Base de dados : MEDLINE
Pesquisa : D23.050.422.500 [Categoria DeCS]
Referências encontradas : 323 [refinar]
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[PMID]:28711658
[Au] Autor:Sutariya B; Taneja N; Saraf M
[Ad] Endereço:Department of Pharmacology, Bombay College of Pharmacy, Kalina, Santacruz (East), Mumbai, 400068, Maharashtra, India.
[Ti] Título:Betulinic acid, isolated from the leaves of Syzygium cumini (L.) Skeels, ameliorates the proteinuria in experimental membranous nephropathy through regulating Nrf2/NF-κB pathways.
[So] Source:Chem Biol Interact;274:124-137, 2017 Aug 25.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Membranous nephropathy (MN) is associated with increased oxidative stress and inflammatory markers in the kidney. Betulinic acid (BA) is a potent antioxidant and anti-inflammatory compound isolated from the leaves of Syzygium cumini (L.) Skeels. In the present study, we investigated the effects of BA on experimental MN in rats and explored the mechanisms by which it enhances antioxidant activities and resolves inflammatory condition in experimental MN. Passive Heymann nephritis (PHN) was induced in Sprague-Dawley rats by a single tail vein injection of anti- Fx1A antiserum. The rats were orally administered BA (25 and 50 mg kg  d ) or dexamethasone (DEX; 0.07 mg kg-1, reference compound) for 4 weeks after the induction of PHN. Blood, urine, and kidney tissue were collected for analysis at the end of the study. Treatment of PHN rats with BA or DEX significantly attenuated renal dysfunction, histopathological alterations and reduced immune complex deposition in the kidneys. Furthermore, BA ameliorated mRNA and protein expression of NF-κB, iNOS, TNF-α, Nrf2, HO-1 and NQO1 in the kidney. BA also restored malondialdehyde level and antioxidant enzyme activities in the kidney. In a nutshell, the protective effect of BA can be explained by its anti-inflammatory and anti-oxidant activities, which in turn is due to downregulation of NF-κB pathway and activation of Nrf2. The results indicated that BA can effectively suppress experimental PHN in rats by regulating Nrf2/NF-κB pathways.
[Mh] Termos MeSH primário: Glomerulonefrite Membranosa/prevenção & controle
Proteinúria/prevenção & controle
Transdução de Sinais/efeitos dos fármacos
Syzygium/química
Triterpenos/farmacologia
[Mh] Termos MeSH secundário: Animais
Anticorpos/administração & dosagem
Anticorpos/imunologia
Antioxidantes/metabolismo
Dexametasona/farmacologia
Feminino
Glomerulonefrite Membranosa/patologia
Complexo Antigênico da Nefrite de Heymann/imunologia
Rim/efeitos dos fármacos
Rim/metabolismo
Rim/patologia
Peroxidação de Lipídeos/efeitos dos fármacos
Masculino
Malondialdeído/sangue
Fator 2 Relacionado a NF-E2/genética
Fator 2 Relacionado a NF-E2/metabolismo
NF-kappa B/genética
NF-kappa B/metabolismo
Folhas de Planta/química
Folhas de Planta/metabolismo
Coelhos
Ratos
Ratos Sprague-Dawley
Syzygium/metabolismo
Triterpenos/química
Triterpenos/isolamento & purificação
Triterpenos/uso terapêutico
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Antioxidants); 0 (Heymann Nephritis Antigenic Complex); 0 (NF-E2-Related Factor 2); 0 (NF-kappa B); 0 (Triterpenes); 0 (Tumor Necrosis Factor-alpha); 4G6A18707N (betulinic acid); 4Y8F71G49Q (Malondialdehyde); 7S5I7G3JQL (Dexamethasone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170717
[St] Status:MEDLINE


  2 / 323 MEDLINE  
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[PMID]:26253709
[Au] Autor:Nassirpour R; Homer BL; Mathur S; Li Y; Li Z; Brown T; Carraher D; Warneke J; Bailey S; Percival K; O'Neil SP; Whiteley LO
[Ad] Endereço:*Drug Safety, Pfizer Worldwide Research and Development; rounak.nassirpour@pfizer.com.
