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[PMID]:28864895
[Au] Autor:Vasilenko MA; Kirienkova EV; Skuratovskaia DA; Zatolokin PA; Mironyuk NI; Litvinova LS
[Ad] Endereço:Immanuel Kant Baltic Federal University, Kaliningrad, 236041, Russia.
[Ti] Título:The role of production of adipsin and leptin in the development of insulin resistance in patients with abdominal obesity.
[So] Source:Dokl Biochem Biophys;475(1):271-276, 2017 Jul.
[Is] ISSN:1608-3091
[Cp] País de publicação:Russia (Federation)
[La] Idioma:eng
[Ab] Resumo:We investigated the tissue-specific features of the production of adipokines (leptin and adipsin) by adipose tissue in obese patients depending on the degree of obesity and the state of carbohydrate metabolism. An increase in the content of adipsin and leptin in the blood plasma was found. In patients with varying degrees of obesity with and without type 2 diabetes mellitus (DM 2), we determined the level of tissue-specific expression of LEP and CFD genes encoding leptin and adipsin, respectively. The contribution of different adipose tissue depots to the blood plasma level of adipsin and leptin in obese patients with and without DM 2 was established. The disturbance of reciprocal relationships between adipsin and leptin in obesity is associated with the development of insulin resistance.
[Mh] Termos MeSH primário: Fator D do Complemento/biossíntese
Resistência à Insulina
Leptina/biossíntese
Obesidade Abdominal/metabolismo
[Mh] Termos MeSH secundário: Adulto
Feminino
Seres Humanos
Gordura Intra-Abdominal/metabolismo
Masculino
Obesidade Abdominal/patologia
Gordura Subcutânea/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Leptin); EC 3.4.21.46 (Complement Factor D)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170903
[St] Status:MEDLINE
[do] DOI:10.1134/S160767291704010X


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[PMID]:28651038
[Au] Autor:Korman BD; Marangoni RG; Hinchcliff M; Shah SJ; Carns M; Hoffmann A; Ramsey-Goldman R; Varga J
[Ad] Endereço:Northwestern University, Chicago, Illinois.
[Ti] Título:Brief Report: Association of Elevated Adipsin Levels With Pulmonary Arterial Hypertension in Systemic Sclerosis.
[So] Source:Arthritis Rheumatol;69(10):2062-2068, 2017 Oct.
[Is] ISSN:2326-5205
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Adipose tissues secrete adipokines, peptides with potent effects modulating fibrosis, inflammation, and vascular homeostasis. Dysregulated adipose tissue biology and adipokine balance have recently been implicated in systemic sclerosis (SSc). This study was undertaken to determine whether altered circulating adipokine levels correlate with SSc disease subsets or clinical manifestations. METHODS: Multiplex assays were used to measure circulating adipokine levels in 198 patients with SSc and 33 healthy controls. Data were evaluated for correlations between serum adipokine levels and demographic and clinical features, including pulmonary arterial hypertension (PAH). To assess the relevance of adipsin, an adipokine involved in complement pathway activation, in SSc, we analyzed publicly available genetic and transcriptomic data. RESULTS: Levels of adiponectin and adipsin differed significantly between controls and patients. Adipsin was significantly elevated in patients with limited cutaneous SSc (odds ratio [OR] 28.3 [95% confidence interval (95% CI) 7.0-113.8]; P < 0.0001), and its levels were associated with serum autoantibody status, pulmonary function and cardiovascular parameters, and PAH (OR 3.3 [95% CI 1.3-8.7]; P = 0.02). Elevated adipsin was more strongly associated with PAH than B-type natriuretic peptide was. Moreover, in SSc patients, adipsin gene single-nucleotide polymorphisms were associated with PAH. Transcriptome data set analysis demonstrated elevated adipsin expression in patients with SSc-related PAH. CONCLUSION: We identify adipsin as a novel adipose tissue-derived marker of SSc-related PAH. Circulating adipsin levels might serve as predictive biomarkers in SSc. Mechanistically, adipsin might represent a pathogenic link between adipocyte dysfunction and complement pathway activation and play an important role in the pathogenesis of SSc-related PAH.
