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[PMID]:29182680
[Au] Autor:Ahrens JM; Jones JD; Nieves NJ; Mitzey AM; DeLuca HF; Clagett-Dame M
[Ad] Endereço:Biochemistry Department, University of Wisconsin-Madison, Madison, Wisconsin, United States of America.
[Ti] Título:Differential activity of 2-methylene-19-nor vitamin D analogs on growth factor gene expression in rhino mouse skin and comparison to all-trans retinoic acid.
[So] Source:PLoS One;12(11):e0188887, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:While all 2-methylene-19-nor analogs of 1α,25-dihydroxyvitamin D3 (1α,25(OH)2D3) tested produce an increase in epidermal thickness in the rhino mouse, only a subset reduce utricle size (comedolysis). All-trans retinoic acid (atRA) also causes epidermal thickening and a reduction in utricle size in the rhino mouse. We now report that 2-methylene-19-nor-(20S)-1α-hydroxybishomopregnacalciferol (2MbisP), a comedolytic analog, increases epidermal thickening more rapidly than does atRA, while both reduce utricle area at an equal rate. Whereas unlike atRA, 2MbisP does not alter the epidermal growth factor receptor ligand, heparin-binding epidermal growth factor-like growth factor, it does increase the expression of both amphiregulin and epigen mRNA, even after a single dose. In situ hybridization reveals an increase in these transcripts throughout the closing utricle as well as in the interfollicular epidermis. The mRNAs for other EGFR ligands including betacellulin and transforming growth factor-α, as well as the epidermal growth factor receptor are largely unaffected by 2MbisP. Another analog, 2-methylene-19-nor-(20S)-26,27-dimethylene-1α,25-dihydroxyvitamin D3 (CAGE-3), produces epidermal thickening but fails to reduce utricle size or increase AREG mRNA levels. CAGE-3 modestly increases epigen mRNA levels, but only after 5 days of dosing. Thus, 2-MbisP produces unique changes in epidermal growth factor receptor ligand mRNAs that may be responsible for both epidermal proliferation and a reduction in utricle size.
[Mh] Termos MeSH primário: Calcitriol/análogos & derivados
Fator de Crescimento Semelhante a EGF de Ligação à Heparina/genética
Pele/efeitos dos fármacos
Tretinoína/farmacologia
[Mh] Termos MeSH secundário: Animais
Calcitriol/química
Calcitriol/farmacologia
Feminino
Fator de Crescimento Semelhante a EGF de Ligação à Heparina/metabolismo
Ligantes
Masculino
Camundongos
RNA Mensageiro/genética
Receptor do Fator de Crescimento Epidérmico/metabolismo
Receptores de Calcitriol/metabolismo
Pele/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-methylene-1,25-dihydroxy-19-norvitamin D3); 0 (Heparin-binding EGF-like Growth Factor); 0 (Ligands); 0 (RNA, Messenger); 0 (Receptors, Calcitriol); 5688UTC01R (Tretinoin); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); FXC9231JVH (Calcitriol)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188887


  2 / 1323 MEDLINE  
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[PMID]:28970067
[Au] Autor:Séry Q; Rabé M; Oliver L; Vallette FM; Gratas C
[Ad] Endereço:Team 9 "Apoptosis and Tumor Progression" CRCINA-INSERM U1232, France; Faculté de Médecine, Université de Nantes, Nantes, France; LaBCT, Institut de Cancérologie de L'Ouest (ICO), St Herblain, Nantes, France.
[Ti] Título:HB-EGF is associated with DNA damage and Mcl-1 turnover in human glioma cell lines treated by Temozolomide.
