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[PMID]:26978230
[Au] Autor:Saryeva OP; Salakhova LM; Kulida LV; Malyshkina AI
[Ad] Endereço:Laboratory of Pathomorphology and Electron Microscopy, V.N. Gorodkov Ivanovo Research Institute of Maternity and Childhood, Ministry of Health of Russia, Ivanovo, Russia.
[Ti] Título:[Immunomorphological aspects of miscarriage at late gestational ages].
[So] Source:Arkh Patol;78(1):8-12, 2016 Jan-Feb.
[Is] ISSN:0004-1955
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:AIM: to reveal the morphological features of placentas and to define a role of the lectin pathway for activation of the complement system in the development of premature birth. MATERIAL AND METHODS: A complex morphological study was conducted to examine 37 placentas, 25 of which were obtained from women with clinical signs of threatened miscarriage and 12 placentas from apparently healthy pregnant women. RESULTS: Placental tissue CD59 expression was ascertained to be significantly less in the women with threatened miscarriage than in those having full-term babies. CONCLUSION: Decreased CD59 expression in threatened miscarriage at late gestational ages leads to additional activation of a maternal immune response and serves as a possible predictor for premature birth.
[Mh] Termos MeSH primário: Aborto Espontâneo/genética
Antígenos CD59/biossíntese
Nascimento Prematuro/genética
[Mh] Termos MeSH secundário: Aborto Espontâneo/patologia
Adulto
Antígenos CD59/genética
Feminino
Regulação da Expressão Gênica no Desenvolvimento
Idade Gestacional
Humanos
Placenta/metabolismo
Placenta/patologia
Gravidez
Nascimento Prematuro/patologia
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD59); 101754-01-2 (CD59 protein, human)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:160316
[Lr] Data última revisão:
160316
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160316
[St] Status:MEDLINE


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[PMID]:26928779
[Au] Autor:Yamanaka K; Kakuta Y; Miyagawa S; Nakazawa S; Kato T; Abe T; Imamura R; Okumi M; Maeda A; Okuyama H; Mizuno M; Nonomura N
[Ad] Endereço:Department of Urology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
[Ti] Título:Depression of Complement Regulatory Factors in Rat and Human Renal Grafts Is Associated with the Progress of Acute T-Cell Mediated Rejection.
[So] Source:PLoS One;11(2):e0148881, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The association of complement with the progression of acute T cell mediated rejection (ATCMR) is not well understood. We investigated the production of complement components and the expression of complement regulatory proteins (Cregs) in acute T-cell mediated rejection using rat and human renal allografts. METHODS: We prepared rat allograft and syngeneic graft models of renal transplantation. The expression of Complement components and Cregs was assessed in the rat grafts using quantitative real-time PCR (qRT-PCR) and immunofluorescent staining. We also administered anti-Crry and anti-CD59 antibodies to the rat allograft model. Further, we assessed the relationship between the expression of membrane cofactor protein (MCP) by immunohistochemical staining in human renal grafts and their clinical course. RESULTS: qRT-PCR results showed that the expression of Cregs, CD59 and rodent-specific complement regulator complement receptor 1-related gene/protein-y (Crry), was diminished in the rat allograft model especially on day 5 after transplantation in comparison with the syngeneic model. In contrast, the expression of complement components and receptors: C3, C3a receptor, C5a receptor, Factor B, C9, C1q, was increased, but not the expression of C4 and C5, indicating a possible activation of the alternative pathway. When anti-Crry and anti-CD59 mAbs were administered to the allograft, the survival period for each group was shortened. In the human ATCMR cases, the group with higher MCP expression in the grafts showed improved serum creatinine levels after the ATCMR treatment as well as a better 5-year graft survival rate. CONCLUSIONS: We conclude that the expression of Cregs in allografts is connected with ATCMR. Our results suggest that controlling complement activation in renal grafts can be a new strategy for the treatment of ATCMR.
