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[PMID]:28701356
[Au] Autor:Bera A; Das F; Ghosh-Choudhury N; Mariappan MM; Kasinath BS; Ghosh Choudhury G
[Ad] Endereço:Department of Medicine, UT Health San Antonio, San Antonio, Texas.
[Ti] Título:Reciprocal regulation of miR-214 and PTEN by high glucose regulates renal glomerular mesangial and proximal tubular epithelial cell hypertrophy and matrix expansion.
[So] Source:Am J Physiol Cell Physiol;313(4):C430-C447, 2017 Oct 01.
[Is] ISSN:1522-1563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Aberrant expression of microRNAs (miRs) contributes to diabetic renal complications, including renal hypertrophy and matrix protein accumulation. Reduced expression of phosphatase and tensin homolog (PTEN) by hyperglycemia contributes to these processes. We considered involvement of miR in the downregulation of PTEN. In the renal cortex of type 1 diabetic mice, we detected increased expression of miR-214 in association with decreased levels of PTEN and enhanced Akt phosphorylation and fibronectin expression. Mesangial and proximal tubular epithelial cells exposed to high glucose showed augmented expression of miR-214. Mutagenesis studies using 3'-UTR of PTEN in a reporter construct revealed PTEN as a direct target of miR-214, which controls its expression in both of these cells. Overexpression of miR-214 decreased the levels of PTEN and increased Akt activity similar to high glucose and lead to phosphorylation of its substrates glycogen synthase kinase-3ß, PRAS40, and tuberin. In contrast, quenching of miR-214 inhibited high-glucose-induced Akt activation and its substrate phosphorylation; these changes were reversed by small interfering RNAs against PTEN. Importantly, respective expression of miR-214 or anti-miR-214 increased or decreased the mammalian target of rapamycin complex 1 (mTORC1) activity induced by high glucose. Furthermore, mTORC1 activity was controlled by miR-214-targeted PTEN via Akt activation. In addition, neutralization of high-glucose-stimulated miR-214 expression significantly inhibited cell hypertrophy and expression of the matrix protein fibronectin. Finally, the anti-miR-214-induced inhibition of these processes was reversed by the expression of constitutively active Akt kinase and hyperactive mTORC1. These results uncover a significant role of miR-214 in the activation of mTORC1 that contributes to high-glucose-induced mesangial and proximal tubular cell hypertrophy and fibronectin expression.
[Mh] Termos MeSH primário: Glicemia/metabolismo
Proliferação Celular
Diabetes Mellitus Tipo 1/enzimologia
Nefropatias Diabéticas/enzimologia
Células Epiteliais/enzimologia
Glomérulos Renais/enzimologia
Túbulos Renais Proximais/enzimologia
MicroRNAs/metabolismo
PTEN Fosfo-Hidrolase/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Animais
Células Cultivadas
Diabetes Mellitus Tipo 1/sangue
Diabetes Mellitus Tipo 1/genética
Diabetes Mellitus Tipo 1/patologia
Nefropatias Diabéticas/sangue
Nefropatias Diabéticas/genética
Nefropatias Diabéticas/patologia
Modelos Animais de Doenças
Células Epiteliais/patologia
Fibronectinas/metabolismo
Regulação Enzimológica da Expressão Gênica
Mesângio Glomerular/metabolismo
Mesângio Glomerular/patologia
Hipertrofia
Glomérulos Renais/patologia
Túbulos Renais Proximais/patologia
Alvo Mecanístico do Complexo 1 de Rapamicina
Camundongos
MicroRNAs/genética
Complexos Multiproteicos/metabolismo
PTEN Fosfo-Hidrolase/genética
Fosforilação
Proteínas Proto-Oncogênicas c-akt/metabolismo
Interferência de RNA
Ratos
Transdução de Sinais
Serina-Treonina Quinases TOR/metabolismo
Transfecção
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Blood Glucose); 0 (Fibronectins); 0 (MicroRNAs); 0 (Mirn214 microRNA, mouse); 0 (Mirn214 microRNA,rat); 0 (Multiprotein Complexes); 0 (Transforming Growth Factor beta); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.1.3.67 (Pten protein, mouse); EC 3.1.3.67 (Pten protein, rat)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170714
[St] Status:MEDLINE
[do] DOI:10.1152/ajpcell.00081.2017


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[PMID]:28584011
[Au] Autor:Chiasson VL; Pakanati AR; Hernandez M; Young KJ; Bounds KR; Mitchell BM
[Ad] Endereço:From the Department of Internal Medicine (V.L.C., A.R.P., M.H., K.J.Y., K.R.B., B.M.M.) and Department of Medical Physiology (B.M.M.), Texas A&M University Health Science Center, College of Medicine, Baylor Scott & White Health, Temple.
