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Pesquisa : D12.776.157.125.050.100 [Categoria DeCS]
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[PMID]:29378549
[Au] Autor:Li S; Pasquin S; Eid HM; Gauchat JF; Saleem A; Haddad PS
[Ad] Endereço:Department of Pharmacology and Physiology, Université de Montréal, P.O. Box 6128, Downtown Postal Station, Montreal, (Quebec), H3C 3J7, Canada.
[Ti] Título:Anti-apoptotic potential of several antidiabetic medicinal plants of the eastern James Bay Cree pharmacopeia in cultured kidney cells.
[So] Source:BMC Complement Altern Med;18(1):37, 2018 Jan 30.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Our team has identified 17 Boreal forest species from the traditional pharmacopeia of the Eastern James Bay Cree that presented promising in vitro and in vivo biological activities in the context of type 2 diabetes (T2D). We now screened the 17 plants extracts for potential anti-apoptotic activity in cultured kidney cells and investigated the underlying mechanisms. METHODS: MDCK (Madin-Darnby Canine Kidney) cell damage was induced by hypertonic medium (700 mOsm/L) in the presence or absence of maximal nontoxic concentrations of each of the 17 plant extracts. After 18 h' treatment, cells were stained with Annexin V (AnnV) and Propidium iodide (PI) and subjected to flow cytometry to assess the cytoprotective (AnnV /PI ) and anti-apoptotic (AnnV /PI ) potential of the 17 plant extracts. We then selected a representative subset of species (most cytoprotective, moderately so or neutral) to measure the activity of caspases 3, 8 and 9. RESULTS: Gaultheria hispidula and Abies balsamea are amongst the most powerful cytoprotective and anti-apoptotic plants and appear to exert their modulatory effect primarily by inhibiting caspase 9 in the mitochondrial apoptotic signaling pathway. CONCLUSION: We conclude that several Cree antidiabetic plants exert anti-apoptotic activity that may be relevant in the context of diabetic nephropathy (DN) that affects a significant proportion of Cree diabetics.
[Mh] Termos MeSH primário: Hipoglicemiantes/farmacologia
Medicina Tradicional
Extratos Vegetais/farmacologia
Plantas Medicinais/química
Substâncias Protetoras/farmacologia
[Mh] Termos MeSH secundário: Animais
Anexina A5/química
Apoptose/efeitos dos fármacos
Canadá
Caspases/metabolismo
Nefropatias Diabéticas/metabolismo
Cães
Hipoglicemiantes/química
Células Madin Darby de Rim Canino
Extratos Vegetais/química
Propídio/química
Substâncias Protetoras/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A5); 0 (Hypoglycemic Agents); 0 (Plant Extracts); 0 (Protective Agents); 36015-30-2 (Propidium); EC 3.4.22.- (Caspases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180131
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-018-2104-1


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[PMID]:27771353
[Au] Autor:Peng W
[Ad] Endereço:Institute of Rheumatology and Immunology, Affiliated Hospital of North Sichuan Medical College, Nanchong City, Sichuan 637000, P. R. China; Laboratory of Experimental Surgery, Hadassah-Hebrew University Medical Center, Mount Scopus, Sderot Churchill, Jerusalem, 91240, Israel. Electronic address: pengwei39@hotmail.com.
[Ti] Título:G-CSF treatment promotes apoptosis of autoreactive T cells to restrict the inflammatory cascade and accelerate recovery in experimental allergic encephalomyelitis.