[Mh] Termos MeSH primário: Antígenos CD59/metabolismo
Antígenos de Superfície/metabolismo
Rejeição de Enxerto/imunologia
Rejeição de Enxerto/metabolismo
Transplante de Rim
Receptores de Superfície Celular/metabolismo
Linfócitos T/imunologia
Linfócitos T/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Aloenxertos
Animais
Anticorpos Monoclonais/farmacologia
Via Alternativa do Complemento/genética
Via Alternativa do Complemento/imunologia
Proteínas do Sistema Complemento/genética
Proteínas do Sistema Complemento/imunologia
Proteínas do Sistema Complemento/metabolismo
Modelos Animais de Doenças
Feminino
Regulação da Expressão Gênica
Rejeição de Enxerto/genética
Sobrevivência de Enxerto/efeitos de drogas
Sobrevivência de Enxerto/genética
Sobrevivência de Enxerto/imunologia
Humanos
Masculino
Meia-Idade
Ratos
Receptores de Superfície Celular/antagonistas & inibidores
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antigens, CD59); 0 (Antigens, Surface); 0 (Crry protein, rat); 0 (Receptors, Cell Surface); 9007-36-7 (Complement System Proteins)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:160308
[Lr] Data última revisão:
160308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160301
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0148881


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[PMID]:26891237
[Au] Autor:Wang W; Wang X; Yang L; Fu W; Pan D; Liu J; Ye J; Zhao Q; Zhu H; Cheng T; Xia N
[Ad] Endereço:State Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, National Institute of Diagnostics and Vaccine Development in Infectious Diseases, School of Life Science, Xiamen University, Xiamen 361102, PR China.
[Ti] Título:Modulation of host CD59 expression by varicella-zoster virus in human xenografts in vivo.
[So] Source:Virology;491:96-105, 2016 Apr.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Varicella-zoster virus (VZV) is the causative agent of both chickenpox (varicella) and shingles (zoster). VZV survives host defenses, even with an intact immune system, and disseminates in the host before causing disease. To date, several diverse immunomodulatory strategies used by VZV to undermine host immunity have been identified; however, few studies have addressed the complement evasion strategies used by this virus. Here, we show that expression of CD59, which is a key member of host regulators of complement activation (RCA), is significantly upregulated in response to VZV infection in human T cells and dorsal root ganglia (DRG) but not in human skin xenografts in SCID-hu mice in vivo. This is the first report demonstrating that VZV infection upregulates host CD59 expression in a tissue-specific manner in vivo, which may aid VZV in complement evasion and pathogenesis.
[Mh] Termos MeSH primário: Antígenos CD59/genética
Varicela/genética
Herpesvirus Humano 3/fisiologia
[Mh] Termos MeSH secundário: Animais
Antígenos CD59/metabolismo
Varicela/metabolismo
Varicela/patologia
Varicela/virologia
Modelos Animais de Doenças
Gânglios Espinais/metabolismo
Gânglios Espinais/patologia
Gânglios Espinais/virologia
Herpesvirus Humano 3/genética
Interações Hospedeiro-Patógeno
Humanos
Fígado/metabolismo
Fígado/patologia
Fígado/virologia
Masculino
Camundongos
Camundongos SCID
Timo/metabolismo
Timo/patologia
Timo/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD59)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:160309
[Lr] Data última revisão:
160309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160309
[St] Status:MEDLINE


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[PMID]:26842754
[Au] Autor:Carver KA; Yang D
[Ti] Título:N-Acetylcysteine Amide Protects Against Oxidative Stress-Induced Microparticle Release From Human Retinal Pigment Epithelial Cells.
[So] Source:Invest Ophthalmol Vis Sci;57(2):360-71, 2016 Feb.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Oxidative stress is a major factor involved in retinal pigment epithelium (RPE) apoptosis that underlies AMD. Drusen, extracellular lipid- and protein-containing deposits, are strongly associated with the development of AMD. Cell-derived microparticles (MPs) are small membrane-bound vesicles shed from cells. The purpose of this study was to determine if oxidative stress drives MP release from RPE cells, to assess whether these MPs carry membrane complement regulatory proteins (mCRPs: CD46, CD55, and CD59), and to evaluate the effects of a thiol antioxidant on oxidative stress-induced MP release. METHODS: Retinal pigment epithelium cells isolated from human donor eyes were cultured and treated with hydrogen peroxide (H2O2) to induce oxidative stress. Isolated MPs were fixed for transmission electron microscopy or processed for component analysis by flow cytometry, Western blot analysis, and confocal microscopy. RESULTS: Transmission electron microscopy showed that MPs ranged in diameter from 100 to 1000 nm. H2O2 treatment led to time- and dose-dependent elevations in MPs with externalized phosphatidylserine and phosphatidylethanolamine, known markers of MPs. These increases were strongly correlated to RPE apoptosis. Oxidative stress significantly increased the release of mCRP-positive MPs, which were prevented by a thiol antioxidant, N-acetylcysteine amide (NACA). CONCLUSIONS: This is the first evidence that oxidative stress induces cultured human RPE cells to release MPs that carry mCRPs on their surface. The levels of released MPs are strongly correlated with RPE apoptosis. N-acetylcysteine amide prevents oxidative stress-induced effects. Our findings indicate that oxidative stress reduces mCRPs on the RPE surface through releasing MPs.