[Ti] Título:Regulatory T-Cell Augmentation or Interleukin-17 Inhibition Prevents Calcineurin Inhibitor-Induced Hypertension in Mice.
[So] Source:Hypertension;70(1):183-191, 2017 Jul.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The immunosuppressive calcineurin inhibitors cyclosporine A and tacrolimus alter T-cell subsets and can cause hypertension, vascular dysfunction, and renal toxicity. We and others have reported that cyclosporine A and tacrolimus decrease anti-inflammatory regulatory T cells and increase proinflammatory interleukin-17-producing T cells; therefore, we hypothesized that inhibition of these effects using noncellular therapies would prevent the hypertension, endothelial dysfunction, and renal glomerular injury induced by calcineurin inhibitor therapy. Daily treatment of mice with cyclosporine A or tacrolimus for 1 week significantly decreased CD4 /FoxP3 regulatory T cells in the spleen and lymph nodes, as well as induced hypertension, vascular injury and dysfunction, and glomerular mesangial expansion in mice. Daily cotreatment with all-trans retinoic acid reported to increase regulatory T cells and decrease interleukin-17-producing T cells, prevented all of the detrimental effects of cyclosporine A and tacrolimus. All-trans retinoic acid also increased regulatory T cells and prevented the hypertension, endothelial dysfunction, and glomerular injury in genetically modified mice that phenocopy calcineurin inhibitor-treated mice (FKBP12-Tie2 knockout). Treatment with an interleukin-17-neutralizing antibody also increased regulatory T-cell levels and prevented the hypertension, endothelial dysfunction, and glomerular injury in cyclosporine A-treated and tacrolimus-treated mice and FKBP12-Tie2 knockout mice, whereas an isotype control had no effect. Augmenting regulatory T cells and inhibiting interleukin-17 signaling using noncellular therapies prevents the cardiovascular and renal toxicity of calcineurin inhibitors in mice.
[Mh] Termos MeSH primário: Ciclosporina/farmacologia
Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos
Hipertensão
Interleucina-17/metabolismo
Insuficiência Renal
Linfócitos T Reguladores/fisiologia
Tacrolimo/farmacologia
[Mh] Termos MeSH secundário: Animais
Inibidores de Calcineurina/farmacologia
Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos/metabolismo
Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos/patologia
Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos/prevenção & controle
Endotélio Vascular/efeitos dos fármacos
Endotélio Vascular/metabolismo
Endotélio Vascular/patologia
Mesângio Glomerular/efeitos dos fármacos
Mesângio Glomerular/metabolismo
Mesângio Glomerular/patologia
Hipertensão/metabolismo
Hipertensão/prevenção & controle
Imunossupressores/farmacologia
Inflamação/metabolismo
Inflamação/patologia
Camundongos
Insuficiência Renal/metabolismo
Insuficiência Renal/prevenção & controle
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcineurin Inhibitors); 0 (Immunosuppressive Agents); 0 (Interleukin-17); 83HN0GTJ6D (Cyclosporine); WM0HAQ4WNM (Tacrolimus)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170824
[Lr] Data última revisão:
170824
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170607
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.117.09374


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[PMID]:28552941
[Au] Autor:Lu G; Zhang X; Shen L; Qiao Q; Li Y; Sun J; Zhang J
[Ad] Endereço:Department of Internal Medicine, Division of Nephrology, the First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, People's Republic of China.
[Ti] Título:CCL20 secreted from IgA1-stimulated human mesangial cells recruits inflammatory Th17 cells in IgA nephropathy.