[So] Source:Exp Neurol;289:73-84, 2017 03.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:G-CSF is a hematopoietic growth factor that regulates the proliferation, differentiation and survival of myeloid lineage cells, which has protective effects in autoimmune neuroinflammatory diseases such as EAE. Here we use EAE model treated by G-CSF to address the hypothesis that G-CSF inhibits the proliferative response of splenic T cells via the enhancement of apoptosis, and this priming effect of G-CSF depends on the cell cycle. Our results show that G-CSF administration reduced EAE frequency and severity of attacks. The inflammatory cells and demyelination areas were decreased in the CNS of G-CSF-treated mice. G-CSF treatment altered cytokine profiles in vivo to inhibit the productions of IFN-γ, IL-1ß, IL-2, TNF-α, IL-17 and NO, while the secretions of IL-4 and IL-10 were increased. Splenic T cells from G-CSF-treated mice showed significantly lower proliferative response to specific antigen MOG stimulation. G-CSF enhanced the percentage of a CD4 CD25 T cell subset in spleen T cells. Moreover, G-CSF promoted the G0/G1 to S phase transition of MOG autoreactive T cells inducing apoptosis and elevating Bax gene expression of apoptosis marker. These findings indicate that G-CSF treatment induces the apoptosis of MOG autoreactive T cells, which decreases the production of pro-inflammatory cytokines and NO, suppresses the proliferation of autoreactive T cells and elevates a CD4 CD25 T cell subset to inhibit inflammatory infiltration and demyelination within CNS of EAE. The conclusions of G-CSF treatment in EAE mice suggest that G-CSF is clinically applicable and may be considered for future use in therapeutic measures for multiple sclerosis treatment.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Linfócitos T CD4-Positivos/efeitos dos fármacos
Encefalomielite Autoimune Experimental/tratamento farmacológico
Encefalomielite Autoimune Experimental/fisiopatologia
Fator Estimulador de Colônias de Granulócitos/uso terapêutico
Recuperação de Função Fisiológica/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Anexina A5/metabolismo
Ciclo Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Citocinas/metabolismo
Modelos Animais de Doenças
Encefalomielite Autoimune Experimental/induzido quimicamente
Feminino
Adjuvante de Freund/toxicidade
Expressão Gênica/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos C57BL
Glicoproteína Mielina-Oligodendrócito/toxicidade
Óxido Nítrico/metabolismo
Fragmentos de Peptídeos/toxicidade
Toxina Pertussis/toxicidade
Baço/patologia
Proteína X Associada a bcl-2/genética
Proteína X Associada a bcl-2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A5); 0 (Cytokines); 0 (Myelin-Oligodendrocyte Glycoprotein); 0 (Peptide Fragments); 0 (bcl-2-Associated X Protein); 0 (myelin oligodendrocyte glycoprotein (35-55)); 143011-72-7 (Granulocyte Colony-Stimulating Factor); 31C4KY9ESH (Nitric Oxide); 9007-81-2 (Freund's Adjuvant); EC 2.4.2.31 (Pertussis Toxin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:180218
[Lr] Data última revisão:
180218
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:28466971
[Au] Autor:Baig AM; Lalani S; Khan NA
[Ad] Endereço:Department of Biological and Biomedical Sciences, Aga Khan University, Karachi, Pakistan.
[Ti] Título:Apoptosis in Acanthamoeba castellanii belonging to the T4 genotype.
[So] Source:J Basic Microbiol;57(7):574-579, 2017 Jul.
[Is] ISSN:1521-4028
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Here we describe features of apoptosis in unicellular Acanthamoeba castellanii belonging to the T4 genotype. When exposed to apoptosis-inducing compounds such as doxorubicin, A. castellanii trophozoites exhibited cell shrinkage and membrane blebbing as observed microscopically, DNA fragmentation using agarose gel electrophoresis, and phosphatidylserine (PS) externalization using annexin V immunostaining. Overall, these findings suggest the existence of apoptosis in A. castellanii possibly mediated by intrinsic apoptotic cascade. Further research in this field could provide avenues to selectively induce apoptosis in A. castellanii by triggering intrinsic apoptotic cascade.
[Mh] Termos MeSH primário: Acanthamoeba castellanii/citologia
Acanthamoeba castellanii/fisiologia
Apoptose
[Mh] Termos MeSH secundário: Acanthamoeba castellanii/efeitos dos fármacos
Acanthamoeba castellanii/genética
Animais
Anexina A5/análise
Fragmentação do DNA
Doxorrubicina/farmacologia
Genótipo
Trofozoítos/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A5); 80168379AG (Doxorubicin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180117
[Lr] Data última revisão:
180117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1002/jobm.201700025


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[PMID]:29267398
[Au] Autor:Stöhr R; Schurgers L; van Gorp R; Jaminon A; Marx N; Reutelingsperger C
[Ad] Endereço:Medizinische Klinik I, RWTH Aachen University, Aachen, Germany.
[Ti] Título:Annexin A5 reduces early plaque formation in ApoE -/- mice.