[Mh] Termos MeSH primário: Acetilcisteína/análogos & derivados
Micropartículas Derivadas de Células/metabolismo
Estresse Oxidativo/efeitos de drogas
Epitélio Pigmentado da Retina/efeitos de drogas
[Mh] Termos MeSH secundário: Acetilcisteína/farmacologia
Antígenos CD46/metabolismo
Antígenos CD55/metabolismo
Antígenos CD59/metabolismo
Western Blotting
Micropartículas Derivadas de Células/ultraestrutura
Células Cultivadas
Citometria de Fluxo
Humanos
Peróxido de Hidrogênio/farmacologia
Masculino
Microscopia Confocal
Microscopia Eletrônica de Transmissão
Meia-Idade
Oxidantes/farmacologia
Epitélio Pigmentado da Retina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD46); 0 (Antigens, CD55); 0 (Antigens, CD59); 0 (CD46 protein, human); 0 (Oxidants); 101754-01-2 (CD59 protein, human); 4N69717RKW (N-Acetylcysteinamide); BBX060AN9V (Hydrogen Peroxide); WYQ7N0BPYC (Acetylcysteine)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160204
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.15-17117


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[PMID]:26828585
[Au] Autor:Martindale RG; Warren MM; McClave SA
[Ad] Endereço:aDepartment of Surgery, Oregon Health and Science University, Portland, Oregon bDepartment of Medicine, University of Louisville, Louisville, Kentucky, USA.
[Ti] Título:Does the use of specialized proresolving molecules in critical care offer a more focused approach to controlling inflammation than that of fish oils?
[So] Source:Curr Opin Clin Nutr Metab Care;19(2):151-4, 2016 Mar.
[Is] ISSN:1473-6519
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:PURPOSE OF REVIEW: The literature regarding the use of fish oils in the critically ill to limit the inflammatory and catabolic response have been inconsistent. The objective of this manuscript is to review a newly discovered class of specialized proresolving molecules (SPMs), which could help elucidate the discrepancies reported in the critical care literature regarding the anti-inflammatory benefits of fish oil/ω-3 fatty acids. RECENT FINDINGS: Although use of fish oil has traditionally been thought to reduce or limit the inflammatory process in the critical ill, a new class of endogenously produced highly active lipid mediators derived from arachidonic acid and ω-3 fatty acids (lipoxins, resolvins, protectins, and maresins) have been shown to actively enhance resolution of inflammation. These SPMs stimulate the cardinal signs of resolution of inflammation, which include the cessation of leukocytic infiltration, a countering of the effects of proinflammatory mediators, stimulation of the uptake of apoptotic neutrophils, promotion of the clearance of necrotic cellular debris, and enhancement of the host's ability to eliminate microbial invasion. SUMMARY: By actively turning off inflammation (instead of simply attenuating its natural course), SPMs have shown more consistent effects in decreasing pain and risk of sepsis, increasing epithelialization and wound healing, promoting tissue regeneration, potentiating the effects of antibiotics, and enhancing adaptive immunity.
[Mh] Termos MeSH primário: Óleos de Peixe/uso terapêutico
Inflamação/quimioterapia
Unidades de Terapia Intensiva
[Mh] Termos MeSH secundário: Imunidade Adaptativa/efeitos de drogas
Anti-Inflamatórios/uso terapêutico
Antígenos CD59/uso terapêutico
Ácido Araquidônico/uso terapêutico
Estado Terminal
Ácidos Docosa-Hexaenoicos/uso terapêutico
Humanos
Lipoxinas/farmacologia
Dor/quimioterapia
Regeneração/efeitos de drogas
Cicatrização/efeitos de drogas
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antigens, CD59); 0 (Fish Oils); 0 (Lipoxins); 25167-62-8 (Docosahexaenoic Acids); 27YG812J1I (Arachidonic Acid)
[Em] Mês de entrada:1611
[Cu] Atualização por classe:161103
[Lr] Data última revisão:
161103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160205
[St] Status:MEDLINE
[do] DOI:10.1097/MCO.0000000000000250


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[PMID]:26772976
[Au] Autor:Gonzalez-Calero L; Martin-Lorenzo M; de la Cuesta F; Maroto AS; Baldan-Martin M; Ruiz-Hurtado G; Pulido-Olmo H; Segura J; Barderas MG; Ruilope LM; Vivanco F; Alvarez-Llamas G
[Ad] Endereço:Departamento de Inmunologia, Laboratorio de Inmunoalergia y Proteomica, IIS-Fundacion Jimenez Diaz, UAM, REDinREN, Avda Reyes Catolicos 2, 28040, Madrid, Spain. laura.gcalero@fjd.es.