[So] Source:PLoS One;12(5):e0178352, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:IgA nephropathy (IgAN) is the most common primary glomerulonephritis characterized by human mesangial cells (HMC) proliferation and extracellular matrix expansion associated with immune deposits consisting of galactose-deficient IgA1. However, how IgA1 contributes to IgAN has yet to be completely elucidated. In this study, the expression profile of chemokines was more altered in IgA1-treated HMC than in the control group. CCL20 was significantly higher either in the serum of IgAN patients or in IgA1-treated HMC. Further experiments demonstrated that CCR6, the only receptor of CCL20, was highly expressed in activated T cells. Intracellular staining assay and cytokine expression profile implied that CCR6+ T cells produced high IL-17 levels. Transwell experiment immunohistochemistry and immunofluorescence experiments extensively demonstrated that CCL20 could recruit inflammatory Th17 cells to the kidneys. These phenomena caused a series of immune inflammatory responses and further damaged the kidneys. Therefore, HMC stimulated by IgA1 could produce CCL20 and consequently recruit inflammatory Th17 cells to the kidneys to induce further lesion in IgA nephropathy.
[Mh] Termos MeSH primário: Quimiocina CCL20/secreção
Mesângio Glomerular/metabolismo
Glomerulonefrite por IGA/imunologia
Imunoglobulina A/imunologia
Células Th17/imunologia
[Mh] Termos MeSH secundário: Adulto
Células Cultivadas
Técnicas de Cocultura
Feminino
Mesângio Glomerular/patologia
Seres Humanos
Ativação Linfocitária
Masculino
Meia-Idade
Reação em Cadeia da Polimerase em Tempo Real
Linfócitos T/imunologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL20 protein, human); 0 (Chemokine CCL20); 0 (Immunoglobulin A)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170530
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178352


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[PMID]:28495185
[Au] Autor:Jayachandran I; Sundararajan S; Paramasivam P; Venkatesan B; Subramanian SC; Balasubramanyam M; Mohan V; Manickam N
[Ad] Endereço:Madras Diabetes Research Foundation and Dr. Mohan's Diabetes Specialties Centre, WHO Collaborating Centre for Non-Communicable Diseases Prevention, Gopalapuram, Chennai 600086, India.
[Ti] Título:Association of circulatory asymmetric dimethylarginine (ADMA) with diabetic nephropathy in Asian Indians and its causative role in renal cell injury.
[So] Source:Clin Biochem;50(15):835-842, 2017 Oct.
[Is] ISSN:1873-2933
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIM: Asymmetric dimethylarginine (ADMA) is involved in the regulation of nitric oxide synthesis and in the maintenance of vascular tone and structure. But the role and status of ADMA in diabetes induced kidney injury is not clear. Hence this study is investigating the role of ADMA in the progression of kidney injury and its circulatory status in Asian Indians with and without diabetic nephropathy. METHODS: Recruited study subjects were divided into normal glucose tolerance (NGT), type 2 diabetes mellitus (T2DM) and T2DM with micro or macroalbuminuria. Albuminuria was calculated using urinary albumin and creatinine ratio (UACR). ADMA was measured using ELISA. Kidney cell damage in terms of fibrotic markers and ADMA metabolism in terms of DDAH activity were investigated in kidney fibroblasts and mesangial cells. RESULTS: There was a significant elevation in plasma ADMA levels in micro and macroalbuminuric diabetic patients. We found a significant positive correlation between ADMA and UACR, serum creatinine, HbA1C and fasting plasma glucose. A cut-off value of ADMA, 0.666µM/l had a sensitivity and specificity of 70.0% and 65.6%, respectively for detecting diabetic nephropathy. DDAH activity was significantly decreased and fibrotic markers such as fibronectin and α-SMA were significantly increased upon high glucose and ADMA treatment. CONCLUSION: We are suggesting a causative role of ADMA in the development of kidney injury in terms of renal fibrosis and also a cut point of 0.666µM/l of plasma ADMA level appears to be a predictive risk threshold for diabetic nephropathy in south Asian Indian population.