[Mh] Termos MeSH primário: Hipertensão Pulmonar/genética
Esclerodermia Difusa/genética
Esclerodermia Limitada/genética
[Mh] Termos MeSH secundário: Adiponectina/metabolismo
Adulto
Idoso
Autoanticorpos/imunologia
Fator D do Complemento/genética
Fator D do Complemento/metabolismo
Citocinas/metabolismo
Feminino
Perfilação da Expressão Gênica
Seres Humanos
Hipertensão Pulmonar/etiologia
Hipertensão Pulmonar/metabolismo
Leptina/metabolismo
Masculino
Meia-Idade
Peptídeo Natriurético Encefálico/metabolismo
Nicotinamida Fosforribosiltransferase/metabolismo
Razão de Chances
Polimorfismo de Nucleotídeo Único
Resistina/metabolismo
Esclerodermia Difusa/complicações
Esclerodermia Difusa/imunologia
Esclerodermia Difusa/metabolismo
Esclerodermia Limitada/complicações
Esclerodermia Limitada/imunologia
Esclerodermia Limitada/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ADIPOQ protein, human); 0 (Adiponectin); 0 (Autoantibodies); 0 (Cytokines); 0 (Leptin); 0 (RETN protein, human); 0 (Resistin); 114471-18-0 (Natriuretic Peptide, Brain); EC 2.4.2.12 (Nicotinamide Phosphoribosyltransferase); EC 2.4.2.12 (nicotinamide phosphoribosyltransferase, human); EC 3.4.21.46 (Complement Factor D); EC 3.4.21.46 (complement factor D, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170627
[St] Status:MEDLINE
[do] DOI:10.1002/art.40193


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[PMID]:28621538
[Au] Autor:Lorthiois E; Anderson K; Vulpetti A; Rogel O; Cumin F; Ostermann N; Steinbacher S; Mac Sweeney A; Delgado O; Liao SM; Randl S; Rüdisser S; Dussauge S; Fettis K; Kieffer L; de Erkenez A; Yang L; Hartwieg C; Argikar UA; La Bonte LR; Newton R; Kansara V; Flohr S; Hommel U; Jaffee B; Maibaum J
[Ad] Endereço:Novartis Pharma AG, Novartis Institutes for BioMedical Research , Novartis Campus, CH-4056 Basel, Switzerland.
[Ti] Título:Discovery of Highly Potent and Selective Small-Molecule Reversible Factor D Inhibitors Demonstrating Alternative Complement Pathway Inhibition in Vivo.
[So] Source:J Med Chem;60(13):5717-5735, 2017 Jul 13.
[Is] ISSN:1520-4804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The highly specific S1 serine protease factor D (FD) plays a central role in the amplification of the complement alternative pathway (AP) of the innate immune system. Genetic associations in humans have implicated AP activation in age-related macular degeneration (AMD), and AP dysfunction predisposes individuals to disorders such as paroxysmal nocturnal hemoglobinuria (PNH) and atypical hemolytic uremic syndrome (aHUS). The combination of structure-based hit identification and subsequent optimization of the center (S)-proline-based lead 7 has led to the discovery of noncovalent reversible and selective human factor D (FD) inhibitors with drug-like properties. The orally bioavailable compound 2 exerted excellent potency in 50% human whole blood in vitro and blocked AP activity ex vivo after oral administration to monkeys as demonstrated by inhibition of membrane attack complex (MAC) formation. Inhibitor 2 demonstrated sustained oral and ocular efficacy in a model of lipopolysaccharide (LPS)-induced systemic AP activation in mice expressing human FD.