[So] Source:Biochem Biophys Res Commun;493(4):1377-1383, 2017 Dec 02.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Temozolomide (TMZ) is the main chemotherapeutic agent used for treating newly diagnosed Glioblastoma Multiforme (GBM), the most frequent malignant brain tumors in adults. This alkylating agent induces DNA double strand breaks (DSBs) which in turn lead to apoptosis by activating the Bcl-2 controlled mitochondrial pathway. However, GBM invariably recur as tumors become resistant to TMZ. We investigated the implication of EGFR ligands in this resistance and we found that the pro Heparin Binding Epidermal Growth Factor (proHB-EGF) expression is linked to the early response to TMZ in human glioma cell lines. However, HB-EGF does not affect apoptosis per se although its expression is associated with the degradation of Mcl-1. HB-EGF is implicated in DSBs repair as silencing of HB-EGF increased γH2AX foci half-life as well as USP9X expression, two features that could be linked to the observed effect on Mcl-1. Our data demonstrate a new role for HB-EGF in TMZ treated cell lines.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/farmacologia
Neoplasias Encefálicas/tratamento farmacológico
Neoplasias Encefálicas/metabolismo
Dacarbazina/análogos & derivados
Glioblastoma/tratamento farmacológico
Glioblastoma/metabolismo
Fator de Crescimento Semelhante a EGF de Ligação à Heparina/metabolismo
Proteína de Sequência 1 de Leucemia de Células Mieloides/metabolismo
[Mh] Termos MeSH secundário: Neoplasias Encefálicas/genética
Linhagem Celular Tumoral
Quebras de DNA de Cadeia Dupla
Reparo do DNA
Dacarbazina/farmacologia
Resistência a Medicamentos Antineoplásicos/fisiologia
Técnicas de Silenciamento de Genes
Glioblastoma/genética
Fator de Crescimento Semelhante a EGF de Ligação à Heparina/genética
Histonas/metabolismo
Seres Humanos
Proteólise/efeitos dos fármacos
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
RNA Neoplásico/genética
RNA Neoplásico/metabolismo
Ubiquitina Tiolesterase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 0 (H2AFX protein, human); 0 (Heparin-binding EGF-like Growth Factor); 0 (Histones); 0 (MCL1 protein, human); 0 (Myeloid Cell Leukemia Sequence 1 Protein); 0 (RNA, Messenger); 0 (RNA, Neoplasm); 7GR28W0FJI (Dacarbazine); EC 3.1.2.15 (USP9X protein, human); EC 3.4.19.12 (Ubiquitin Thiolesterase); YF1K15M17Y (temozolomide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE


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[PMID]:28864379
[Au] Autor:Guo Y; Ding Q; Chen L; Ji C; Hao H; Wang J; Qi W; Xie X; Ma J; Li A; Jiang X; Li X; Jiang H
[Ad] Endereço:Department of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, Shijiazhuang, Hebei, China.
[Ti] Título:Overexpression of Heparin-Binding Epidermal Growth Factor-Like Growth Factor Mediates Liver Fibrosis in Transgenic Mice.
[So] Source:Am J Med Sci;354(2):199-210, 2017 Aug.
[Is] ISSN:1538-2990
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The role of heparin-binding epidermal growth factor-like growth factor (HB-EGF) in liver fibrosis is not clear and is sometimes even contradictory. To clarify this role, a HB-EGF transgenic (Tg) mouse model was, for the first time, used to evaluate the functions of HB-EGF in liver fibrosis. MATERIALS AND METHODS: For the in vivo study, carbon tetrachloride injection and bile duct ligation treatment were used to induce liver fibrosis in HB-EGF Tg mice and wild-type (WT) mice, respectively. Primary hepatic satellite cells (HSCs) were isolated from HB-EGF Tg and WT mice for the in vitro study. RESULTS: Compared with the WT mice, HB-EGF Tg mice were shown to develop more severe liver fibrosis when treated with carbon tetrachloride or bile duct ligation, with increased matrix metalloproteinases 13 activity and enhanced expression of fibrogenic genes including α-smooth muscle actin and collagen I. HB-EGF gene transfer led to an increase in proliferation and a decrease in apoptosis in primary HSCs. The ERK signaling pathway was more highly activated in primary HSCs from HB-EGF Tg mice than in those from WT mice. CONCLUSIONS: Our investigation confirmed the profibrotic effect of HB-EGF on the liver using a Tg mouse model. This result may contribute to the elucidation of HB-EGF as a therapeutic target in liver fibrosis.
