Base de dados : MEDLINE
Pesquisa : D12.644.276.200.100 [Categoria DeCS]
Referências encontradas : 2606 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 261 ir para página                         

  1 / 2606 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29408622
[Au] Autor:Zeng Y; Shen Z; Gu W; Wu M
[Ad] Endereço:Department of Medical Oncology, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, Jiangsu 210009, China; The First Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023, China. Ele
[Ti] Título:Inhibition of hepatocellular carcinoma tumorigenesis by curcumin may be associated with CDKN1A and CTGF.
[So] Source:Gene;651:183-193, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:This study aimed to explore crucial genes, transcription factors (TFs), and microRNAs (miRNAs) associated with the effects of curcumin against hepatocellular carcinoma (HCC). We downloaded data (GSE59713) from Gene Expression Omnibus to analyze differentially expressed genes (DEGs) between curcumin-treated and untreated HCC cell lines. Then, we identified the disease ontology (DO) and functional enrichment analysis of these DEGs and analyzed their protein-protein interactions (PPIs). Additionally, we constructed TF-target gene and miRNA-target gene regulatory networks and explored the potential functions of these DEGs. Finally, we detected the expression of CDKN1A, CTGF, LEF1 TF and MIR-19A regulated by curcumin in PLC/PRF/5 cells using RT-PCR. In total, 345 upregulated and 212 downregulated genes were identified. The main enriched pathway of upregulated genes was the TNF signaling pathway. The downregulated genes were significantly enriched in TGF-beta signaling pathway. In addition, most DEGs were significantly enriched in DO terms such as liver cirrhosis, hepatitis, hepatitis C and cholestasis (eg., CTGF). In the constructed PPI network, CDKN1A and CTGF were the key proteins. Moreover, LEF1, CDKN1A, and miR-19A that regulated CTGF were highlighted in the regulatory networks. Furthermore, the expression of CDKN1A, CTGF, LEF1 TF and miR-19A regulated by curcumin in PLC/PRF/5 cells was consistent with the aforementioned bioinformatics analysis results. To conclude, curcumin might exert its protective effects against HCC tumorigenesis by downregulating LEF1 and downregulating CTGF regulated by MIR-19A and upregulating CDKN1A expression.
[Mh] Termos MeSH primário: Carcinogênese/efeitos dos fármacos
Carcinoma Hepatocelular/tratamento farmacológico
Fator de Crescimento do Tecido Conjuntivo/genética
Curcumina/uso terapêutico
Inibidor de Quinase Dependente de Ciclina p21/genética
[Mh] Termos MeSH secundário: Carcinoma Hepatocelular/genética
Linhagem Celular Tumoral
Bases de Dados Genéticas
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Neoplasias Hepáticas/genética
Fator 1 de Ligação ao Facilitador Linfoide/genética
MicroRNAs/genética
Proteínas de Neoplasias/genética
Mapas de Interação de Proteínas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDKN1A protein, human); 0 (CTGF protein, human); 0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (LEF1 protein, human); 0 (Lymphoid Enhancer-Binding Factor 1); 0 (MIRN19 microRNA, human); 0 (MicroRNAs); 0 (Neoplasm Proteins); 139568-91-5 (Connective Tissue Growth Factor); IT942ZTH98 (Curcumin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE


  2 / 2606 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28460443
[Au] Autor:Fan Q; Cheng Y; Chang HM; Deguchi M; Hsueh AJ; Leung PCK
[Ad] Endereço:Department of Obstetrics and Gynaecology, British Columbia Children's Hospital Research Institute, University of British Columbia, Vancouver, British Columbia, V5Z 4H4, Canada.
[Ti] Título:Sphingosine-1-phosphate promotes ovarian cancer cell proliferation by disrupting Hippo signaling.
[So] Source:Oncotarget;8(16):27166-27176, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Epithelial ovarian carcinomas account for more than 90% of human ovarian cancers and have become the primary cause of death for gynecological malignancies. Unlimited cell proliferation and resistance to cell apoptosis contribute to the development of ovarian cancers. However, the underlying mechanisms involved in these processes in epithelial ovarian carcinomas are yet poorly understood. In the present study, we examined the Hippo signaling gene expression and investigated the effects of Sphingosine 1-phosphate (S1P) on cell proliferation and the underlying mechanisms in human ovarian cancer cell lines, OVCAR3 and SKOV3. Our results demonstrate that S1P disrupts Hippo signaling by reducing YAP phosphorylation and increasing the expression of CCN1 and CCN2 in both ovarian cancer cells. Furthermore, the increase in CCN1/CCN2 expression contributes to the S1P-induced increase in cancer cell proliferation.