[Ti] Título:Identification of Promising Urinary MicroRNA Biomarkers in Two Rat Models of Glomerular Injury.
[So] Source:Toxicol Sci;148(1):35-47, 2015 Nov.
[Is] ISSN:1096-0929
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:MicroRNAs (miRNAs) are small, noncoding RNAs that regulate protein levels posttranscriptionally. miRNAs play important regulatory roles in many cellular processes and have been implicated in several diseases. Recent studies have reported significant levels of miRNAs in a variety of body fluids, raising the possibility that miRNAs could serve as useful biomarkers. Here, changes in miRNA expression patterns are described in 2 different rodent models of glomerular injury (acute puromycin aminonucleoside nephropathy and passive Heymann nephritis). By employing 2 different modes of glomerular insult, oxidative stress and immune-mediated toxicity, miRNA changes in both isolated glomeruli as well as urine specimens allow for identification of urinary miRNA biomarkers that are suggestive of drug-induced injury specifically to the glomerulus. Subsets of glomerular urinary miRNAs associated with these different modes of glomerular toxicity seem to be dependent on the mechanism of the induced injury, while 9 miRNAs that changed early in both glomerular and urine specimens were common to both studies. We further show that the miRNAs identified as mechanism-specific early glomerular injury biomarkers target key pathways and transcripts relevant to the type of insult, while the insult-independent changes might serve as ideal glomerular injury biomarkers.
[Mh] Termos MeSH primário: Lesão Renal Aguda/urina
Modelos Animais de Doenças
Glomerulonefrite Membranosa/metabolismo
Glomérulos Renais/metabolismo
MicroRNAs/urina
[Mh] Termos MeSH secundário: Lesão Renal Aguda/metabolismo
Lesão Renal Aguda/patologia
Lesão Renal Aguda/fisiopatologia
Animais
Biomarcadores/metabolismo
Biomarcadores/urina
Progressão da Doença
Regulação da Expressão Gênica/efeitos dos fármacos
Glomerulonefrite Membranosa/imunologia
Glomerulonefrite Membranosa/patologia
Glomerulonefrite Membranosa/fisiopatologia
Complexo Antigênico da Nefrite de Heymann/química
Soros Imunes/toxicidade
Glomérulos Renais/imunologia
Glomérulos Renais/fisiopatologia
Glomérulos Renais/ultraestrutura
Microdissecção e Captura a Laser
Masculino
Metabolômica/métodos
MicroRNAs/metabolismo
Microscopia Eletrônica de Transmissão
Estresse Oxidativo/efeitos dos fármacos
Podócitos/efeitos dos fármacos
Podócitos/imunologia
Podócitos/metabolismo
Podócitos/ultraestrutura
Puromicina Aminonucleosídeo/toxicidade
Ratos Sprague-Dawley
Carneiro Doméstico
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Heymann Nephritis Antigenic Complex); 0 (Immune Sera); 0 (MicroRNAs); 58-60-6 (Puromycin Aminonucleoside)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:151027
[Lr] Data última revisão:
151027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150809
[St] Status:MEDLINE
[do] DOI:10.1093/toxsci/kfv167


  3 / 323 MEDLINE  
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[PMID]:25845564
[Au] Autor:Wang YM; Lee VW; Wu H; Harris DC; Alexander SI
[Ad] Endereço:Centre for Kidney Research, Children's Hospital at Westmead, Sydney, New South Wales, Australia.
[Ti] Título:Heymann nephritis in Lewis rats.
[So] Source:Curr Protoc Immunol;109:15.29.1-6, 2015 Apr 01.
[Is] ISSN:1934-368X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human membranous nephritis is a major cause of end-stage kidney disease. Active Heymann nephritis (HN) is an auto-immune model of membranous nephritis induced in Lewis rats by immunization with a crude renal tubular antigen (Fx1A) or megalin (gp330). The pathogenesis of HN is through the binding of anti-Fx1A autoantibodies to the auto-antigen expressed on glomerular epithelial cells, resulting in severe glomerular injury and proteinuria. The pathological features of HN include immune deposits in glomeruli and infiltration of glomeruli and the tubulointerstitium by macrophages and T cells. This unit describes the method of the preparation of Fx1A and the induction of HN in Lewis rats by immunization with Fx1A.