[Mh] Termos MeSH primário: Fator D do Complemento/antagonistas & inibidores
Via Alternativa do Complemento/efeitos dos fármacos
Prolina/análogos & derivados
Prolina/farmacologia
[Mh] Termos MeSH secundário: Administração Oral
Animais
Síndrome Hemolítico-Urêmica Atípica/tratamento farmacológico
Síndrome Hemolítico-Urêmica Atípica/imunologia
Fator D do Complemento/imunologia
Complexo de Ataque à Membrana do Sistema Complemento/antagonistas & inibidores
Complexo de Ataque à Membrana do Sistema Complemento/imunologia
Feminino
Haplorrinos
Seres Humanos
Macaca fascicularis
Degeneração Macular/tratamento farmacológico
Degeneração Macular/imunologia
Masculino
Camundongos
Prolina/administração & dosagem
Prolina/farmacocinética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Complement Membrane Attack Complex); 9DLQ4CIU6V (Proline); EC 3.4.21.46 (Complement Factor D)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170617
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jmedchem.7b00425


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[PMID]:28219679
[Au] Autor:Wuertz BR; Darrah L; Wudel J; Ondrey FG
[Ad] Endereço:Molecular Oncology Program, Department of Otolaryngology, University of Minnesota, Minneapolis, MN 55455, USA. Electronic address: knier003@umn.edu.
[Ti] Título:Thiazolidinediones abrogate cervical cancer growth.
[So] Source:Exp Cell Res;353(2):63-71, 2017 Apr 15.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Peroxisome proliferator-activated receptor gamma (PPAR γ) is activated by thiazolidinedione drugs (TZDs) and can promote anti-cancer properties. We used three TZDs (pioglitazone, rosiglitazone, and ciglitazone) to target cervical cancer cell lines and a nude mouse animal model. Each agent increased activation of PPAR γ, as judged by a luciferase reporter gene assay in three HPV-associated cell lines (CaSki, SiHa, and HeLa cells) while decreasing cellular proliferation in a dose-dependent manner. They also promoted Oil Red O accumulation in treated cell lines and upregulated the lipid differentiation marker adipsin. Interestingly, xenograft HeLa tumors in nude mice treated with 100mg/kg/day pioglitazone exhibited decreased growth compared to control mice or mice treated with standard cervical chemotherapy. In conclusion, TZDs slow tumor cell growth in vitro and in vivo with decreases in cell proliferation and increases in PPAR γ and adipsin. These agents may be interesting treatments or treatment adjuncts for HPV-associated cancers or perhaps even precancerous conditions.
[Mh] Termos MeSH primário: Proliferação Celular/efeitos dos fármacos
PPAR gama/biossíntese
Tiazolidinedionas/administração & dosagem
Neoplasias do Colo do Útero/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/efeitos dos fármacos
Fator D do Complemento/biossíntese
Fator D do Complemento/genética
Modelos Animais de Doenças
Feminino
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Células HeLa
Seres Humanos
Camundongos
PPAR gama/genética
Papillomaviridae/efeitos dos fármacos
Papillomaviridae/patogenicidade
Neoplasias do Colo do Útero/genética
Neoplasias do Colo do Útero/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (PPAR gamma); 0 (Thiazolidinediones); 05V02F2KDG (rosiglitazone); EC 3.4.21.46 (Complement Factor D); EC 3.4.21.46 (complement factor D, human); U8QXS1WU8G (ciglitazone); X4OV71U42S (pioglitazone)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170524
[Lr] Data última revisão:
170524
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170222
[St] Status:MEDLINE


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[PMID]:28189761
[Au] Autor:Sandhu HS; Puri S; Sharma R; Sokhi J; Singh G; Matharoo K; Bhanwer A
[Ad] Endereço:Department of Human Genetics, Guru Nanak Dev University, Amritsar 143005, India; Centre for Stem Cell and Tissue Engineering, Panjab University, Chandigarh 160014, India.
[Ti] Título:Associating genetic variation at Perilipin 1, Complement Factor D and Adiponectin loci to the bone health status in North Indian population.