[Mh] Termos MeSH primário: Albuminúria/sangue
Grupo com Ancestrais do Continente Asiático
Diabetes Mellitus Tipo 2/sangue
Nefropatias Diabéticas/sangue
Mesângio Glomerular/lesões
[Mh] Termos MeSH secundário: Adulto
Albuminúria/urina
Animais
Arginina/análogos & derivados
Biomarcadores/sangue
Biomarcadores/urina
Linhagem Celular
Creatinina/sangue
Creatinina/urina
Diabetes Mellitus Tipo 2/etnologia
Diabetes Mellitus Tipo 2/urina
Nefropatias Diabéticas/etnologia
Nefropatias Diabéticas/urina
Feminino
Fibroblastos/metabolismo
Mesângio Glomerular/metabolismo
Hemoglobina A Glicada/metabolismo
Seres Humanos
Índia/etnologia
Masculino
Meia-Idade
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Glycated Hemoglobin A); 0 (hemoglobin A1c protein, human); 63CV1GEK3Y (N,N-dimethylarginine); 94ZLA3W45F (Arginine); AYI8EX34EU (Creatinine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170513
[St] Status:MEDLINE


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[PMID]:28228399
[Au] Autor:Kriz W; Löwen J; Federico G; van den Born J; Gröne E; Gröne HJ
[Ad] Endereço:Department of Neuroanatomy, Medical Faculty Mannheim, University Heidelberg, Germany; wilhelm.kriz@urz.uni-heidelberg.de.
[Ti] Título:Accumulation of worn-out GBM material substantially contributes to mesangial matrix expansion in diabetic nephropathy.
[So] Source:Am J Physiol Renal Physiol;312(6):F1101-F1111, 2017 Jun 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thickening of the glomerular basement membrane (GBM) and expansion of the mesangial matrix are hallmarks of diabetic nephropathy (DN), generally considered to emerge from different sites of overproduction: GBM components from podocytes and mesangial matrix from mesangial cells. Reevaluation of 918 biopsies with DN revealed strong evidence that these mechanisms are connected to each other, wherein excess GBM components fail to undergo degradation and are deposited in the mesangium. These data do not exclude that mesangial cells also synthesize components that contribute to the accumulation of matrix in the mesangium. Light, electron microscopic, immunofluorescence, and in situ hybridization studies clearly show that the thickening of the GBM is due not only to overproduction of components of the mature GBM (α3 and α5 chains of collagen IV and agrin) by podocytes but also to resumed increased synthesis of the α1 chain of collagen IV and of perlecan by endothelial cells usually seen during embryonic development. We hypothesize that these abnormal production mechanisms are caused by different processes: overproduction of mature GBM-components by the diabetic milieu and regression of endothelial cells to an embryonic production mode by decreased availability of mediators from podocytes.
[Mh] Termos MeSH primário: Nefropatias Diabéticas/patologia
Membrana Basal Glomerular/ultraestrutura
Mesângio Glomerular/ultraestrutura
Podócitos/ultraestrutura
[Mh] Termos MeSH secundário: Agrina/análise
Autoantígenos/análise
Biópsia
Microambiente Celular
Colágeno Tipo IV/análise
Nefropatias Diabéticas/metabolismo
Progressão da Doença
Membrana Basal Glomerular/química
Mesângio Glomerular/química
Proteoglicanas de Heparan Sulfato/análise
Seres Humanos
Imuno-Histoquímica
Microscopia Eletrônica de Transmissão
Podócitos/química
Esclerose
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Agrin); 0 (Autoantigens); 0 (COL4A1 protein, human); 0 (COL4A5 protein, human); 0 (Collagen Type IV); 0 (Heparan Sulfate Proteoglycans); 0 (type IV collagen alpha3 chain); 143972-95-6 (perlecan)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170224
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00020.2017


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[PMID]:28194406
[Au] Autor:Lu M; Yin N; Liu W; Cui X; Chen S; Wang E
[Ad] Endereço:Department of Nephrology, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou 121000, China.
[Ti] Título:Curcumin Ameliorates Diabetic Nephropathy by Suppressing NLRP3 Inflammasome Signaling.
[So] Source:Biomed Res Int;2017:1516985, 2017.