[Mh] Termos MeSH primário: Glomerulonefrite Membranosa/etiologia
Glomerulonefrite Membranosa/patologia
[Mh] Termos MeSH secundário: Animais
Biópsia
Modelos Animais de Doenças
Complexo Antigênico da Nefrite de Heymann/administração & dosagem
Complexo Antigênico da Nefrite de Heymann/imunologia
Masculino
Ratos
Ratos Endogâmicos Lew
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Heymann Nephritis Antigenic Complex)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:161021
[Lr] Data última revisão:
161021
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150408
[St] Status:MEDLINE
[do] DOI:10.1002/0471142735.im1529s109


  4 / 323 MEDLINE  
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[PMID]:22595305
[Au] Autor:Wang L; Hong Q; Lv Y; Feng Z; Zhang X; Wu L; Cui S; Hou K; Su H; Huang Z; Wu D; Chen X
[Ad] Endereço:Department of Nephrology, State Key Laboratory of Kidney Disease, Chinese PLA General Hospital, Beijing 100853, PR China.
[Ti] Título:Autophagy can repair endoplasmic reticulum stress damage of the passive Heymann nephritis model as revealed by proteomics analysis.
[So] Source:J Proteomics;75(13):3866-76, 2012 Jul 16.
[Is] ISSN:1876-7737
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Membranous nephropathy is a common cause of nephrotic syndrome in adults. Although many mechanisms have been proposed, whole proteomic research is still lacking. We analyzed the passive Heymann nephritis animal model using label-free quantitative proteome technology. Results showed 160 differential proteins between control and PHN model groups at days 14 and 21. The expression level of endoplasmic reticulum stress (ERS)-associated protein GRP78 and GRP94 protein was up-regulated on day 14 or 21, which was confirmed by Western blotting. The results also showed that the autophagy marker LC3 was up-regulated in the models. Furthermore, we used tunicamycin to induce ERS of podocytes in vitro to investigate the mechanism. Results of Western blotting revealed that the expression of GRP78, GRP94, and LC3 was up-regulated, while that of the cytoskeletal protein tubulin-ß was down-regulated, and immunofluorescence displayed disordered distribution of tubulin-ß. These suggest that ERS plays an important role in podocyte damage. Autophagy can repair the cytoskeleton damage caused by ERS as a protective mechanism. This provides an important basis for a thorough understanding of the mechanism of podocyte damage and the pathogenesis of membranous nephropathy.
[Mh] Termos MeSH primário: Autofagia/fisiologia
Estresse do Retículo Endoplasmático/fisiologia
Glomerulonefrite Membranosa/patologia
Podócitos/patologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Modelos Animais de Doenças
Proteínas de Choque Térmico/biossíntese
Complexo Antigênico da Nefrite de Heymann/imunologia
Glicoproteínas de Membrana/biossíntese
Camundongos
Proteínas Associadas aos Microtúbulos/biossíntese
Podócitos/metabolismo
Proteômica
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Heat-Shock Proteins); 0 (Heymann Nephritis Antigenic Complex); 0 (Hspa5 protein, rat); 0 (LC3 protein, rat); 0 (Membrane Glycoproteins); 0 (Microtubule-Associated Proteins); 0 (endoplasmin)
[Em] Mês de entrada:1210
[Cu] Atualização por classe:160518
[Lr] Data última revisão:
160518
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120519
[St] Status:MEDLINE
[do] DOI:10.1016/j.jprot.2012.04.016


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[PMID]:22103575
[Au] Autor:Barabas AZ; Cole CD; Sensen M; Lafreniere R
[Ad] Endereço:Department of Surgery, University of Calgary, Calgary, Alberta, Canada. barabas@ucalgary.ca
[Ti] Título:Production of heterologous IgG antibody against Heymann nephritis antigen by injections of immune complexes.
[So] Source:Int J Exp Pathol;93(1):11-7, 2012 Feb.