[So] Source:Gene;610:80-89, 2017 Apr 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Osteoporosis, the most common bone metabolic disease affecting nearly 200 million people worldwide is under the strong influence of genetic components. Simultaneously, adipogenesis and osteogenesis are two highly coordinated processes imperative for the maintenance of bone quality and quantity, where any perturbation leads to pathological conditions of obesity, osteopenia and osteoporosis. To delineate this adipogenic-osteogenic connection, a total of 254 cases (T-score<-1.0 SD) and 250 age, gender and ethnicity matched healthy controls (T-score≥-1.0 SD) were recruited from North India after analyzing bone health status employing quantitative ultrasound (QUS) bone densitometer. The genetic variants of Perilipin 1 (PLIN1), Complement Factor D (CFD) and Adiponectin (ADIPOQ) were genotyped using the PCR-RFLP/ARMS-PCR approach. Subjects with CC+CT (PLIN1 rs2304795) and CC+CG (CFD rs1683563) genotypes conferred nearly 1.54-1.87 fold increased risk towards bone deterioration. Predicted RNA secondary structures of rs2304795 corroborated the risk associated with wild type C allele. G allele carriers at the ADIPOQ locus (rs1501299) were more likely to have a lower bone health (1.57-fold). Haplotype analysis revealed the ADIPOQ variants rs1501299 and rs3774261 in slight linkage disequilibrium (LD), nonetheless G/G haplotype was associated with increased risk. 3-locus and 5-locus gene-gene interaction models revealed a greater likelihood of bone deterioration. In conclusion, certain variants of adipogenic genes might serve as potential biomarkers for determining the genetic predisposition towards bone loss in the North Indian population, further, emphasizing the role of impaired metabolism in bone health.
[Mh] Termos MeSH primário: Adipogenia
Adiponectina/genética
Osteogênese
Osteoporose/genética
Perilipina-1/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Osso e Ossos/metabolismo
Fator D do Complemento/genética
Epistasia Genética
Gorduras/metabolismo
Feminino
Seres Humanos
Índia/epidemiologia
Masculino
Meia-Idade
Conformação de Ácido Nucleico
Osteoporose/epidemiologia
Polimorfismo de Nucleotídeo Único
Estabilidade de RNA
RNA Mensageiro/química
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ADIPOQ protein, human); 0 (Adiponectin); 0 (Fats); 0 (PLIN1 protein, human); 0 (Perilipin-1); 0 (RNA, Messenger); EC 3.4.21.46 (Complement Factor D); EC 3.4.21.46 (complement factor D, human)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170315
[Lr] Data última revisão:
170315
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170213
[St] Status:MEDLINE


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[PMID]:28157311
[Au] Autor:Vulpetti A; Randl S; Rüdisser S; Ostermann N; Erbel P; Mac Sweeney A; Zoller T; Salem B; Gerhartz B; Cumin F; Hommel U; Dalvit C; Lorthiois E; Maibaum J
[Ad] Endereço:Novartis Institutes for BioMedical Research, Novartis Pharma AG , Novartis Campus, CH-4056 Basel, Switzerland.
[Ti] Título:Structure-Based Library Design and Fragment Screening for the Identification of Reversible Complement Factor D Protease Inhibitors.
[So] Source:J Med Chem;60(5):1946-1958, 2017 Mar 09.
[Is] ISSN:1520-4804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chronic dysregulation of alternative complement pathway activation has been associated with diverse clinical disorders including age-related macular degeneration and paroxysmal nocturnal hemoglobinurea. Factor D is a trypsin-like serine protease with a narrow specificity for arginine in the P1 position, which catalyzes the first enzymatic reaction of the amplification loop of the alternative pathway. In this article, we describe two hit finding approaches leading to the discovery of new chemical matter for this pivotal protease of the complement system: in silico active site mapping for hot spot identification to guide rational structure-based design and NMR screening of focused and diverse fragment libraries. The wealth of information gathered by these complementary approaches enabled the identification of ligands binding to different subpockets of the latent Factor D conformation and was instrumental for understanding the binding requirements for the generation of the first known potent noncovalent reversible Factor D inhibitors.
[Mh] Termos MeSH primário: Inibidores de Proteases/farmacologia
[Mh] Termos MeSH secundário: Domínio Catalítico
Fator D do Complemento/química
Desenho de Drogas
Seres Humanos
Espectroscopia de Ressonância Magnética
Estrutura Molecular
Inibidores de Proteases/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Protease Inhibitors); EC 3.4.21.46 (Complement Factor D); EC 3.4.21.46 (complement factor D, human)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170204
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jmedchem.6b01684


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[PMID]:27928850
[Au] Autor:Peng B; Zhang L; Yan J; Qi H; Zhang W; Fan L; Hu Y; Lin L; Li X; Hu R; Xie L; Zhang J; Wu Y; Li L; Zhou R
[Ad] Endereço:Department of Obstetrics and Gynecology, West China Second University Hospital, Sichuan University, Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University), Ministry of Education, Chengdu, China.