[Is] ISSN:2314-6141
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Diabetic nephropathy (DN) is the leading cause of end-stage renal disease, partly because of the lack of effective treatments for DN. Curcumin has been shown to exert strong antifibrotic effects in DN, but the underlying mechanisms are not well characterized. In this study, we sought to determine the effects of curcumin on diabetic renal disease in db/db mice and characterize the underlying mechanism of action. We administered curcumin to db/db mice for 16 weeks. In comparison to mock-treated db/db mice, curcumin-treated mice showed diminished renal hypertrophy, reduced mesangial matrix expansion, and a lower level of albuminuria. Furthermore, the upregulated protein and mRNA expressions of collagen IV and fibronectin in the renal cortices of the db/db mice were inhibited by curcumin treatment. Additionally, curcumin treatment was associated with significant reductions in mature interleukin-1 , cleaved caspase-1, and NLRP3 protein levels in the renal cortices of db/db mice as well as in HK-2 cells exposed to high glucose concentration. In summary, curcumin, a potent antifibrotic agent, is a promising treatment for DN, and its renoprotective effects appear to be mediated by the inhibition of NLRP3 inflammasome activity.
[Mh] Termos MeSH primário: Curcumina/farmacologia
Diabetes Mellitus Experimental/tratamento farmacológico
Nefropatias Diabéticas/tratamento farmacológico
Inflamassomos/metabolismo
Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Caspase 1/metabolismo
Diabetes Mellitus Experimental/metabolismo
Diabetes Mellitus Experimental/patologia
Nefropatias Diabéticas/metabolismo
Nefropatias Diabéticas/patologia
Matriz Extracelular/metabolismo
Matriz Extracelular/patologia
Mesângio Glomerular/metabolismo
Mesângio Glomerular/patologia
Interleucina-1beta/metabolismo
Masculino
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IL1B protein, mouse); 0 (Inflammasomes); 0 (Interleukin-1beta); 0 (NLR Family, Pyrin Domain-Containing 3 Protein); 0 (Nlrp3 protein, mouse); EC 3.4.22.36 (Caspase 1); IT942ZTH98 (Curcumin)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170224
[Lr] Data última revisão:
170224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170215
[St] Status:MEDLINE
[do] DOI:10.1155/2017/1516985


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[PMID]:28157068
[Au] Autor:Yang N; Wang X; Xu F; Zeng C; Wang J; Liu Z
[Ti] Título:Clinical and pathological characteristics of Fabry disease combined with IgA nephropathy in Chinese patients
.
[So] Source:Clin Nephrol;87 (2017)(4):188-195, 2017 Apr.
[Is] ISSN:0301-0430
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:AIMS: To improve diagnosis and treatment, we characterized Fabry disease combined with IgA nephropathy and its response to treatment clinically and pathologically in Chinese patients. MATERIALS AND METHODS: Clinical and pathological characteristics of 6 Chinese patients with renal biopsy-proven Fabry disease combined with IgA nephropathy were retrospectively analyzed. RESULTS: There were 4 males and 2 females in this study. All of the 6 patients presented with proteinuria. Microscopic hematuria was observed in case 4. Extrarenal symptoms included: acroparesthesia in case 1, 2, and 6, hypohidrosis in case 6 and angiokeratomas with hearing loss in case 3. By light microscopy, podocyte distension, with vacuolization, mesangial expansion, and interstitial lesions were found in all 6 cases; and focal segmental glomerulosclerosis was observed in 3 cases. Immunofluorescence microscopy showed deposition of IgA or predominant IgA with C3 in the mesangium. By electron microscopy, myelin figures and/or zebra bodies as well as electron-dense materials, were observed in the mesangium in the 6 cases. After admission and treatment with angiotensin converting enzyme inhibitors (ACEI) or angiotensin receptor blocker (ARB) together with immunosuppressant, glomerular filtration rate (GFR) decreased in 3 cases while it increased in the other 3 without statistical differences. CONCLUSIONS: The clinical and pathological features of Fabry disease combined with IgA nephropathy are diverse. Therefore, it is important to combine family history, clinical manifestations, α-galactosidase A activity and pathological features, especially ultrastructural changes, to improve the diagnosis and treatment of the disease.
.