[Mh] Termos MeSH primário: Lisofosfolipídeos/farmacologia
Neoplasias Ovarianas/metabolismo
Proteínas Serina-Treonina Quinases/metabolismo
Transdução de Sinais/efeitos dos fármacos
Esfingosina/análogos & derivados
[Mh] Termos MeSH secundário: Transporte Ativo do Núcleo Celular
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Fator de Crescimento do Tecido Conjuntivo/genética
Fator de Crescimento do Tecido Conjuntivo/metabolismo
Proteína Rica em Cisteína 61/genética
Proteína Rica em Cisteína 61/metabolismo
Feminino
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Proteínas Nucleares/metabolismo
Neoplasias Ovarianas/genética
Neoplasias Ovarianas/mortalidade
Neoplasias Ovarianas/patologia
Fosforilação
Fosfotransferases (Aceptor do Grupo Álcool)/genética
Fosfotransferases (Aceptor do Grupo Álcool)/metabolismo
Prognóstico
Esfingosina/farmacologia
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cysteine-Rich Protein 61); 0 (Lysophospholipids); 0 (Nuclear Proteins); 0 (Transcription Factors); 0 (YY1AP1 protein, human); 139568-91-5 (Connective Tissue Growth Factor); 26993-30-6 (sphingosine 1-phosphate); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor)); EC 2.7.1.- (sphingosine kinase); EC 2.7.1.91 (sphingosine kinase 2, human); EC 2.7.11.1 (Hippo protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); NGZ37HRE42 (Sphingosine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15677


  3 / 2606 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28460256
[Au] Autor:Rubis P; Wisniowska-Smialek S; Wypasek E; Rudnicka-Sosin L; Hlawaty M; Lesniak-Sobelga A; Kostkiewicz M; Podolec P
[Ad] Endereço:Department of Cardiac and Vascular Diseases, John Paul II Hospital, 31-202 Krakow, Pradnicka Street 80, Poland. Electronic address: pawelrub@poczta.onet.pl.
[Ti] Título:12-month patterns of serum markers of collagen synthesis, transforming growth factor and connective tissue growth factor are similar in new-onset and chronic dilated cardiomyopathy in patients both with and without cardiac fibrosis.
[So] Source:Cytokine;96:217-227, 2017 08.
[Is] ISSN:1096-0023
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The dynamics of the extracellular matrix (ECM) fibrosis process in dilated cardiomyopathy (DCM) may be assessed non-invasively by means of serum markers of fibrosis. AIM: To explore the kinetics of serum markers of fibrosis during a 12-month follow-up in DCM. METHODS: We included 70 consecutive DCM patients (pts) (48±12.1years, EF 24.4±7.4%) with new-onset (n=35, duration <6months) and chronic DCM (n=35, >6months). Markers of collagen type I and III synthesis - procollagens type I and III carboxy- and amino-terminal peptides (PICP, PINP, PIIICP, PIIINP), and ECM metabolism controlling factors - tumor growth factor beta-1 (TGF1-ß), and connective tissue growth factor (CTGF) - were measured in serum at baseline, and at 3- and 12-month follow-up. All pts underwent endomyocardial biopsy to determine the presence and extent of ECM fibrosis. RESULTS: Markers of collagen type I synthesis (PICP and PINP) were almost homogenously increased over the 3- and 12-month period, whereas PIIINP values decreased and PIIICP levels were unchanged in new-onset and chronic DCM, and in pts with and without ECM fibrosis. Both TGF-ß and CTGF levels decreased over the observation period. Kinetics of serum markers of collagen synthesis and fibrosis controlling factors did not differ between DCM pts categorized according to disease duration and fibrosis status. CONCLUSIONS: The kinetics of collagen type I and III synthesis in DCM move in opposite directions, with production of collagen type I consistently increasing, and the synthesis of collagen type III decreasing. Levels of TGF and CTGF, which are proven fibrosis-stimulating factors, had a tendency to decrease. Regardless of disease duration or fibrosis status, the kinetics of serum markers of collagen synthesis, TGF and CTGF were similar in DCM. A better understanding of the kinetics of serum markers of fibrosis in DCM may help to develop more tailored therapeutic approaches to fibrosis.