[Is] ISSN:1365-2613
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Heterologous IgG antibody (ab) can be produced against Heymann nephritis (HN) antigen (ag) in rabbits by administering it in Freund's complete adjuvant. The developing abs reacted at high titre with rat kidney brush border (BB) regions of the renal proximal tubules in an indirect fluorescence ab test. A single IV injection of the heterologous ab into a susceptible strain of rat resulted in the localization of IgG ab to glomerular fixed ags, producing immune complex glomerular nephritis. The injected ab also reacted with the BB region of the renal proximal tubules. The aim of this experiment was to find out whether heterologous IgG ab against the HN ag can also be produced in recipient rabbits by injecting immune complexes (ICs) composed of a rat kidney tubular preparation [rat kidney fraction 3 (rKF3)] and donor rabbit-derived rabbit anti-rKF3 IgG ab. We found that anti-rKF3 IgG ab--against the BB region of the renal proximal tubules--could be induced in rabbits injected with ICs, and the resulting ab was able to initiate passive HN in rats. This was the first time a pathogenic IgG ab was produced against HN ag in rabbits without the use of adjuvant. Ab responses in recipient rabbits were achieved by ab information transfer. Recipient rabbits injected with the IC produced the same class of immunoglobulin with the same specificity against the target ag rKF3, as was present in the innoculum, namely rabbit anti-rKF3 IgG ab.
[Mh] Termos MeSH primário: Complexo Antígeno-Anticorpo/imunologia
Complexo Antigênico da Nefrite de Heymann/imunologia
Imunoglobulina G/metabolismo
Túbulos Renais Proximais/metabolismo
[Mh] Termos MeSH secundário: Animais
Especificidade de Anticorpos
Complexo Antígeno-Anticorpo/administração & dosagem
Feminino
Técnica Indireta de Fluorescência para Anticorpo
Adjuvante de Freund/administração & dosagem
Adjuvante de Freund/imunologia
Injeções
Túbulos Renais Proximais/patologia
Masculino
Microvilosidades/metabolismo
Microvilosidades/patologia
Modelos Animais
Coelhos
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigen-Antibody Complex); 0 (Heymann Nephritis Antigenic Complex); 0 (Immunoglobulin G); 9007-81-2 (Freund's Adjuvant)
[Em] Mês de entrada:1204
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:111123
[St] Status:MEDLINE
[do] DOI:10.1111/j.1365-2613.2011.00792.x


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[PMID]:20947506
[Au] Autor:Liu H; Tian N; Arany I; Bigler SA; Waxman DJ; Shah SV; Baliga R
[Ad] Endereço:Department of Pediatrics, 5 P42 ES07381 , USA.
[Ti] Título:Cytochrome P450 2B1 mediates complement-dependent sublytic injury in a model of membranous nephropathy.
[So] Source:J Biol Chem;285(52):40901-10, 2010 Dec 24.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Membranous nephropathy is a disease that affects the filtering units of the kidney, the glomeruli, and results in proteinuria accompanied by loss of kidney function. Passive Heymann nephritis is an experimental model that mimics membranous nephropathy in humans, wherein the glomerular epithelial cell (GEC) injury induced by complement C5b-9 leads to proteinuria. We examined the role of cytochrome P450 2B1 (CYP2B1) in this complement-mediated sublytic injury. Overexpression of CYP2B1 in GECs significantly increased the formation of reactive oxygen species, cytotoxicity, and collapse of the actin cytoskeleton following treatment with anti-tubular brush-border antiserum (anti-Fx1A). In contrast, silencing of CYP2B1 markedly attenuated anti-Fx1A-induced reactive oxygen species generation and cytotoxicity with preservation of the actin cytoskeleton. Gelsolin, which maintains an organized actin cytoskeleton, was significantly decreased by complement C5b-9-mediated injury but was preserved in CYP2B1-silenced cells. In rats injected with anti-Fx1A, the cytochrome P450 inhibitor cimetidine blocked an increase in catalytic iron and ROS generation, reduced the formation of malondialdehyde adducts, maintained a normal distribution of nephrin in the glomeruli, and provided significant protection at the onset of proteinuria. Thus, GEC CYP2B1 contributes to complement C5b-9-mediated injury and plays an important role in the pathogenesis of passive Heymann nephritis.