[Mh] Termos MeSH primário: Colágeno/metabolismo
Regulação Neoplásica da Expressão Gênica
Fator de Crescimento Semelhante a EGF de Ligação à Heparina/genética
Cirrose Hepática/genética
[Mh] Termos MeSH secundário: Animais
Tetracloreto de Carbono/toxicidade
Fator de Crescimento Semelhante a EGF de Ligação à Heparina/metabolismo
Cirrose Hepática/induzido quimicamente
Cirrose Hepática/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hbegf protein, mouse); 0 (Heparin-binding EGF-like Growth Factor); 9007-34-5 (Collagen); CL2T97X0V0 (Carbon Tetrachloride)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170903
[St] Status:MEDLINE


  4 / 1323 MEDLINE  
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[PMID]:28792970
[Au] Autor:Kim S; Yang L; Kim S; Lee RG; Graham MJ; Berliner JA; Lusis AJ; Cai L; Temel RE; Rateri DL; Lee S
[Ad] Endereço:Saha Cardiovascular Research Center at the University of Kentucky College of Medicine, Lexington, Kentucky, United States of America.
[Ti] Título:Targeting hepatic heparin-binding EGF-like growth factor (HB-EGF) induces anti-hyperlipidemia leading to reduction of angiotensin II-induced aneurysm development.
[So] Source:PLoS One;12(8):e0182566, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The upregulated expression of heparin binding EGF-like growth factor (HB-EGF) in the vessel and circulation is associated with risk of cardiovascular disease. In this study, we tested the effects of HB-EGF targeting using HB-EGF-specific antisense oligonucleotide (ASO) on the development of aortic aneurysm in a mouse aneurysm model. APPROACH AND RESULTS: Low-density lipoprotein receptor (LDLR) deficient mice (male, 16 weeks of age) were injected with control and HB-EGF ASOs for 10 weeks. To induce aneurysm, the mice were fed a high fat diet (22% fat, 0.2% cholesterol; w/w) at 5 week point of ASO administration and infused with angiotensin II (AngII, 1,000ng/kg/min) for the last 4 weeks of ASO administration. We confirmed that the HB-EGF ASO administration significantly downregulated HB-EGF expression in multiple tissues including the liver. Importantly, the HB-EGF ASO administration significantly suppressed development of aortic aneurysms including thoracic and abdominal types. Interestingly, the HB-EGF ASO administration induced a remarkable anti-hyperlipidemic effect by suppressing very low density lipoprotein (VLDL) level in the blood. Mechanistically, the HB-EGF targeting suppressed hepatic VLDL secretion rate without changing heparin-releasable plasma triglyceride (TG) hydrolytic activity or fecal neutral cholesterol excretion rate. CONCLUSION: This result suggested that the HB-EGF targeting induced protection against aneurysm development through anti-hyperlipidemic effects. Suppression of hepatic VLDL production process appears to be a key mechanism for the anti-hyperlipidemic effects by the HB-EGF targeting.
[Mh] Termos MeSH primário: Angiotensina II/efeitos adversos
Aneurisma Aórtico/prevenção & controle
Fator de Crescimento Semelhante a EGF de Ligação à Heparina/administração & dosagem
Hiperlipidemias/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Aneurisma Aórtico/induzido quimicamente
Aterosclerose/prevenção & controle
Modelos Animais de Doenças
Hiperlipidemias/induzido quimicamente
Fígado/metabolismo
Masculino
Camundongos
Receptores de LDL/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Heparin-binding EGF-like Growth Factor); 0 (Receptors, LDL); 11128-99-7 (Angiotensin II)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182566


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[PMID]:28698257
[Au] Autor:Li Y; Shen XZ; Li L; Zhao TV; Bernstein KE; Johnson AK; Lyden P; Fang J; Shi P
[Ad] Endereço:From the School of Life Science and Technology, Tongji University, Shanghai, China (Y.L., T.V.Z., J.F.); The Second Affiliated Hospital of Zhejiang University (P.S.), Institute of Translational Medicine (P.S.), and Department of Physiology (X.Z.S.), Zhejiang University School of Medicine, Hangzhou,
[Ti] Título:Brain Transforming Growth Factor-ß Resists Hypertension Via Regulating Microglial Activation.