[Mh] Termos MeSH primário: Cardiomiopatia Dilatada/sangue
Colágeno Tipo III/sangue
Colágeno Tipo I/sangue
Fator de Crescimento do Tecido Conjuntivo/sangue
Fibrose Endomiocárdica/sangue
Fibrose/sangue
Fatores de Crescimento Transformadores/sangue
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/sangue
Cardiomiopatia Dilatada/complicações
Colágeno Tipo I/biossíntese
Colágeno Tipo III/biossíntese
Fibrose Endomiocárdica/complicações
Feminino
Fibrose/terapia
Seguimentos
Seres Humanos
Cinética
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Collagen Type I); 0 (Collagen Type III); 139568-91-5 (Connective Tissue Growth Factor); 76057-06-2 (Transforming Growth Factors)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


  4 / 2606 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29287092
[Au] Autor:Chatterjee A; Barnard J; Moravec C; Desnoyer R; Tirupula K; Karnik SS
[Ad] Endereço:Department of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, United States of America.
[Ti] Título:Connective tissue growth factor dependent collagen gene expression induced by MAS agonist AR234960 in human cardiac fibroblasts.
[So] Source:PLoS One;12(12):e0190217, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Perspectives on whether the functions of MAS, a G protein-coupled receptor, are beneficial or deleterious in the heart remain controversial. MAS gene knockout reduces coronary vasodilatation leading to ischemic injury. G protein signaling activated by MAS has been implicated in progression of adaptive cardiac hypertrophy to heart failure and fibrosis. In the present study, we observed increased expression of MAS, connective tissue growth factor (CTGF) and collagen genes in failing (HF) human heart samples when compared to non-failing (NF). Expression levels of MAS are correlated with CTGF in HF and NF leading to our hypothesis that MAS controls CTGF production and the ensuing expression of collagen genes. In support of this hypothesis we show that the non-peptide MAS agonist AR234960 increases both mRNA and protein levels of CTGF via ERK1/2 signaling in HEK293-MAS cells and adult human cardiac fibroblasts. MAS-mediated CTGF expression can be specifically blocked by MAS inverse agonist AR244555 and also by MEK1 inhibition. Expression of CTGF gene was essential for MAS-mediated up-regulation of different collagen subtype genes in HEK293-MAS cells and human cardiac fibroblasts. Knockdown of CTGF by RNAi disrupted collagen gene regulation by the MAS-agonist. Our data indicate that CTGF mediates the profibrotic effects of MAS in cardiac fibroblasts. Blocking MAS-CTGF-collagen pathway should be considered for pharmacological intervention for HF.
[Mh] Termos MeSH primário: Colágeno/genética
Fator de Crescimento do Tecido Conjuntivo/metabolismo
Expressão Gênica/efeitos dos fármacos
Miócitos Cardíacos/efeitos dos fármacos
Sulfonas/uso terapêutico
[Mh] Termos MeSH secundário: Western Blotting
Células Cultivadas
Células HEK293
Seres Humanos
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Miócitos Cardíacos/metabolismo
Fosforilação
Reação em Cadeia da Polimerase em Tempo Real
Sulfonas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (AR234960); 0 (Sulfones); 139568-91-5 (Connective Tissue Growth Factor); 9007-34-5 (Collagen); EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171230
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190217


  5 / 2606 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27771699
[Au] Autor:van Breda GF; Bongartz LG; Zhuang W; van Swelm RP; Pertijs J; Braam B; Cramer MJ; Swinkels DW; Doevendans PA; Verhaar MC; Masereeuw R; Joles JA; Gaillard CA
[Ad] Endereço:Department of Nephrology and Immunology, University of Alberta, Edmonton, Alta., Canada.
[Ti] Título:Cardiac Hepcidin Expression Associates with Injury Independent of Iron.
[So] Source:Am J Nephrol;44(5):368-378, 2016.