[Mh] Termos MeSH primário: Complexo de Ataque à Membrana do Sistema Complemento/metabolismo
Citocromo P-450 CYP2B1/metabolismo
Glomerulonefrite Membranosa/enzimologia
Glomérulos Renais/enzimologia
Túbulos Renais/metabolismo
Espécies Reativas de Oxigênio/metabolismo
[Mh] Termos MeSH secundário: Animais
Anticorpos/farmacologia
Cimetidina/farmacologia
Complexo de Ataque à Membrana do Sistema Complemento/genética
Citocromo P-450 CYP2B1/antagonistas & inibidores
Citocromo P-450 CYP2B1/genética
Modelos Animais de Doenças
Inibidores Enzimáticos/farmacologia
Inativação Gênica
Glomerulonefrite Membranosa/genética
Glomerulonefrite Membranosa/patologia
Complexo Antigênico da Nefrite de Heymann/metabolismo
Glomérulos Renais/patologia
Túbulos Renais/patologia
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Microvilosidades/metabolismo
Microvilosidades/patologia
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies); 0 (Complement Membrane Attack Complex); 0 (Enzyme Inhibitors); 0 (Heymann Nephritis Antigenic Complex); 0 (Membrane Proteins); 0 (Reactive Oxygen Species); 0 (nephrin); 80061L1WGD (Cimetidine); EC 1.14.14.1 (Cytochrome P-450 CYP2B1)
[Em] Mês de entrada:1101
[Cu] Atualização por classe:161202
[Lr] Data última revisão:
161202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:101016
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M110.165498


  7 / 323 MEDLINE  
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[PMID]:20375980
[Au] Autor:Chen ZH; Qin WS; Zeng CH; Zheng CX; Hong YM; Lu YZ; Li LS; Liu ZH
[Ad] Endereço:Research Institute of Nephrology, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China.
[Ti] Título:Triptolide reduces proteinuria in experimental membranous nephropathy and protects against C5b-9-induced podocyte injury in vitro.
[So] Source:Kidney Int;77(11):974-88, 2010 Jun.
[Is] ISSN:1523-1755
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Membranous nephropathy is a major cause of nephrotic syndrome in adults where podocyte injuries were found to mediate the development of proteinuria. Triptolide, a major active component of Tripterygium wilfordii Hook F, has potent immunosuppressive, anti-inflammatory and antiproteinuric effects. To study its antiproteinuric properties, we established an experimental rat model of passive Heymann nephritis and a C5b-9 injury model of podocytes in vitro. Treatment or pretreatment with triptolide markedly reduced established proteinuria as well as the titer of circulating rat anti-rabbit IgG antibodies in these nephritic rats, accompanied by a reduction in glomerular C5b-9 deposits. Expression of desmin, a marker of podocyte injury, diminished after triptolide treatment, whereas quantitative analysis of mean foot process width showed that effacement of foot processes was substantially reversed. In in vitro studies we found that triptolide deactivated NADPH oxidase, suppressed reactive oxygen species generation and p38 mitogen-activated protein kinase, and restored RhoA signaling activity. Triptolide did not interfere with the formation of C5b-9 on the membrane of podocytes. Thus, triptolide reduces established heavy proteinuria and podocyte injuries in rats with passive Heymann nephritis, and protects podocytes from C5b-9-mediated injury.