[Mh] Termos MeSH primário: Antagonistas de Receptores de Angiotensina/uso terapêutico
Inibidores da Enzima Conversora de Angiotensina/uso terapêutico
Doença de Fabry/metabolismo
Glomerulonefrite por IGA/tratamento farmacológico
Imunossupressores/uso terapêutico
alfa-Galactosidase/metabolismo
[Mh] Termos MeSH secundário: Adulto
Grupo com Ancestrais do Continente Asiático
Doença de Fabry/complicações
Feminino
Taxa de Filtração Glomerular
Mesângio Glomerular/patologia
Mesângio Glomerular/ultraestrutura
Glomerulonefrite por IGA/complicações
Glomerulosclerose Segmentar e Focal/tratamento farmacológico
Hematúria/etiologia
Seres Humanos
Masculino
Microscopia Eletrônica
Meia-Idade
Podócitos/patologia
Podócitos/ultraestrutura
Proteinúria/etiologia
Estudos Retrospectivos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin Receptor Antagonists); 0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Immunosuppressive Agents); EC 3.2.1.22 (alpha-Galactosidase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170602
[Lr] Data última revisão:
170602
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170204
[St] Status:MEDLINE
[do] DOI:10.5414/CN108986


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[PMID]:27900943
[Au] Autor:Chen X; Wang H; Xu W; Zhu J
[Ti] Título:Collagen type III glomerulopathy: case report and review of the literature
.
[So] Source:Clin Nephrol;87 (2017)(1):39-46, 2017 Jan.
[Is] ISSN:0301-0430
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:To summarize the clinical and pathological features of collagen type III glomerulopathy, the present report describes a case of collagen type III glomerulopathy and reviewed more than 60 cases recorded by other groups in English literature over the last few years. A 24-year-old female patient was admitted because of lower limbs edema, without any other discomforts. The lab examination of the patient reported proteinuria (2.42 g/24 h urine), microscopic hematuria, and the serum creatinine was 71 µmol/L. She received renal biopsy. The immunofluorescence staining results showed that collagen type III expression was positive. The electron microscopy examination showed that the mesangial regions were widened, with visible fine fibers in it. The periodic stripes of collagen fibers could be seen on some fine fiber-like substance under a high-magnification microscope, the diameters of the fiber-like substances were 40 - 70 nm. Serum collagen type III N-peptide (PIIIP N-P) was 97.94 ng/mL. After the patient received benazepril 10 mg per day and symptomatic treatments (Chinese drug, Cordyceps Capsules 0.5 g per day), her proteinuria resolved (~ 0.5 g/24 hour urine).
[Mh] Termos MeSH primário: Colágeno Tipo III/ultraestrutura
Mesângio Glomerular/patologia
Nefropatias/patologia
[Mh] Termos MeSH secundário: Colágeno Tipo III/metabolismo
Feminino
Hematúria/etiologia
Seres Humanos
Nefropatias/complicações
Nefropatias/tratamento farmacológico
Microscopia Eletrônica
Fragmentos de Peptídeos/sangue
Pró-Colágeno/sangue
Proteinúria/etiologia
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Collagen Type III); 0 (Peptide Fragments); 0 (Procollagen); 0 (procollagen Type III-N-terminal peptide)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161201
[St] Status:MEDLINE


  9 / 5437 MEDLINE  
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[PMID]:27590500
[Au] Autor:Zhao X; Hao J; Duan H; Rong Z; Li F
[Ad] Endereço:1 Department of Pathology, Hebei Medical University, Shijiazhuang 050017, China.
[Ti] Título:Phosphoinositide 3-kinase/protein kinase B/periostin mediated platelet-derived growth factor-induced cell proliferation and extracellular matrix production in lupus nephritis.
[So] Source:Exp Biol Med (Maywood);242(2):160-168, 2017 Jan.