[Ti] Título:Urinary alpha-1 antitrypsin and CD59 glycoprotein predict albuminuria development in hypertensive patients under chronic renin-angiotensin system suppression.
[So] Source:Cardiovasc Diabetol;15:8, 2016 Jan 16.
[Is] ISSN:1475-2840
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Hypertension is a multi-factorial disease of increasing prevalence and a major risk factor for cardiovascular mortality even in the presence of adequate treatment. Progression of cardiovascular disease (CVD) occurs frequently during chronic renin-angiotensin-system (RAS) suppression, and albuminuria is a marker of CV risk. High prevalence of albuminuria in treated hypertensive patients has been demonstrated, but there are no available markers able to predict evolution. The aim of this study was the identification of novel indicators of albuminuria progression measurable in urine of diabetic and non-diabetic patients. METHODS: 1143 hypertensive patients under chronic treatment were followed for a minimum period of 3 years. Among them, 105 diabetic and non-diabetic patients were selected and classified in three groups according to albuminuria development during follow-up: (a) patients with persistent normoalbuminuria; (b) patients developing de novo albuminuria; (c) patients with maintained albuminuria. Differential urine analysis was performed by 2D gel electrophoresis (2D-DIGE) and further confirmed by liquid chromatography-mass spectrometry. Non-parametric statistical tests were applied. RESULTS: CD59 glycoprotein and alpha-1 antitrypsin (AAT) resulted already altered in patients developing albuminuria de novo, with a similar response in those with maintained albuminuria. A prospective study in a sub-group of normoalbuminuric patients who were clinically followed up for at least 1 year from urine sampling, revealed CD59 and AAT proteins significantly varied in the urine collected from normoalbuminurics who will negatively progress, serving as predictors of future albuminuria development. CONCLUSIONS: CD59 and AAT proteins are significantly altered in hypertensive patients developing albuminuria. Interestingly, CD59 and AAT are able to predict, in normoalbuminuric individuals, who will develop albuminuria in the future, being potential predictors of vascular damage and CV risk. These findings contribute to early identify patients at risk of developing albuminuria even when this classical predictor is still in the normal range, constituting a novel strategy towards a prompt and more efficient therapeutic intervention with better outcome.
[Mh] Termos MeSH primário: Albuminúria/etiologia
Antígenos CD59/urina
Anti-Hipertensivos/uso terapêutico
Nefropatias Diabéticas/etiologia
Hipertensão/quimioterapia
Sistema Renina-Angiotensina/efeitos de drogas
alfa 1-Antitripsina/urina
[Mh] Termos MeSH secundário: Idoso
Albuminúria/diagnóstico
Albuminúria/fisiopatologia
Albuminúria/urina
Biomarcadores/urina
Estudos de Casos e Controles
Cromatografia Líquida
Nefropatias Diabéticas/diagnóstico
Nefropatias Diabéticas/fisiopatologia
Nefropatias Diabéticas/urina
Eletroforese em Gel Bidimensional
Feminino
Humanos
Hipertensão/complicações
Hipertensão/diagnóstico
Hipertensão/fisiopatologia
Hipertensão/urina
Masculino
Meia-Idade
Valor Preditivo dos Testes
Estudos Prospectivos
Proteômica/métodos
Medição de Risco
Fatores de Risco
Espectrometria de Massas em Tandem
Fatores de Tempo
Urinálise
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD59); 0 (Antihypertensive Agents); 0 (Biomarkers); 0 (SERPINA1 protein, human); 0 (alpha 1-Antitrypsin); 101754-01-2 (CD59 protein, human)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161110
[Lr] Data última revisão:
161110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160116
[St] Status:MEDLINE
[do] DOI:10.1186/s12933-016-0331-7


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[PMID]:26738794
[Au] Autor:Emin M; Wang G; Castagna F; Rodriguez-Lopez J; Wahab R; Wang J; Adams T; Wei Y; Jelic S
[Ad] Endereço:Division of Pulmonary, Allergy, and Critical Care Medicine, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.