[So] Source:PLoS One;12(12):e0190229, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Annexin A5 (AnxA5) exerts anti-inflammatory, anticoagulant and anti-apoptotic effects through its binding to cell surface expressed phosphatidylserine. We previously showed that AnxA5 can stabilize advanced atherosclerotic plaques by reducing macrophage infiltration. We now investigated the effects of AnxA5 administration on the onset of atherosclerosis development. Eight-week-old ApoE-/-mice were fed a western diet while being administered AnxA5 or control (M1234) for a total of 6 weeks. AnxA5 administration reduced plaque size in the aortic root as well as the aortic arch by 36% and 55% respectively. As determined by immunohistochemistry, administration of AnxA5 further stabilized plaque by reducing macrophage content and increasing smooth muscle cell content. Furthermore, the pre-treatment of HUVEC's with AnxA5 reduced monocyte adhesion under flow-conditions. Finally, AnxA5 administration results in a trend to reduced cell death more pronounced in the aortic arch than the aortic root. In conclusion, treatment with AnxA5 before the onset of atherosclerosis reduces plaque formation in a murine model of atherosclerosis in part by reducing apoptotic rates further to its beneficial effect on macrophage infiltration and activation.
[Mh] Termos MeSH primário: Anexina A5/fisiologia
Apolipoproteínas E/genética
Placa Aterosclerótica/metabolismo
[Mh] Termos MeSH secundário: Animais
Anexina A5/genética
Apoptose
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Camundongos
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A5); 0 (Apolipoproteins E)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190229


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[PMID]:28748286
[Au] Autor:Klaihmon P; Vimonpatranon S; Noulsri E; Lertthammakiat S; Anurathapan U; Sirachainan N; Hongeng S; Pattanapanyasat K
[Ad] Endereço:Graduate Program in Immunology, Department of Immunology, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.
[Ti] Título:Normalized levels of red blood cells expressing phosphatidylserine, their microparticles, and activated platelets in young patients with ß-thalassemia following bone marrow transplantation.
[So] Source:Ann Hematol;96(10):1741-1747, 2017 Oct.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Bone marrow transplantation (BMT) serves as the only curative treatment for patients with ß-thalassemia major; however, hemostatic changes have been observed in these BMT patients. Aggregability of thalassemic red blood cells (RBCs) and increased red blood cell-derived microparticles (RMPs) expressing phosphatidylserine (PS) are thought to participate in thromboembolic events by initially triggering platelet activation. To our knowledge, there has been no report providing quantitation of these circulating PS-expressing RBCs and RMPs in young ß-thalassemia patients after BMT. Whole blood from each subject was fluorescently labeled to detect RBC markers (CD235a) and annexin-V together with the known number TruCount™ beads. PS-expressing RBCs, RMPs, and activated platelets were identified by flow cytometry. In our randomized study, we found the decreased levels of three aforementioned factors compared to levels in patients receiving regular blood transfusion (RT). This study showed that BMT in ß-thalassemia patients decreases the levels of circulating PS-expressing RBCs, their MPs, and procoagulant platelets when compared to patients who received RT. Normalized levels of these coagulation markers may provide the supportive evidence of the effectiveness of BMT for curing thalassemia.
[Mh] Termos MeSH primário: Plaquetas/metabolismo
Transplante de Medula Óssea
Micropartículas Derivadas de Células/metabolismo
Eritrócitos/metabolismo
Fosfatidilserinas/sangue
Ativação Plaquetária
Talassemia beta
[Mh] Termos MeSH secundário: Adolescente
Aloenxertos
Anexina A5/sangue
Criança
Feminino
Seres Humanos
Masculino
Talassemia beta/sangue
Talassemia beta/terapia
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A5); 0 (Phosphatidylserines)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171129
[Lr] Data última revisão:
171129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-017-3070-2


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[PMID]:28409836
[Au] Autor:Wang Y; Zhang S; Luo L; Norström E; Braun OÖ; Mörgelin M; Thorlacius H
[Ad] Endereço:Department of Clinical Sciences, Section for Surgery, Lund University, Malmö, Sweden.
[Ti] Título:Platelet-derived microparticles regulates thrombin generation via phophatidylserine in abdominal sepsis.