[Ti] Título:Assessment of the diagnostic value of a urinary adipsin rapid strip test for pre-eclampsia: A prospective multicenter study.
[So] Source:J Obstet Gynaecol Res;43(1):30-33, 2017 Jan.
[Is] ISSN:1447-0756
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:AIM: The purpose of the present study was to evaluate the clinical value of the rapid strip test of urinary adipsin for the quick diagnosis of pre-eclampsia. METHODS: In a multicenter diagnostic test study, we studied the diagnostic accuracy of the rapid strip test of urinary adipsin in women presenting with pre-eclampsia. A total of 204 pre-eclampsia patients and 254 healthy pregnant women were recruited for this study, respectively. The rapid strip test of urinary adipsin was used to detect the adipsin in the urine of each patient. RESULTS: The diagnostic value of the rapid strip test of urinary adipsin for pre-eclampsia was demonstrated by its high sensitivity and specificity (95.10% and 97.64%, respectively). The diagnostic accuracy was 96.51%. The consistency analysis showed that the kappa value was 0.93 compared with the gold standard diagnosis of pre-eclampsia. CONCLUSION: The rapid strip test of urinary adipsin is a non-invasive test for the diagnosis of pre-eclampsia with high sensitivity and specificity. It could help the quick diagnosis of pre-eclampsia in clinical practice greatly.
[Mh] Termos MeSH primário: Pré-Eclâmpsia/diagnóstico
[Mh] Termos MeSH secundário: Adulto
Fator D do Complemento/urina
Feminino
Seres Humanos
Pré-Eclâmpsia/urina
Gravidez
Fitas Reagentes
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Reagent Strips); EC 3.4.21.46 (Complement Factor D); EC 3.4.21.46 (complement factor D, human)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170425
[Lr] Data última revisão:
170425
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161209
[St] Status:MEDLINE
[do] DOI:10.1111/jog.13156


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[PMID]:27810992
[Au] Autor:Yuan X; Gavriilaki E; Thanassi JA; Yang G; Baines AC; Podos SD; Huang Y; Huang M; Brodsky RA
[Ad] Endereço:Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
[Ti] Título:Small-molecule factor D inhibitors selectively block the alternative pathway of complement in paroxysmal nocturnal hemoglobinuria and atypical hemolytic uremic syndrome.
[So] Source:Haematologica;102(3):466-475, 2017 Mar.
[Is] ISSN:1592-8721
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Paroxysmal nocturnal hemoglobinuria and atypical hemolytic uremic syndrome are diseases of excess activation of the alternative pathway of complement that are treated with eculizumab, a humanized monoclonal antibody against the terminal complement component C5. Eculizumab must be administered intravenously, and moreover some patients with paroxysmal nocturnal hemoglobinuria on eculizumab have symptomatic extravascular hemolysis, indicating an unmet need for additional therapeutic approaches. We report the activity of two novel small-molecule inhibitors of the alternative pathway component Factor D using correlates of both paroxysmal nocturnal hemoglobinuria and atypical hemolytic uremic syndrome. Both compounds bind human Factor D with high affinity and effectively inhibit its proteolytic activity against purified Factor B in complex with C3b. When tested using the traditional Ham test with cells from paroxysmal nocturnal hemoglobinuria patients, the Factor D inhibitors significantly reduced complement-mediated hemolysis at concentrations as low as 0.01 µM. Additionally the compound ACH-4471 significantly decreased C3 fragment deposition on paroxysmal nocturnal hemoglobinuria erythrocytes, indicating a reduced potential relative to eculizumab for extravascular hemolysis. Using the recently described modified Ham test with serum from patients with atypical hemolytic uremic syndrome, the compounds reduced the alternative pathway-mediated killing of -null reagent cells, thus establishing their potential utility for this disease of alternative pathway of complement dysregulation and validating the modified Ham test as a system for pre-clinical drug development for atypical hemolytic uremic syndrome. Finally, ACH-4471 blocked alternative pathway activity when administered orally to cynomolgus monkeys. In conclusion, the small-molecule Factor D inhibitors show potential as oral therapeutics for human diseases driven by the alternative pathway of complement, including paroxysmal nocturnal hemoglobinuria and atypical hemolytic uremic syndrome.