[So] Source:Stroke;48(9):2557-2564, 2017 Sep.
[Is] ISSN:1524-4628
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: Hypertension is the major risk factor for stroke. Recent work unveiled that hypertension is associated with chronic neuroinflammation; microglia are the major players in neuroinflammation, and the activated microglia elevate sympathetic nerve activity and blood pressure. This study is to understand how brain homeostasis is kept from hypertensive disturbance and microglial activation at the onset of hypertension. METHODS: Hypertension was induced by subcutaneous delivery of angiotensin II, and blood pressure was monitored in conscious animals. Microglial activity was analyzed by flow cytometry and immunohistochemistry. Antibody, pharmacological chemical, and recombinant cytokine were administered to the brain through intracerebroventricular infusion. Microglial depletion was performed by intracerebroventricular delivering diphtheria toxin to CD11b-diphtheria toxin receptor mice. Gene expression profile in sympathetic controlling nucleus was analyzed by customized qRT-PCR array. RESULTS: Transforming growth factor-ß (TGF-ß) is constitutively expressed in the brains of normotensive mice. Removal of TGF-ß or blocking its signaling before hypertension induction accelerated hypertension progression, whereas supplementation of TGF-ß1 substantially suppressed neuroinflammation, kidney norepinephrine level, and blood pressure. By means of microglial depletion and adoptive transfer, we showed that the effects of TGF-ß on hypertension are mediated through microglia. In contrast to the activated microglia in established hypertension, the resting microglia are immunosuppressive and important in maintaining neural homeostasis at the onset of hypertension. Further, we profiled the signature molecules of neuroinflammation and neuroplasticity associated with hypertension and TGF-ß by qRT-PCR array. CONCLUSIONS: Our results identify that TGF-ß-modulated microglia are critical to keeping brain homeostasis responding to hypertensive disturbance.
[Mh] Termos MeSH primário: Pressão Sanguínea/efeitos dos fármacos
Encéfalo/efeitos dos fármacos
Hipertensão/imunologia
Microglia/efeitos dos fármacos
Fator de Crescimento Transformador beta1/farmacologia
[Mh] Termos MeSH secundário: Transferência Adotiva
Angiotensina II/toxicidade
Animais
Pressão Sanguínea/imunologia
Encéfalo/imunologia
Encéfalo/metabolismo
Encéfalo/fisiopatologia
Antígeno CD11b
Toxina Diftérica
Citometria de Fluxo
Fator de Crescimento Semelhante a EGF de Ligação à Heparina
Hipertensão/induzido quimicamente
Hipertensão/genética
Hipertensão/fisiopatologia
Imuno-Histoquímica
Rim/efeitos dos fármacos
Rim/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Microglia/imunologia
Norepinefrina/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Transdução de Sinais
Sistema Nervoso Simpático
Transcriptoma
Fator de Crescimento Transformador beta1/imunologia
Vasoconstritores/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD11b Antigen); 0 (Diphtheria Toxin); 0 (Heparin-binding EGF-like Growth Factor); 0 (Transforming Growth Factor beta1); 0 (Vasoconstrictor Agents); 11128-99-7 (Angiotensin II); X4W3ENH1CV (Norepinephrine)
[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:170713
[St] Status:MEDLINE
[do] DOI:10.1161/STROKEAHA.117.017370


  6 / 1323 MEDLINE  
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[PMID]:28668900
[Au] Autor:Miyata K; Yotsumoto F; Fukagawa S; Kiyoshima C; Ouk NS; Urushiyama D; Ito T; Katsuda T; Kurakazu M; Araki R; Sanui A; Miyahara D; Murata M; Shirota K; Yagi H; Takono T; Kato K; Yaegashi N; Akazawa K; Kuroki M; Yasunaga S; Miyamoto S
[Ad] Endereço:Department of Obstetrics and Gynecology, School of Medicine, Fukuoka University, Fukuoka, Japan.