[So] Source:J Cell Physiol;233(2):1051-1060, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sepsis is associated with dysfunctional coagulation. Recent data suggest that platelets play a role in sepsis by promoting neutrophil accumulation. Herein, we show that cecal ligation and puncture (CLP) triggered systemic inflammation, which is characterized by formation of IL-6 and CXC chemokines as well as neutrophil accumulation in the lung. Platelet depletion decreased neutrophil accumulation, IL-6, and CXC chemokines formation in septic lungs. Depletion of platelets increased peak thrombin formation and total thrombin generation (TG) in plasma from septic animals. CLP elevated circulating levels of platelet-derived microparticles (PMPs). In vitro generated PMPs were a potent inducer of TG. Interestingly, in vitro wild-type recombinant annexin V abolished PMP-induced thrombin formation whereas a mutant annexin V protein, which does not bind to phosphatidylserine (PS), had no effect. Administration of wild-type, but not mutant annexin V, significantly inhibited thrombin formation in septic animals. Moreover, CLP-induced formation of thrombin-antithrombin complexes were reduced in platelet-depleted mice and in animals pretreated with annexin V. PMP-induced TG attenuated in FXII- and FVII-deficient plasma. These findings suggest that sepsis-induced TG is dependent on platelets. Moreover, PMPs formed in sepsis are a potent inducer of TG via PS exposure, and activation of both the intrinsic and extrinsic pathway of coagulation. In conclusion, these observations suggest that PMPs and PS play an important role in dysfunctional coagulation in abdominal sepsis.
[Mh] Termos MeSH primário: Coagulação Sanguínea
Plaquetas/metabolismo
Micropartículas Derivadas de Células/metabolismo
Fosfatidilserinas/sangue
Sepse/sangue
Trombina/metabolismo
[Mh] Termos MeSH secundário: Animais
Anexina A5/sangue
Antitrombina III
Plaquetas/imunologia
Plaquetas/microbiologia
Plaquetas/ultraestrutura
Micropartículas Derivadas de Células/imunologia
Micropartículas Derivadas de Células/microbiologia
Micropartículas Derivadas de Células/ultraestrutura
Quimiocinas CXC/metabolismo
Modelos Animais de Doenças
Inflamação/sangue
Inflamação/imunologia
Inflamação/microbiologia
Interleucina-6/metabolismo
Pulmão/imunologia
Pulmão/metabolismo
Pulmão/microbiologia
Masculino
Camundongos Endogâmicos C57BL
Infiltração de Neutrófilos
Peptídeo Hidrolases/sangue
Sepse/imunologia
Sepse/microbiologia
Sepse/patologia
Transdução de Sinais
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A5); 0 (Chemokines, CXC); 0 (Interleukin-6); 0 (Phosphatidylserines); 0 (antithrombin III-protease complex); 0 (interleukin-6, mouse); 9000-94-6 (Antithrombin III); EC 3.4.- (Peptide Hydrolases); EC 3.4.21.5 (Thrombin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170415
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25959


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[PMID]:28793293
[Au] Autor:Al Mamun Bhuyan A; Cao H; Lang F
[Ad] Endereço:Department of Internal Medicine III, Tuebingen, Germany.
[Ti] Título:Triggering of Eryptosis, the Suicidal Erythrocyte Death by Mammalian Target of Rapamycin (mTOR) inhibitor Temsirolimus.
[So] Source:Cell Physiol Biochem;42(4):1575-1591, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: The mammalian target of rapamycin (mTOR) inhibitor temsirolimus is utilized for the treatment of malignancy. Temsirolimus is at least in part effective by triggering suicidal tumor cell death. The most common side effect of temsirolimus treatment is anemia. At least in theory, the anemia following temsirolimus treatment could result from stimulation of eryptosis, the suicidal erythrocyte death. Hallmarks of eryptosis include cell shrinkage and cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface. Signaling involved in the orchestration of eryptosis include increase of cytosolic Ca2+ activity ([Ca2+]i), oxidative stress, ceramide, as well as activation of staurosporine and chelerythrine sensitive protein kinase C, SB203580 sensitive p38 kinase, D4476 sensitive casein kinase 1, and zVAD sensitive caspases. The purpose of the present study was to test whether temsirolimus influences eryptosis and, if so, to shed light on the signaling involved. METHODS: Flow cytometry was employed to estimate cell volume from forward scatter, phosphatidylserine exposure at the cell surface from annexin-V-binding, [Ca2+]i from Fluo3-fluorescence, reactive oxygen species (ROS) abundance from DCFDA dependent fluorescence, and ceramide abundance utilizing specific antibodies. Hemolysis was determined from hemoglobin concentration in the supernatant. RESULTS: A 48 hours exposure of human erythrocytes to temsirolimus (5 - 20 µg/ml) significantly decreased forward scatter and significantly increased the percentage of annexin-V-binding cells. Temsirolimus significantly increased Fluo3-fluorescence, DCFDA fluorescence and ceramide abundance at the erythrocyte surface. The effect of temsirolimus on annexin-V-binding was significantly blunted but not abolished by removal of extracellular Ca2+ and by addition of staurosporine (1 µM) or chelerythrine (10 µM) but not significantly modified by addition of SB203580 (2 µM), D4476 (10 µM), or zVAD (10 µM). Chelerythrine (10 µM) further significantly blunted the effect of temsirolimus on DCFDA fluorescence but not ceramide formation. Removal of extracellular Ca2+ had no effect on temsirolimus induced ROS formation or ceramide abundance. CONCLUSIONS: Temsirolimus triggers eryptosis with cell shrinkage and phospholipid scrambling of the erythrocyte cell membrane, an effect at least in part due to Ca2+ entry, oxidative stress, ceramide and activation of staurosporine/Chelerythrine sensitive kinase(s).