[Is] ISSN:1535-3699
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In the present study, the effect and mechanism of periostin on renal proliferation and extracellular matrix accumulation of lupus mice were investigated. MRL /lpr mice, known as lupus mice, were revealed to show enhanced periostin, proliferating cell nuclear antigen (PCNA), and extracellular matrix accumulation in the kidney accompanied by increased serum platelet-derived growth factor (PDGF). Again, cultured mouse mesangial cells (MMCs) were treated with PDGF, then periostin, and PCNA and secreted fibronectin were detected. The results showed that intracellular periostin and PCNA were respectively enhanced by 2.691 and 2.308 times in PDGF-treated MMC cells at 6 h after stimulation. In addition, secreted fibronectin was increased by 1.442 times. Next, the transfection of periostin shRNA vector in PDGF-stimulated MMC cells effectively suppressed periostin, PCNA and secreted fibronectin by 45.27%, 47.75%, and 39.95%, compared with PDGF-stimulated cells transfected with control vector. Furthermore, it was found that PDGF increased the expression of phospho-Akt (Ser 473) from 30 min to 6 h in MMCs. LY294002 effectively inhibited phospho-Akt (Ser 473) expression caused by PDGF stimulation. Then, periostin, PCNA, and fibronectin were respectively decreased by 69.61%, 46.00%, and 46.20%. In the end, phosphoinositide 3-kinase/protein kinase B/periostin was suggested to mediate PDGF-induced cell proliferation and extracellular matrix production in lupus nephritis.
[Mh] Termos MeSH primário: Moléculas de Adesão Celular/metabolismo
Proliferação Celular/fisiologia
Matriz Extracelular/metabolismo
Nefrite Lúpica/patologia
Fosfatidilinositol 3-Quinases/metabolismo
Fator de Crescimento Derivado de Plaquetas/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
[Mh] Termos MeSH secundário: Animais
Moléculas de Adesão Celular/genética
Células Cultivadas
Cromonas/farmacologia
Feminino
Fibronectinas/secreção
Mesângio Glomerular/citologia
Mesângio Glomerular/metabolismo
Rim/metabolismo
Células Mesangiais/metabolismo
Células Mesangiais/secreção
Camundongos
Camundongos Transgênicos
Morfolinas/farmacologia
Fosfatidilinositol 3-Quinases/antagonistas & inibidores
Antígeno Nuclear de Célula em Proliferação/metabolismo
Proteínas Proto-Oncogênicas c-akt/antagonistas & inibidores
Interferência de RNA
RNA Interferente Pequeno/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Adhesion Molecules); 0 (Chromones); 0 (Fibronectins); 0 (Morpholines); 0 (POSTN protein, human); 0 (Platelet-Derived Growth Factor); 0 (Proliferating Cell Nuclear Antigen); 0 (RNA, Small Interfering); 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160904
[St] Status:MEDLINE
[do] DOI:10.1177/1535370216668050


  10 / 5437 MEDLINE  
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[PMID]:26910209
[Au] Autor:Kurihara H; Sakai T
[Ad] Endereço:Department of Anatomy and Life Structure, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan. hidetake@juntendo.ac.jp.
[Ti] Título:Cell biology of mesangial cells: the third cell that maintains the glomerular capillary.
[So] Source:Anat Sci Int;92(2):173-186, 2017 Mar.
[Is] ISSN:1447-073X
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:The renal glomerulus consists of glomerular endothelial cells, podocytes, and mesangial cells, which cooperate with each other for glomerular filtration. We have produced monoclonal antibodies against glomerular cells in order to identify different types of glomerular cells. Among these antibodies, the E30 clone specifically recognizes the Thy1.1 molecule expressed on mesangial cells. An injection of this antibody into rats resulted in mesangial cell-specific injury within 15 min, and induced mesangial proliferative glomerulonephritis in a reproducible manner. We examined the role of mesangial cells in glomerular function using several experimental tools, including an E30-induced nephritis model, mesangial cell culture, and the deletion of specific genes. Herein, we describe the characterization of E30-induced nephritis, formation of the glomerular capillary network, mesangial matrix turnover, and intercellular signaling between glomerular cells. New molecules that are involved in a wide variety of mesangial cell functions are also introduced.
[Mh] Termos MeSH primário: Matriz Extracelular/metabolismo
Mesângio Glomerular/metabolismo
Células Mesangiais/metabolismo
Nefrite/metabolismo
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Citoesqueleto de Actina
Animais
Mesângio Glomerular/patologia
Células Mesangiais/citologia
Nefrite/patologia
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170313
[Lr] Data última revisão:
170313
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160225
[St] Status:MEDLINE
[do] DOI:10.1007/s12565-016-0334-1



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