[Is] ISSN:1421-9670
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Hepcidin regulates systemic iron homeostasis by downregulating the iron exporter ferroportin. Circulating hepcidin is mainly derived from the liver but hepcidin is also produced in the heart. We studied the differential and local regulation of hepcidin gene expression in response to myocardial infarction (MI) and/or chronic kidney disease (CKD). We hypothesized that cardiac hepcidin gene expression is induced by and regulated to severity of cardiac injury, either through direct (MI) or remote (CKD) stimuli, as well as through increased local iron content. METHODS: Nine weeks after subtotal nephrectomy (SNX) or sham surgery (CON), rats were subjected to coronary ligation (CL) or sham surgery to realize 4 groups: CON, SNX, CL and SNX + CL. In week 16, the gene expression of hepcidin, iron and damage markers in cardiac and liver tissues was assessed by quantitative polymerase chain reaction and ferritin protein expression was studied by immunohistochemistry. RESULTS: Cardiac hepcidin messenger RNA (mRNA) expression was increased 2-fold in CL (p = 0.03) and 3-fold in SNX (p = 0.01). Cardiac ferritin staining was not different among groups. Cardiac hepcidin mRNA expression correlated with mRNA expression levels of brain natriuretic peptide (ß = 0.734, p < 0.001) and connective tissue growth factor (ß = 0.431, p = 0.02). In contrast, liver hepcidin expression was unaffected by SNX and CL alone, while it had decreased 50% in SNX + CL (p < 0.05). Hepatic ferritin immunostaining was not different among groups. CONCLUSIONS: Our data indicate differences in hepcidin regulation in liver and heart and suggest a role for injury rather than iron as the driving force for cardiac hepcidin expression in renocardiac failure.
[Mh] Termos MeSH primário: Hepcidinas/metabolismo
Ferro/metabolismo
Fígado/metabolismo
Infarto do Miocárdio/metabolismo
Miocárdio/metabolismo
Insuficiência Renal Crônica/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteína Morfogenética Óssea 6/metabolismo
Proteína alfa Estimuladora de Ligação a CCAAT/metabolismo
Proteínas de Transporte de Cátions/metabolismo
Fator de Crescimento do Tecido Conjuntivo/metabolismo
Citocinas/metabolismo
Regulação da Expressão Gênica
Heme Oxigenase (Desciclizante)/metabolismo
Masculino
Peptídeo Natriurético Encefálico/metabolismo
Ratos Endogâmicos Lew
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bmp6 protein, rat); 0 (Bone Morphogenetic Protein 6); 0 (CCAAT-Enhancer-Binding Protein-alpha); 0 (Cation Transport Proteins); 0 (Ctgf protein, rat); 0 (Cytokines); 0 (Hepcidins); 0 (metal transporting protein 1); 114471-18-0 (Natriuretic Peptide, Brain); 139568-91-5 (Connective Tissue Growth Factor); E1UOL152H7 (Iron); EC 1.14.14.18 (Heme Oxygenase (Decyclizing)); EC 1.14.14.18 (Hmox1 protein, rat)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  6 / 2606 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29198711
[Au] Autor:Xing X; Li Z; Yu Z; Cheng G; Li D; Li Z
[Ad] Endereço:The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) & Key Laboratory of Oral Biomedicine, Ministry of Education, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
[Ti] Título:Effects of connective tissue growth factor (CTGF/CCN2) on condylar chondrocyte proliferation, migration, maturation, differentiation and signalling pathway.
[So] Source:Biochem Biophys Res Commun;495(1):1447-1453, 2018 01 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CCN2, also known as connective tissue growth factor (CTGF), is a 38 kDa cysteine-rich extracellular matrix protein that regulates a sequence of cellular functions and participates in multiple complex biological processes, such as chondrogenesis and osteogenesis. In the present study, we provided the first evidence describing the physiological role of CCN2 in condylar chondrocyte proliferation, migration, maturation and differentiation. CCN2 was widely expressed throughout the whole layers of condylar cartilage and predominantly distributed in the proliferative zone. Recombinant CCN2 promoted the proliferation, migration, proteoglycan synthesis and differentiation capacity of isolated condylar chondrocytes. The stimulatory effect of CCN2 on chondrocyte proliferation was associated with the activation of phosphatidylinositol 3-kinase/Akt signalling pathway. The blocking of this pathway by its inhibitor LY294002 impaired the proliferative effect of CCN2 on chondrocytes. These results suggested a novel physiological role of CCN2 in the development of condylar cartilage.