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Eriptose/efeitos dos fármacos
Eritrócitos/efeitos dos fármacos
Hemólise/efeitos dos fármacos
Inibidores de Proteínas Quinases/farmacologia
Sirolimo/análogos & derivados
Serina-Treonina Quinases TOR/antagonistas & inibidores
[Mh] Termos MeSH secundário: Compostos de Anilina/química
Anexina A5/metabolismo
Benzamidas/farmacologia
Benzofenantridinas/farmacologia
Cálcio/metabolismo
Caseína Quinase I/antagonistas & inibidores
Caseína Quinase I/genética
Caseína Quinase I/metabolismo
Caspases/genética
Caspases/metabolismo
Ceramidas/metabolismo
Eriptose/genética
Eritrócitos/citologia
Eritrócitos/metabolismo
Fluoresceínas/química
Regulação da Expressão Gênica
Seres Humanos
Imidazóis/farmacologia
Oligopeptídeos/farmacologia
Fosfatidilserinas/metabolismo
Cultura Primária de Células
Piridinas/farmacologia
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais
Sirolimo/farmacologia
Estaurosporina/farmacologia
Serina-Treonina Quinases TOR/genética
Serina-Treonina Quinases TOR/metabolismo
Xantenos/química
Proteínas Quinases p38 Ativadas por Mitógeno/antagonistas & inibidores
Proteínas Quinases p38 Ativadas por Mitógeno/genética
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4-(4-(2,3-dihydrobenzo(1,4)dioxin-6-yl)-5-pyridin-2-yl-1H-imidazol-2-yl)benzamide); 0 (Aniline Compounds); 0 (Annexin A5); 0 (Antineoplastic Agents); 0 (Benzamides); 0 (Benzophenanthridines); 0 (Ceramides); 0 (Fluoresceins); 0 (Imidazoles); 0 (Oligopeptides); 0 (Phosphatidylserines); 0 (Protein Kinase Inhibitors); 0 (Pyridines); 0 (Reactive Oxygen Species); 0 (Xanthenes); 0 (benzyloxycarbonyl-valyl-alanyl-aspartic acid); 2044-85-1 (diacetyldichlorofluorescein); 23D4W0B50Y (Fluo-3); 624KN6GM2T (temsirolimus); E3B045W6X0 (chelerythrine); EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Casein Kinase I); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); EC 3.4.22.- (Caspases); H88EPA0A3N (Staurosporine); OU13V1EYWQ (SB 203580); SY7Q814VUP (Calcium); W36ZG6FT64 (Sirolimus)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE
[do] DOI:10.1159/000479398


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Mariano, Mário
Texto completo
[PMID]:28598340
[Au] Autor:Macarrão CL; Bachi ALL; Mariano M; Abel LJ
[Ad] Endereço:Universidade Paulista, UNIP, Av. Dr. Bacelar, São Paulo 1212, SP, Brazil E-mail: ljabel@uol.com.br.
[Ti] Título:Effects of drinking desalinated seawater on cell viability and proliferation.
[So] Source:J Water Health;15(3):360-366, 2017 Jun.