[Mh] Termos MeSH primário: Síndrome Hemolítico-Urêmica Atípica/etiologia
Síndrome Hemolítico-Urêmica Atípica/metabolismo
Fator D do Complemento/antagonistas & inibidores
Inativadores do Complemento/farmacologia
Via Alternativa do Complemento/efeitos dos fármacos
Via Alternativa do Complemento/imunologia
Hemoglobinúria Paroxística/etiologia
Hemoglobinúria Paroxística/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Animais
Síndrome Hemolítico-Urêmica Atípica/diagnóstico
Síndrome Hemolítico-Urêmica Atípica/tratamento farmacológico
Biomarcadores
Complemento C3/imunologia
Complemento C3/metabolismo
Fator D do Complemento/imunologia
Fator D do Complemento/metabolismo
Inativadores do Complemento/administração & dosagem
Citotoxicidade Imunológica
Modelos Animais de Doenças
Eritrócitos/imunologia
Eritrócitos/metabolismo
Feminino
Hemoglobinúria Paroxística/diagnóstico
Hemoglobinúria Paroxística/tratamento farmacológico
Hemólise
Seres Humanos
Macaca fascicularis
Masculino
Meia-Idade
Ligação Proteica
Proteólise
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Complement C3); 0 (Complement Inactivating Agents); EC 3.4.21.46 (Complement Factor D)
[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:161105
[St] Status:MEDLINE
[do] DOI:10.3324/haematol.2016.153312


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[PMID]:27721574
[Au] Autor:Guerrero-García JJ; Carrera-Quintanar L; López-Roa RI; Márquez-Aguirre AL; Rojas-Mayorquín AE; Ortuño-Sahagún D
[Ad] Endereço:U.M.A.E. Hospital de Pediatría, C.M.N.O., Instituto Mexicano del Seguro Social, Guadalajara, JAL, Mexico; Instituto de Investigación en Ciencias Biomédicas (IICB), CUCS, Universidad de Guadalajara, Guadalajara, JAL, Mexico.
[Ti] Título:Multiple Sclerosis and Obesity: Possible Roles of Adipokines.
[So] Source:Mediators Inflamm;2016:4036232, 2016.
[Is] ISSN:1466-1861
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Multiple Sclerosis (MS) is an autoimmune disorder of the Central Nervous System that has been associated with several environmental factors, such as diet and obesity. The possible link between MS and obesity has become more interesting in recent years since the discovery of the remarkable properties of adipose tissue. Once MS is initiated, obesity can contribute to increased disease severity by negatively influencing disease progress and treatment response, but, also, obesity in early life is highly relevant as a susceptibility factor and causally related risk for late MS development. The aim of this review was to discuss recent evidence about the link between obesity, as a chronic inflammatory state, and the pathogenesis of MS as a chronic autoimmune and inflammatory disease. First, we describe the main cells involved in MS pathogenesis, both from neural tissue and from the immune system, and including a new participant, the adipocyte, focusing on their roles in MS. Second, we concentrate on the role of several adipokines that are able to participate in the mediation of the immune response in MS and on the possible cross talk between the latter. Finally, we explore recent therapy that involves the transplantation of adipocyte precursor cells for the treatment of MS.