[Mh] Termos MeSH primário: Complexo de Ataque à Membrana do Sistema Complemento/imunologia
Diterpenos/farmacologia
Glomerulonefrite Membranosa/tratamento farmacológico
Imunossupressores/farmacologia
Fenantrenos/farmacologia
Podócitos/efeitos dos fármacos
Proteinúria/prevenção & controle
[Mh] Termos MeSH secundário: Administração Oral
Animais
Linhagem Celular
Citoproteção
Desmina/metabolismo
Modelos Animais de Doenças
Diterpenos/administração & dosagem
Diterpenos/efeitos adversos
Compostos de Epóxi/administração & dosagem
Compostos de Epóxi/efeitos adversos
Compostos de Epóxi/farmacologia
Feminino
Glomerulonefrite Membranosa/imunologia
Glomerulonefrite Membranosa/patologia
Complexo Antigênico da Nefrite de Heymann/imunologia
Imunoglobulina G/sangue
Imunossupressores/administração & dosagem
Imunossupressores/efeitos adversos
Camundongos
NADPH Oxidases/metabolismo
Fenantrenos/administração & dosagem
Fenantrenos/efeitos adversos
Podócitos/imunologia
Podócitos/patologia
Proteinúria/imunologia
Proteinúria/patologia
Coelhos
Ratos
Ratos Sprague-Dawley
Ratos Wistar
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais/efeitos dos fármacos
Tacrolimo/farmacologia
Fatores de Tempo
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
Proteínas rho de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Complement Membrane Attack Complex); 0 (Desmin); 0 (Diterpenes); 0 (Epoxy Compounds); 0 (Heymann Nephritis Antigenic Complex); 0 (Immunoglobulin G); 0 (Immunosuppressive Agents); 0 (Phenanthrenes); 0 (Reactive Oxygen Species); 19ALD1S53J (triptolide); EC 1.6.3.- (NADPH Oxidases); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); EC 3.6.5.2 (RhoA protein, mouse); EC 3.6.5.2 (rho GTP-Binding Proteins); WM0HAQ4WNM (Tacrolimus)
[Em] Mês de entrada:1008
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100409
[St] Status:MEDLINE
[do] DOI:10.1038/ki.2010.41


  8 / 323 MEDLINE  
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[PMID]:20007346
[Au] Autor:Ohse T; Vaughan MR; Kopp JB; Krofft RD; Marshall CB; Chang AM; Hudkins KL; Alpers CE; Pippin JW; Shankland SJ
[Ad] Endereço:Division of Nephrology, University of Washington, Seattle, Washington 98195-6521, USA.
[Ti] Título:De novo expression of podocyte proteins in parietal epithelial cells during experimental glomerular disease.
[So] Source:Am J Physiol Renal Physiol;298(3):F702-11, 2010 Mar.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Studies have shown that certain cells of the glomerular tuft begin to express proteins considered unique to other cell types upon injury. Little is known about the response of parietal epithelial cells (PEC) to injury. To determine whether PECs change their phenotype upon injury to also express proteins traditionally considered podocyte specific, the following four models of glomerular disease were studied: the transforming growth factor (TGF)-beta1 transgenic mouse model of global glomerulosclerosis, the adriamycin model of focal segmental glomerulosclerosis (FSGS), the anti-glomerular basement membrane (GBM) model of crescentic glomerulonephritis, and the passive Heymann nephritis model of membranous nephropathy. Double immunostaining was performed with antibodies to podocyte-specific proteins (synaptopodin and Wilms' tumor 1) and antibodies to PEC specific proteins (paired box gene 8 and claudin-1). No double staining was detected in normal mice. In contrast, the results showed a statistical increase in the number of cells attached to Bowman basement membrane that were double-positive for both podocyte/PEC proteins in TGF-beta1 transgenic, anti-GBM, and membranous animals. Double-positive cells for both podocyte and PEC proteins were also statistically increased in the glomerular tuft in TGF-beta1 transgenic, anti-GBM, and FSGS mice. These results are consistent with glomerular cells coexpressing podocyte and PEC proteins in experimental glomerular disease, but not under normal circumstances.
[Mh] Termos MeSH primário: Doença Antimembrana Basal Glomerular/metabolismo
Células Epiteliais/metabolismo
Glomerulonefrite Membranosa/metabolismo
Glomerulonefrite/metabolismo
Glomerulosclerose Segmentar e Focal/metabolismo
Podócitos/metabolismo
Proteínas/metabolismo
[Mh] Termos MeSH secundário: Animais
Doença Antimembrana Basal Glomerular/imunologia
Doença Antimembrana Basal Glomerular/patologia
Anticorpos
Autoanticorpos
Biomarcadores/metabolismo
Proliferação Celular
Doxorrubicina
Células Epiteliais/patologia
Glomerulonefrite/genética
Glomerulonefrite/patologia
Glomerulonefrite Membranosa/imunologia
Glomerulonefrite Membranosa/patologia
Glomerulosclerose Segmentar e Focal/induzido quimicamente
Glomerulosclerose Segmentar e Focal/patologia
Complexo Antigênico da Nefrite de Heymann/imunologia
Imuno-Histoquímica
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Transgênicos
Fenótipo
Podócitos/patologia
Ratos
Ratos Sprague-Dawley
Fatores de Tempo
Fator de Crescimento Transformador beta1/genética
Fator de Crescimento Transformador beta1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, N.I.H., INTRAMURAL
[Nm] Nome de substância:
0 (Antibodies); 0 (Autoantibodies); 0 (Biomarkers); 0 (Heymann Nephritis Antigenic Complex); 0 (Proteins); 0 (Transforming Growth Factor beta1); 0 (antiglomerular basement membrane antibody); 80168379AG (Doxorubicin)
[Em] Mês de entrada:1003
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:091217
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00428.2009


  9 / 323 MEDLINE  
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[PMID]:19451724
[Au] Autor:Salant DJ
[Ad] Endereço:Boston University Medical Center, Mass. 02118, USA. djsalant@bu.edu
[Ti] Título:In search of the elusive membranous nephropathy antigen.