[Mh] Termos MeSH primário: Condrócitos/citologia
Condrócitos/fisiologia
Condrogênese/fisiologia
Fator de Crescimento do Tecido Conjuntivo/metabolismo
Côndilo Mandibular/citologia
Côndilo Mandibular/metabolismo
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/fisiologia
Crescimento Celular
Movimento Celular/fisiologia
Proliferação Celular/fisiologia
Células Cultivadas
Proteína Oncogênica v-akt/metabolismo
Fosfatidilinositol 3-Quinases/metabolismo
Ratos
Ratos Sprague-Dawley
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ctgf protein, rat); 139568-91-5 (Connective Tissue Growth Factor); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Oncogene Protein v-akt)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE


  7 / 2606 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28977597
[Au] Autor:Cheng JC; Chang HM; Leung PCK
[Ad] Endereço:Department of Obstetrics and Gynaecology, BC Children's Hospital Research Institute, University of British Columbia, Vancouver, British Columbia V5Z 4H4, Canada.
[Ti] Título:TGF-ß1 Inhibits Human Trophoblast Cell Invasion by Upregulating Connective Tissue Growth Factor Expression.
[So] Source:Endocrinology;158(10):3620-3628, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Appropriate trophoblast invasion into the maternal endometrium is essential for successful human implantation and placentation. Connective tissue growth factor (CTGF), also known as CCN2, is a matricellular protein that is expressed in the placenta. Interestingly, the CTGF expression levels in the placenta and serum from patients with severe preeclampsia or fetal growth restriction are higher than those from healthy controls. However, to date, the role of CTGF in the regulation of trophoblast cell invasion remains unclear. Transforming growth factor-ß1 (TGF-ß1) is a potent stimulator of CTGF expression and has been shown to inhibit trophoblast cell invasiveness. However, whether CTGF mediates TGF-ß1-inhibited human trophoblast cell invasion is unknown. In the present study, we show that treatment with TGF-ß1 upregulates CTGF expression in a human trophoblast cell line, HTR-8/SVneo, and in primary human trophoblast cells. Our results also demonstrate that the SMAD2/3 signaling pathways are required for TGF-ß1-induced upregulation of CTGF. Importantly, CTGF knockdown attenuates TGF-ß1-inhibited cell invasion. Furthermore, cell invasiveness is decreased by treatment with recombinant CTGF. These results provide evidence that CTGF mediates TGF-ß1-inhibited human trophoblast cell invasion.
[Mh] Termos MeSH primário: Movimento Celular/efeitos dos fármacos
Fator de Crescimento do Tecido Conjuntivo/efeitos dos fármacos
Fator de Crescimento Transformador beta1/farmacologia
Trofoblastos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Western Blotting
Linhagem Celular
Movimento Celular/genética
Fator de Crescimento do Tecido Conjuntivo/genética
Fator de Crescimento do Tecido Conjuntivo/metabolismo
Feminino
Técnicas de Silenciamento de Genes
Seres Humanos
Gravidez
Primeiro Trimestre da Gravidez
RNA Interferente Pequeno
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Transdução de Sinais
Proteína Smad2/metabolismo
Proteína Smad3/metabolismo
Trofoblastos/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CTGF protein, human); 0 (RNA, Small Interfering); 0 (SMAD2 protein, human); 0 (SMAD3 protein, human); 0 (Smad2 Protein); 0 (Smad3 Protein); 0 (Transforming Growth Factor beta1); 139568-91-5 (Connective Tissue Growth Factor)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00536


  8 / 2606 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28938412
[Au] Autor:Kasper P; Vohlen C; Dinger K; Mohr J; Hucklenbruch-Rother E; Janoschek R; Köth J; Matthes J; Appel S; Dötsch J; Alejandre Alcazar MA
[Ad] Endereço:Translational Experimental Pediatrics, University Hospital for Pediatrics and Adolescent Medicine, Faculty of Medicine, University of Cologne, 50937 Cologne, Germany.
[Ti] Título:Renal Metabolic Programming Is Linked to the Dynamic Regulation of a Leptin-Klf15 Axis and Akt/AMPKα Signaling in Male Offspring of Obese Dams.