[Is] ISSN:1477-8920
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Desalination of seawater is becoming an important means to address the increasing scarcity of freshwater resources in the world. Seawater has been used as drinking water in the health, food, and medical fields and various beneficial effects have been suggested, although not confirmed. Given the presence of 63 minerals and trace elements in drinking desalinated seawater (63 DSW), we evaluated their effects on the behavior of tumorigenic and nontumorigenic cells through the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay and annexin-V-fluorescein isothiocyanate/propidium iodide staining. Our results showed that cell viability and proliferation in the presence of 63 DSW were significantly greater than in mineral water and in the presence of fetal bovine serum in a dose-dependent manner. Furthermore, 63 DSW showed no toxic effect on murine embryonic fibroblast (NIH-3T3) and murine melanoma (B16-F10) cells. In another assay, we also showed that pre-treatment of non-adherent THP-1 cells with 63 DSW reduces apoptosis incidence, suggesting a protective effect against cell death. We conclude that cell viability and proliferation were improved by the mineral components of 63 DSW and this effect can guide further studies on health effects associated with DSW consumption.
[Mh] Termos MeSH primário: Água Potável/química
Minerais/farmacologia
Água do Mar/análise
Purificação da Água
[Mh] Termos MeSH secundário: Animais
Anexina A5/química
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Corantes/química
Fluoresceína-5-Isotiocianato/química
Camundongos
Células NIH 3T3
Propídio/química
Água do Mar/química
Coloração e Rotulagem
Sais de Tetrazólio/química
Tiazóis/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A5); 0 (Coloring Agents); 0 (Drinking Water); 0 (Minerals); 0 (Tetrazolium Salts); 0 (Thiazoles); 36015-30-2 (Propidium); EUY85H477I (thiazolyl blue); I223NX31W9 (Fluorescein-5-isothiocyanate)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170610
[St] Status:MEDLINE
[do] DOI:10.2166/wh.2017.252


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[PMID]:28522568
[Au] Autor:Green DE; Murphy TC; Kang BY; Bedi B; Yuan Z; Sadikot RT; Hart CM
[Ad] Endereço:Department of Medicine, Division of Pulmonary, Allergy, and Critical Care Medicine, Atlanta Veterans Affairs Medical Center/Emory University, Atlanta, Georgia degree4@emory.edu.
[Ti] Título:Peroxisome proliferator-activated receptor-γ enhances human pulmonary artery smooth muscle cell apoptosis through microRNA-21 and programmed cell death 4.
[So] Source:Am J Physiol Lung Cell Mol Physiol;313(2):L371-L383, 2017 Aug 01.
[Is] ISSN:1522-1504
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pulmonary hypertension (PH) is a progressive disorder whose cellular pathogenesis involves enhanced smooth muscle cell (SMC) proliferation and resistance to apoptosis signals. Existing evidence demonstrates that the tumor suppressor programmed cell death 4 (PDCD4) affects patterns of cell growth and repair responses in the systemic vasculature following experimental injury. In the current study, the regulation PDCD4 and its functional effects on growth and apoptosis susceptibility in pulmonary artery smooth muscle cells were explored. We previously demonstrated that pharmacological activation of the nuclear transcription factor peroxisome proliferator-activated receptor-γ (PPARγ) attenuated hypoxia-induced proliferation of human pulmonary artery smooth muscle cells (HPASMCs) by inhibiting the expression and mitogenic functions of microRNA-21 (miR-21). In the current study, we hypothesize that PPARγ stimulates PDCD4 expression and HPASMC apoptosis by inhibiting miR-21. Our findings demonstrate that PDCD4 is reduced in the mouse lung upon exposure to chronic hypoxia (10% O for 3 wk) and in hypoxia-exposed HPASMCs (1% O ). HPASMC apoptosis was reduced by hypoxia, by miR-21 overexpression, or by siRNA-mediated PPARγ and PDCD4 depletion. Activation of PPARγ inhibited miR-21 expression and resultant proliferation, while restoring PDCD4 levels and apoptosis to baseline. Additionally, pharmacological activation of PPARγ with rosiglitazone enhanced PDCD4 protein expression and apoptosis in a dose-dependent manner as demonstrated by increased annexin V detection by flow cytometry. Collectively, these findings demonstrate that PPARγ confers growth-inhibitory signals in hypoxia-exposed HPASMCs through suppression of miR-21 and the accompanying derepression of PDCD4 that augments HPASMC susceptibility to undergo apoptosis.