[So] Source:Nephron Physiol;112(1):p11-2, 2009.
[Is] ISSN:1660-2137
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Mh] Termos MeSH primário: Glomerulonefrite Membranosa/imunologia
Complexo Antigênico da Nefrite de Heymann/imunologia
Rim/imunologia
Modelos Imunológicos
[Mh] Termos MeSH secundário: Animais
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Heymann Nephritis Antigenic Complex)
[Em] Mês de entrada:0908
[Cu] Atualização por classe:170118
[Lr] Data última revisão:
170118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090520
[St] Status:MEDLINE
[do] DOI:10.1159/000212068


  10 / 323 MEDLINE  
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[PMID]:18332711
[Au] Autor:Ahn SY; Ingulli E
[Ad] Endereço:Department of Pediatrics, University of California, San Diego and Rady Children's Hospital, La Jolla, California 92093-0815, USA.
[Ti] Título:Acute poststreptococcal glomerulonephritis: an update.
[So] Source:Curr Opin Pediatr;20(2):157-62, 2008 Apr.
[Is] ISSN:1040-8703
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE OF REVIEW: Acute poststreptococcal glomerulonephritis, the most common form of acute glomerulonephritis in children, continues to be a major concern worldwide. This review summarizes the recent advances in the pathogenesis, host susceptibility factors, diverse clinical presentations, and treatment of the condition. RECENT FINDINGS: Several recent advances have been made in identifying streptococcal antigens that may play a pathogenic role in acute poststreptococcal glomerulonephritis. Nephritis-associated streptococcal plasmin receptor and streptococcal pyrogenic exotoxin B are currently considered major putative nephritogens. Host susceptibility factors including HLA-DRB1*03011 have been found at a higher frequency in acute poststreptococcal glomerulonephritis patients than in healthy controls. Reversible posterior leukoencephalopathy and autoimmune hemolytic anemia are newly reported clinical associations with the disease. Studies from developing countries question whether the outcome is always benign. Treatment remains mostly conservative; however, controversy exists over the use of aggressive therapy with poor prognostic factors. SUMMARY: Severe group A streptococcal disease including acute poststreptococcal glomerulonephritis remains a cause of morbidity and mortality in developing countries and among impoverished populations. Various reports on the diverse clinical manifestations that can be associated with the condition will aid physicians in prompt diagnosis and intervention, while studies focusing on better understanding of immunopathogenesis may facilitate vaccine development and prevention.
[Mh] Termos MeSH primário: Glomerulonefrite/imunologia
Doenças do Complexo Imune/complicações
Infecções Estreptocócicas/complicações
[Mh] Termos MeSH secundário: Animais
Criança
Ativação do Complemento
Suscetibilidade a Doenças
Glomerulonefrite/diagnóstico
Glomerulonefrite/tratamento farmacológico
Complexo Antigênico da Nefrite de Heymann/imunologia
Seres Humanos
Mimetismo Molecular
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Heymann Nephritis Antigenic Complex)
[Em] Mês de entrada:0808
[Cu] Atualização por classe:080311
[Lr] Data última revisão:
080311
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:080312
[St] Status:MEDLINE
[do] DOI:10.1097/MOP.0b013e3282f45bcf



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