[So] Source:Endocrinology;158(10):3399-3415, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Childhood obesity is associated with renal diseases. Maternal obesity is a risk factor linked to increased adipocytokines and metabolic disorders in the offspring. Therefore, we studied the impact of maternal obesity on renal-intrinsic insulin and adipocytokine signaling and on renal function and structure. To induce maternal obesity, female mice were fed a high-fat diet (HFD) or a standard diet (SD; control group) prior to mating, during gestation, and throughout lactation. A third group of dams was fed HFD only during lactation (HFD-Lac). After weaning at postnatal day (P)21, offspring of all groups received SD. Clinically, HFD offspring were overweight and insulin resistant at P21. Although no metabolic changes were detected at P70, renal sodium excretion was reduced by 40%, and renal matrix deposition increased in the HFD group. Mechanistically, two stages were differentiated. In the early stage (P21), compared with the control group, HFD showed threefold increased white adipose tissue, impaired glucose tolerance, hyperleptinemia, and hyperinsulinemia. Renal leptin/Stat3-signaling was activated. In contrast, the Akt/ AMPKα cascade and Krüppel-like factor 15 expression were decreased. In the late stage (P70), although no metabolic differences were detected in HFD when compared with the control group, leptin/Stat3-signaling was reduced, and Akt/AMPKα was activated in the kidneys. This effect was linked to an increase of proliferative (cyclinD1/D2) and profibrotic (ctgf/collagen IIIα1) markers, similar to leptin-deficient mice. HFD-Lac mice exhibited metabolic changes at P21 similar to HFD, but no other persistent changes. This study shows a link between maternal obesity and metabolic programming of renal structure and function and intrinsic-renal Stat3/Akt/AMPKα signaling in the offspring.
[Mh] Termos MeSH primário: Intolerância à Glucose/metabolismo
Insulina/metabolismo
Rim/metabolismo
Leptina/metabolismo
Obesidade/metabolismo
Sobrepeso/metabolismo
Complicações na Gravidez/metabolismo
Efeitos Tardios da Exposição Pré-Natal/metabolismo
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/metabolismo
Adipocinas
Tecido Adiposo Branco
Animais
Colágeno Tipo III/metabolismo
Fator de Crescimento do Tecido Conjuntivo/metabolismo
Ciclina D1/metabolismo
Ciclina D2/metabolismo
Proteínas de Ligação a DNA/metabolismo
Dieta Hiperlipídica
Feminino
Resistência à Insulina
Masculino
Camundongos
Gravidez
Proteínas Proto-Oncogênicas c-akt/metabolismo
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais
Sódio/urina
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adipokines); 0 (COL3A1 protein, mouse); 0 (Ccnd1 protein, mouse); 0 (Ccnd2 protein, mouse); 0 (Collagen Type III); 0 (Ctgf protein, mouse); 0 (Cyclin D2); 0 (DNA-Binding Proteins); 0 (Insulin); 0 (Klf15 protein, mouse); 0 (Leptin); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, mouse); 0 (Transcription Factors); 136601-57-5 (Cyclin D1); 139568-91-5 (Connective Tissue Growth Factor); 9NEZ333N27 (Sodium); EC 2.7.11.1 (AMPK alpha1 subunit, mouse); EC 2.7.11.1 (AMPK alpha2 subunit, mouse); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.31 (AMP-Activated Protein Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00489


  9 / 2606 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28815607
[Au] Autor:Waters JP; Richards YC; Skepper JN; Southwood M; Upton PD; Morrell NW; Pober JS; Bradley JR
[Ad] Endereço:Department of Medicine, University of Cambridge, Addenbrooke's Hospital and NIHR Cambridge Biomedical Research Centre, Cambridge, UK.
[Ti] Título:A 3D tri-culture system reveals that activin receptor-like kinase 5 and connective tissue growth factor drive human glomerulosclerosis.
[So] Source:J Pathol;243(3):390-400, 2017 Nov.