[Mh] Termos MeSH primário: Proteínas Reguladoras de Apoptose/metabolismo
Apoptose/fisiologia
MicroRNAs/metabolismo
Miócitos de Músculo Liso/metabolismo
PPAR gama/metabolismo
Artéria Pulmonar/metabolismo
Proteínas de Ligação a RNA/metabolismo
[Mh] Termos MeSH secundário: Animais
Anexina A5/genética
Anexina A5/metabolismo
Apoptose/genética
Proteínas Reguladoras de Apoptose/genética
Proliferação Celular/efeitos dos fármacos
Proliferação Celular/genética
Células Cultivadas
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/genética
Seres Humanos
Hipertensão Pulmonar/genética
Hipertensão Pulmonar/metabolismo
Pulmão/efeitos dos fármacos
Pulmão/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
MicroRNAs/genética
Miócitos de Músculo Liso/efeitos dos fármacos
PPAR gama/genética
Artéria Pulmonar/efeitos dos fármacos
RNA Interferente Pequeno/genética
Proteínas de Ligação a RNA/genética
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/genética
Tiazolidinedionas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A5); 0 (Apoptosis Regulatory Proteins); 0 (MIRN21 microRNA, human); 0 (MicroRNAs); 0 (PDCD4 protein, human); 0 (PPAR gamma); 0 (RNA, Small Interfering); 0 (RNA-Binding Proteins); 0 (Thiazolidinediones); 05V02F2KDG (rosiglitazone)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170520
[St] Status:MEDLINE
[do] DOI:10.1152/ajplung.00532.2016


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[PMID]:28429360
[Au] Autor:Ding XM; Li JX; Wang K; Wu ZS; Yao AH; Jiao CY; Qian JJ; Bai DS; Li XC
[Ad] Endereço:Liver Transplantation Center, The First Affiliated Hospital of Nanjing Medical University, Key Laboratory of Living Donor Liver Transplantation, Nanjing, Jiangsu Province, China. xcli7900@163.com.
[Ti] Título:Effects of silencing annexin A5 on proliferation and invasion of human cholangiocarcinoma cell line.
[So] Source:Eur Rev Med Pharmacol Sci;21(7):1477-1488, 2017 Apr.
[Is] ISSN:2284-0729
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: We investigated the expression of annexin A5 (ANXA5) in human cholangiocarcinoma (CCA) cell line and its effect on proliferation, migration, and apoptosis of human CCA cells. MATERIALS AND METHODS: Expression of ANXA5 was detected by fluorescent quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and western blotting method in 2 human CCA cell lines, QBC939 and RBE. 3 shRNA plasmids for ANXA5 silencing (ANXA5-sh1, ANXA5-sh2, ANXA5-sh3) and 1 negative control plasmid were constructed to infect QBC939 cells. The infection efficiency, expression of ANXA5, apoptosis and cell cycle of QBC939 cell were measured separately. RESULTS: The expression of ANXA5 in QBC939 cell was significantly higher than RBE cell. Expressed ANXA5 protein in the QBC939-KD cell (QBC939 cell treated by RNAi) was significantly lower than QBC939-BC (QBC939 cell) and QBC939-NC cells (QBC939 cell treated by scramble plasmid). The ratio of G0/1 phase cells and apoptosis rate increased in QBC939-KD cell. The proliferation activity and invasion ability decreased in QBC939-KD cell compared with QBC939-NC and QBC939-BC cells. CONCLUSIONS: ANXA5 play important role in the migration and apoptosis of CCA cells. Inhibiting the expression of ANXA5 significantly reduce the proliferation, migration and invasion ability of QBC939 cells, and increase the apoptosis of QBC939 cells.
[Mh] Termos MeSH primário: Anexina A5/genética
Neoplasias dos Ductos Biliares
Colangiocarcinoma
[Mh] Termos MeSH secundário: Apoptose/genética
Neoplasias dos Ductos Biliares/genética
Neoplasias dos Ductos Biliares/patologia
Linhagem Celular Tumoral
Movimento Celular/genética
Proliferação Celular/genética
Colangiocarcinoma/genética
Colangiocarcinoma/patologia
Inativação Gênica
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A5)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170422
[St] Status:MEDLINE



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