[Ti] Título:Increased internalization of complement inhibitor CD59 may contribute to endothelial inflammation in obstructive sleep apnea.
[So] Source:Sci Transl Med;8(320):320ra1, 2016 Jan 06.
[Is] ISSN:1946-6242
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Obstructive sleep apnea (OSA), characterized by intermittent hypoxia (IH) during transient cessation of breathing, triples the risk for cardiovascular diseases. We used a phage display peptide library as an unbiased approach to investigate whether IH, which is specific to OSA, activates endothelial cells (ECs) in a distinctive manner. The target of a differentially bound peptide on ECs collected from OSA patients was identified as CD59, a major complement inhibitor that protects ECs from the membrane attack complex (MAC). A decreased proportion of CD59 is located on the EC surface in OSA patients compared with controls, suggesting reduced protection against complement attack. In vitro, IH promoted endothelial inflammation predominantly via augmented internalization of CD59 and consequent MAC deposition. Increased internalization of endothelial CD59 in IH appeared to be cholesterol-dependent and was reversed by statins in a CD59-dependent manner. These studies suggest that reduced complement inhibition may mediate endothelial inflammation and increase vascular risk in OSA patients.
[Mh] Termos MeSH primário: Antígenos CD59/metabolismo
Endocitose
Endotélio Vascular/patologia
Inflamação/patologia
Apneia do Sono Tipo Obstrutiva/patologia
[Mh] Termos MeSH secundário: Transporte Biológico/efeitos de drogas
Estudos de Casos e Controles
Técnicas de Visualização da Superfície Celular
Colesterol/metabolismo
Complexo de Ataque à Membrana do Sistema Complemento/metabolismo
Endocitose/efeitos de drogas
Endotélio Vascular/efeitos de drogas
Células Endoteliais da Veia Umbilical Humana/metabolismo
Humanos
Inibidores de Hidroximetilglutaril-CoA Redutases/farmacologia
Hipóxia/complicações
Hipóxia/patologia
Proteínas de Membrana/metabolismo
Apneia do Sono Tipo Obstrutiva/complicações
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antigens, CD59); 0 (Complement Membrane Attack Complex); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Membrane Proteins); 97C5T2UQ7J (Cholesterol)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160107
[St] Status:MEDLINE
[do] DOI:10.1126/scitranslmed.aad0634


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[PMID]:26721735
[Au] Autor:Bloom AC; Collins FL; Van't Hof RJ; Ryan ES; Jones E; Hughes TR; Morgan BP; Erlandsson M; Bokarewa M; Aeschlimann D; Evans BA; Williams AS
[Ad] Endereço:Institute of Infection and Immunity, School of Medicine, Cardiff University, Cardiff, UK.
[Ti] Título:Deletion of the membrane complement inhibitor CD59a drives age and gender-dependent alterations to bone phenotype in mice.
[So] Source:Bone;84:253-61, 2016 Mar.
[Is] ISSN:1873-2763
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Degenerative joint diseases such as osteoarthritis are characterised by aberrant region-specific bone formation and abnormal bone mineral content. A recent study suggested a role for the complement membrane attack complex in experimental models of osteoarthritis. Since CD59a is the principal regulator of the membrane attack complex in mice, we evaluated the impact of CD59a gene deletion upon maintenance of bone architecture. In vivo bone morphology analysis revealed that male CD59a-deficient mice have increased femur length and cortical bone volume, albeit with reduced bone mineral density. However, this phenomenon was not observed in female mice. Histomorphometric analysis of the trabecular bone showed increased rates of bone homeostasis, with both increased bone resorption and mineral apposition rate in CD59a-deficient male mice. When bone cells were studied in isolation, in vitro osteoclastogenesis was significantly increased in male CD59a-deficient mice, although osteoblast formation was not altered. Our data reveal, for the first time, that CD59a is a regulator of bone growth and homeostasis. CD59a ablation in male mice results in longer and wider bones, but with less density, which is likely a major contributing factor for their susceptibility to osteoarthritis. These findings increase our understanding of the role of complement regulation in degenerative arthritis.