[Is] ISSN:1096-9896
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Glomerular scarring, known as glomerulosclerosis, occurs in many chronic kidney diseases and involves interaction between glomerular endothelial cells (GECs), podocytes, and mesangial cells (MCs), leading to signals that promote extracellular matrix deposition and endothelial cell dysfunction and loss. We describe a 3D tri-culture system to model human glomerulosclerosis. In 3D monoculture, each cell type alters its phenotype in response to TGFß, which has been implicated as an important mediator of glomerulosclerosis. GECs form a lumenized vascular network, which regresses in response to TGFß. MCs respond to TGFß by forming glomerulosclerotic-like nodules with matrix deposition. TGFß treatment of podocytes does not alter cell morphology but increases connective tissue growth factor (CTGF) expression. BMP7 prevents TGFß-induced GEC network regression, whereas TGFß-induced MC nodule formation is prevented by SMAD3 siRNA knockdown or ALK5 inhibitors but not BMP7, and increased phospho-SMAD3 was observed in human glomerulosclerosis. In 3D tri-culture, GECs, podocytes, and MCs form a vascular network in which GECs and podocytes interact intimately within a matrix containing MCs. TGFß treatment induces formation of nodules, but combined inhibition of ALK5 and CTGF is required to prevent TGFß-induced nodule formation in tri-cellular cultures. Identification of therapeutic targets for glomerulosclerosis depends on the 3D culture of all three glomerular cells. Copyright © 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
[Mh] Termos MeSH primário: Fator de Crescimento do Tecido Conjuntivo/metabolismo
Nefropatias Diabéticas/metabolismo
Nefropatias Diabéticas/patologia
Glomérulos Renais/patologia
Proteínas Serina-Treonina Quinases/metabolismo
Receptores de Fatores de Crescimento Transformadores beta/metabolismo
[Mh] Termos MeSH secundário: Matriz Extracelular/metabolismo
Seres Humanos
Nefropatias/patologia
Glomérulos Renais/metabolismo
Células Mesangiais/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CTGF protein, human); 0 (Receptors, Transforming Growth Factor beta); 139568-91-5 (Connective Tissue Growth Factor); EC 2.7.1.11 (TGF-beta type I receptor); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170818
[St] Status:MEDLINE
[do] DOI:10.1002/path.4960


  10 / 2606 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28803990
[Au] Autor:Cai Y; Ma W; Xiao Y; Wu B; Li X; Liu F; Qiu J; Zhang G
[Ad] Endereço:Center of Pharmaceutical Research and Development, Guangzhou Medical University, Guangdong 511436, PR China; The Fifth Affiliated Hospital, Guangzhou Medical University. Guangzhou, Guangdong 511436, PR China. Electronic address: 2012990019@gzhmu.edu.cn.
[Ti] Título:High doses of baicalin induces kidney injury and fibrosis through regulating TGF-ß/Smad signaling pathway.
[So] Source:Toxicol Appl Pharmacol;333:1-9, 2017 Oct 15.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Baicalin is a major flavonoid compound purified from Scutellariae radix, which has been described as an herb in the Chinese Pharmacopoeia. Previous studies have suggested baicalin possessed extensive anti-inflammatory, anti-cancer, anti-viral properties. However, up to known, there have been no reports of safety and toxicity in the rats following oral administration of baicalin. In this present study, we showed the first evidence that treatment of baicalin (400, 800 and 1600mg/kg/day) induced significantly kidney injury and fibrosis. The collagen synthesis and fibrosis-related protein expression were increased in the kidney of Sprague-Dawley (SD) rats after treatment with high doses of baicalin. We further investigated the potential molecular mechanism of baicalin-mediated renal fibrosis and revealed that baicalin activated the transforming growth factor-ß (TGF-ß)/Smad signaling pathway in a dose-dependent manner. Moreover, we also observed that baicalin induced Smad3 interaction with transcriptional coactivator p300 accompanying with increment of Smad3 acetylation. Our results may contribute to better understanding of the future pharmacological and toxicological studies of Scutellaria baicalensis Georgi and its active compounds on the human disease.
[Mh] Termos MeSH primário: Flavonoides/toxicidade
Nefropatias/induzido quimicamente
[Mh] Termos MeSH secundário: Actinas/genética
Actinas/metabolismo
Animais
Anti-Inflamatórios não Esteroides/toxicidade
Antineoplásicos/toxicidade
Antivirais/toxicidade
Fator de Crescimento do Tecido Conjuntivo/genética
Fator de Crescimento do Tecido Conjuntivo/metabolismo
Fibronectinas/genética
Fibronectinas/metabolismo
Fibrose
Rim/efeitos dos fármacos
Rim/metabolismo
Rim/patologia
Nefropatias/metabolismo
Nefropatias/patologia
Ratos Sprague-Dawley
Scutellaria baicalensis
Transdução de Sinais/efeitos dos fármacos
Proteína Smad3/metabolismo
Fator de Crescimento Transformador beta1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acta2 protein, rat); 0 (Actins); 0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Antineoplastic Agents); 0 (Antiviral Agents); 0 (Ctgf protein, rat); 0 (Fibronectins); 0 (Flavonoids); 0 (Madh3 protein, rat); 0 (Smad3 Protein); 0 (Transforming Growth Factor beta1); 139568-91-5 (Connective Tissue Growth Factor); 347Q89U4M5 (baicalin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170815
[St] Status:MEDLINE



página 1 de 261 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde