematology/Oncology, Boston Children's Hospital and Dana Farber Cancer Institute, Howard Hughes Medical Institute, Harvard Stem Cell Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.
[Ti] Título:Clonal fate mapping quantifies the number of haematopoietic stem cells that arise during development.
[So] Source:Nat Cell Biol;19(1):17-27, 2017 Jan.
[Is] ISSN:1476-4679
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Haematopoietic stem cells (HSCs) arise in the developing aorta during embryogenesis. The number of HSC clones born has been estimated through transplantation, but experimental approaches to assess the absolute number of forming HSCs in a native setting have remained challenging. Here, we applied single-cell and clonal analysis of HSCs in zebrafish to quantify developing HSCs. Targeting creER in developing cd41:eGFP HSCs enabled long-term assessment of their blood contribution. We also applied the Brainbow-based multicolour Zebrabow system with drl:creER that is active in early haematopoiesis to induce heritable colour barcoding unique to each HSC and its progeny. Our findings reveal that approximately 21 HSC clones exist prior to HSC emergence and 30 clones are present during peak production from aortic endothelium. Our methods further reveal that stress haematopoiesis, including sublethal irradiation and transplantation, reduces clonal diversity. Our findings provide quantitative insights into the early clonal events that regulate haematopoietic development.
[Mh] Termos MeSH primário: Linhagem da Célula
Desenvolvimento Embrionário
Células-Tronco Hematopoéticas/citologia
[Mh] Termos MeSH secundário: Envelhecimento
Animais
Vasos Sanguíneos/embriologia
Células da Medula Óssea/citologia
Transplante de Medula Óssea
Contagem de Células
Células Clonais
Embrião não Mamífero/citologia
Células Eritroides/citologia
Granulócitos/citologia
Hematopoese
Lasers
Glicoproteína IIb da Membrana de Plaquetas/metabolismo
Coloração e Rotulagem
Transgenes
Peixe-Zebra/embriologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Platelet Membrane Glycoprotein IIb)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161122
[St] Status:MEDLINE
[do] DOI:10.1038/ncb3444


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[PMID]:27534900
[Au] Autor:Wang Q; You T; Fan H; Wang Y; Chu T; Poncz M; Zhu L
[Ad] Endereço:a Cyrus Tang Hematology Center , Soochow University , Suzhou , China.
[Ti] Título:Rapamycin and bafilomycin A1 alter autophagy and megakaryopoiesis.
[So] Source:Platelets;28(1):82-89, 2017 Jan.
[Is] ISSN:1369-1635
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Autophagy is an effective strategy for cell development by recycling cytoplasmic constituents. Genetic deletion of autophagy mediator Atg7 in hematopoietic stem cells (HSCs) can lead to failure of megakaryopoiesis and enhanced autophagy has been implicated in various hematological disorders such as immune thrombocytopenia and myelodysplastic syndrome. Here, we examined the hypothesis that optimal autophagy is essential for megakaryopoiesis and thrombopoiesis by altering autophagy using pharmacological approaches. When autophagy was induced by rapamycin or inhibited by bafilomycin A1 in fetal liver cells, we observed a significant decrease in high ploidy megakaryocytes, a reduction of CD41 and CD61 co-expressing cells, and less proplatelet or platelet formation. Additionally, reduced cell size was shown in megakaryocytes derived from rapamycin, but not bafilomycin A1-treated mouse fetal liver cells. However, when autophagy was altered in mature megakaryocytes, we observed no significant change in proplatelet formation, which was consistent with normal platelet counts, megakaryocyte numbers, and ploidy in Atg7 PF4-Cre mice with megakaryocyte- and platelet-specific deletion of autophagy-related gene Atg7. Therefore, our findings suggest that either induction or inhibition of autophagy in the early stage of megakaryopoiesis suppresses megakaryopoiesis and thrombopoiesis.
[Mh] Termos MeSH primário: Autofagia/efeitos dos fármacos
Macrolídeos/farmacologia
Sirolimo/farmacologia
Trombopoese/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Biomarcadores
Plaquetas/metabolismo
Diferenciação Celular/efeitos dos fármacos
Diferenciação Celular/genética
Células Cultivadas
Feminino
Citometria de Fluxo
Expressão Gênica
Integrina beta3/genética
Integrina beta3/metabolismo
Megacariócitos/citologia
Megacariócitos/efeitos dos fármacos
Megacariócitos/metabolismo
Camundongos
Camundongos Transgênicos
Contagem de Plaquetas
Glicoproteína IIb da Membrana de Plaquetas/genética
Glicoproteína IIb da Membrana de Plaquetas/metabolismo
Ploidias
Trombopoese/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Integrin beta3); 0 (Macrolides); 0 (Platelet Membrane Glycoprotein IIb); 88899-55-2 (bafilomycin A1); W36ZG6FT64 (Sirolimus)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160819
[St] Status:MEDLINE
[do] DOI:10.1080/09537104.2016.1204436



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