[Mh] Termos MeSH primário: Envelhecimento/patologia
Antígenos CD59/metabolismo
Osso e Ossos/patologia
Proteínas do Sistema Complemento/metabolismo
Deleção de Genes
Caracteres Sexuais
[Mh] Termos MeSH secundário: Animais
Desenvolvimento Ósseo
Células da Medula Óssea/patologia
Remodelação Óssea
Feminino
Masculino
Camundongos Endogâmicos C57BL
Tamanho do Órgão
Osteoblastos/metabolismo
Osteoblastos/patologia
Osteoclastos/metabolismo
Osteoclastos/patologia
Fenótipo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD59); 0 (CD59a protein, mouse); 9007-36-7 (Complement System Proteins)
[Em] Mês de entrada:1611
[Cu] Atualização por classe:161111
[Lr] Data última revisão:
161111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160215
[St] Status:MEDLINE


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[PMID]:26686775
[Au] Autor:Uzawa A; Mori M; Uchida T; Masuda H; Ohtani R; Kuwabara S
[Ad] Endereço:Department of Neurology, Graduate School of Medicine, Chiba University, Japan. Electronic address: auzawa@chiba-u.jp.
[Ti] Título:Increased levels of CSF CD59 in neuromyelitis optica and multiple sclerosis.
[So] Source:Clin Chim Acta;453:131-3, 2016 Jan 30.
[Is] ISSN:1873-3492
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Complement activation is important in multiple sclerosis (MS) and is essential for anti-aquaporin 4 antibodies to damage the central nervous system in neuromyelitis optica (NMO). Little is known about the role of cerebrospinal fluid (CSF) regulators of complement activation in NMO and MS. We determined whether CSF CD59, which is a complement regulator and C5b-9 formation inhibitor, is involved in the pathogenesis of NMO and MS. METHODS: We analyzed CSF levels of CD59 in 30 patients with NMO, 22 patients with MS, and 24 patients with non-inflammatory neurological disorders (NINDs). Possible correlations between CSF CD59 levels and the clinical and laboratory variables in patients with NMO and MS were also reviewed. RESULTS: CSF CD59 levels in patients with NMO and MS were higher than those in patients with NINDs (p<0.001), and those in patients with NMO decreased after treatment. No significant correlations were found between CSF CD59 levels and clinical and laboratory parameters in NMO and MS. CONCLUSION: High CSF CD59 levels in NMO and MS may reflect inflammation, damage, and/or complement activation in the central nervous system.
[Mh] Termos MeSH primário: Antígenos CD59/líquido cefalorraquidiano
Esclerose Múltipla/líquido cefalorraquidiano
Neuromielite Óptica/líquido cefalorraquidiano
[Mh] Termos MeSH secundário: Adulto
Feminino
Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD59)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160118
[St] Status:MEDLINE


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[PMID]:26552688
[Au] Autor:Suzuki KG
[Ad] Endereço:Institute for Integrated Cell-Material Sciences (WPI-iCeMS), Institute for Frontier Medical Sciences, Kyoto University, Kyoto, 606-8507, Japan. ksuzuki@frontier.kyoto-u.ac.jp.
[Ti] Título:Single-Molecule Imaging of Signal Transduction via GPI-Anchored Receptors.
[So] Source:Methods Mol Biol;1376:229-38, 2016.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lipid rafts have been drawing extensive attention as a signaling platform. To investigate molecular interactions in lipid rafts, we often need to observe molecules in the plasma membranes of living cells because chemical fixation and subsequent immunostaining with divalent or multivalent antibodies may change the location of the target molecules. In this chapter, we describe how to examine dynamics of raft-associated glycosylphosphatidylinositol (GPI)-anchored receptors and interactions of the receptors with downstream signaling molecules by single-particle tracking or single-molecule imaging techniques.
[Mh] Termos MeSH primário: Proteínas Ligadas por GPI/metabolismo
Imagem Molecular/métodos
Receptores de Superfície Celular/metabolismo
Transdução de Sinal
[Mh] Termos MeSH secundário: Anticorpos Monoclonais/química
Anticorpos Monoclonais/farmacologia
Antígenos CD59/metabolismo
Cálcio/metabolismo
Corantes Fluorescentes
Proteínas Ligadas por GPI/antagonistas & inibidores
Proteínas Ligadas por GPI/química
Inositol 1,4,5-Trisfosfato/metabolismo
Nanopartículas Metálicas
Ligação Proteica
Receptores de Superfície Celular/antagonistas & inibidores
Receptores de Superfície Celular/química
Coloração e Rotulagem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antigens, CD59); 0 (Fluorescent Dyes); 0 (GPI-Linked Proteins); 0 (Receptors, Cell Surface); 85166-31-0 (Inositol 1,4,5-Trisphosphate); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:151110
[Lr] Data última revisão:
151110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151110
[St] Status:MEDLINE
[do] DOI:10.1007/978-1-4939-3170-5_19



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