[Mh] Termos MeSH primário: Adipocinas/metabolismo
Doenças Autoimunes/complicações
Esclerose Múltipla/complicações
Obesidade/complicações
[Mh] Termos MeSH secundário: Adipócitos/citologia
Adiponectina/metabolismo
Tecido Adiposo/patologia
Animais
Astrócitos/citologia
Doenças Autoimunes/metabolismo
Linfócitos T CD8-Positivos/citologia
Fator D do Complemento/metabolismo
Modelos Animais de Doenças
Encefalomielite Autoimune Experimental/metabolismo
Seres Humanos
Sistema Imunitário
Inflamação
Interleucina-17/metabolismo
Leptina/metabolismo
Células Mesenquimais Estromais/citologia
Camundongos
Microglia/patologia
Esclerose Múltipla/metabolismo
Nicotinamida Fosforribosiltransferase/metabolismo
Obesidade/metabolismo
Oligodendroglia/citologia
Prevalência
Resistina/metabolismo
Risco
Células Th1/citologia
Células Th2/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Adipokines); 0 (Adiponectin); 0 (Interleukin-17); 0 (Leptin); 0 (Resistin); EC 2.4.2.12 (Nicotinamide Phosphoribosyltransferase); EC 3.4.21.46 (Complement Factor D)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170811
[Lr] Data última revisão:
170811
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161011
[St] Status:MEDLINE


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[PMID]:27707997
[Au] Autor:Banda NK; Acharya S; Scheinman RI; Mehta G; Coulombe M; Takahashi M; Sekine H; Thiel S; Fujita T; Holers VM
[Ad] Endereço:Division of Rheumatology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045; Nirmal.Banda@ucdenver.edu.
[Ti] Título:Mannan-Binding Lectin-Associated Serine Protease 1/3 Cleavage of Pro-Factor D into Factor D In Vivo and Attenuation of Collagen Antibody-Induced Arthritis through Their Targeted Inhibition by RNA Interference-Mediated Gene Silencing.
[So] Source:J Immunol;197(9):3680-3694, 2016 Nov 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The complement system is proposed to play an important role in the pathogenesis of rheumatoid arthritis (RA). The complement system mannan-binding lectin-associated serine proteases (MASP)-1/3 cleave pro-factor D (proDf; inactive) into Df (active), but it is unknown where this cleavage occurs and whether inhibition of MASP-1/3 is a relevant therapeutic strategy for RA. In the present study, we show that the cleavage of proDf into Df by MASP-1/3 can occur in the circulation and that inhibition of MASP-1/3 by gene silencing is sufficient to ameliorate collagen Ab-induced arthritis in mice. Specifically, to examine the cleavage of proDf into Df, MASP-1/3-producing Df liver tissue (donor) was transplanted under the kidney capsule of MASP-1/3 (recipient) mice. Five weeks after the liver transplantation, cleaved Df was present in the circulation of MASP-1/3 mice. To determine the individual effects of MASP-1/3 and Df gene silencing on collagen Ab-induced arthritis, mice were injected with scrambled, MASP-1/3-targeted, or Df-targeted small interfering RNAs (siRNAs). The mRNA levels for MASP-1 and -3 decreased in the liver to 62 and 58%, respectively, in mice injected with MASP-1/3 siRNAs, and Df mRNA decreased to 53% in the adipose tissue of mice injected with Df siRNAs; additionally, circulating MASP-1/3 and Df protein levels were decreased. In mice injected with both siRNAs the clinical disease activity, histopathologic injury scores, C3 deposition, and synovial macrophage/neutrophil infiltration were significantly decreased. Thus, MASP-1/3 represent a new therapeutic target for the treatment of RA, likely through both direct effects on the lectin pathway and indirectly through the alternative pathway.
[Mh] Termos MeSH primário: Artrite Experimental/terapia
Artrite Reumatoide/terapia
Fator D do Complemento/metabolismo
Lectina de Ligação a Manose da Via do Complemento
Serina Proteases Associadas a Proteína de Ligação a Manose/metabolismo
Interferência de RNA
[Mh] Termos MeSH secundário: Animais
Artrite Experimental/genética
Artrite Reumatoide/genética
Fator D do Complemento/genética
Seres Humanos
Masculino
Lectina de Ligação a Manose/metabolismo
Serina Proteases Associadas a Proteína de Ligação a Manose/genética
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Proteólise
RNA Interferente Pequeno/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Mannose-Binding Lectin); 0 (RNA, Small Interfering); EC 3.4.21.- (MASP-1 protein, mouse); EC 3.4.21.- (Mannose-Binding Protein-Associated Serine Proteases); EC 3.4.21.46 (Complement Factor D)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161007
[St] Status:MEDLINE



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