[Ti] Título:Serum Heparin-binding Epidermal Growth Factor-like Growth Factor (HB-EGF) as a Biomarker for Primary Ovarian Cancer.
[So] Source:Anticancer Res;37(7):3955-3960, 2017 07.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Ovarian cancer is the most lethal malignancy among gynaecological cancers. Although many anticancer agents have been developed for the treatment of ovarian cancer, it continues to have an extremely poor prognosis. Heparin-binding epidermal growth factor-like grown factor (HB-EGF) has been reported to be a rational therapeutic target for ovarian cancer. Here, we evaluated the clinical significance of serum HB-EGF by examining the association between prognosis and serum HB-EGF levels in patients with primary ovarian cancer. We found that high serum HB-EGF concentrations were significantly associated with poor prognosis in a combined cohort of patients with all stages of ovarian cancer, as well as in a subset of patients with advanced disease. In addition, serum HB-EGF levels increased as the cancer advanced. These data suggest that serum HB-EGF may be a target for the design of novel therapies for ovarian cancer.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/sangue
Fator de Crescimento Semelhante a EGF de Ligação à Heparina/sangue
Neoplasias Ovarianas/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Progressão da Doença
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Meia-Idade
Neoplasias Ovarianas/metabolismo
Prognóstico
Análise de Sobrevida
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (HBEGF protein, human); 0 (Heparin-binding EGF-like Growth Factor)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170703
[St] Status:MEDLINE


  7 / 1323 MEDLINE  
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[PMID]:28668882
[Au] Autor:Yotsumoto F; Fukagawa S; Miyata K; Nam SO; Katsuda T; Miyahara D; Odawara T; Manabe S; Ishikawa T; Yasunaga S; Miyamoto S
[Ad] Endereço:Department of Obstetrics and Gynecology, Faculty of Medicine, Fukuoka University, Fukuoka, Japan yotsumoto@cis.fukuoka-u.ac.jp smiya@cis.fukuoka-u.ac.jp.
[Ti] Título:HB-EGF Is a Promising Therapeutic Target for Lung Cancer with Secondary Mutation of .
[So] Source:Anticancer Res;37(7):3825-3831, 2017 07.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Advanced lung cancer is one of the most lethal malignancies. Many anticancer agents have been developed for lung cancer with epidermal growth factor receptor (EGFR) mutations, but its prognosis remains extremely poor. The development of molecularly-targeted therapies is required for patients with lung cancer with secondary mutation of the EGFR gene. In this study, in order to assess the validity of heparin-binding EGF-like growth factor (HB-EGF) as a therapeutic target for lung cancer with EGFR mutation, we examined the antitumor effects of a specific inhibitor (cross-reacting material 197; CRM197) on lung cancer cells with EGFR mutation. HB-EGF was the most predominantly expressed EGFR ligand in lung cancer cells with EGFR mutation. CRM197 induced significant cell apoptosis and marked suppression of tumorigenicity in lung cancer cells with single or double mutation of EGFR. These results suggest that HB-EGF is a rational target for the treatment of lung cancer with EGFR mutation.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Proteínas de Bactérias/uso terapêutico
Fator de Crescimento Semelhante a EGF de Ligação à Heparina
Neoplasias Pulmonares/tratamento farmacológico
Receptor do Fator de Crescimento Epidérmico/genética
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacologia
Apoptose/efeitos dos fármacos
Proteínas de Bactérias/farmacologia
Linhagem Celular Tumoral
Feminino
Seres Humanos
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/metabolismo
Neoplasias Pulmonares/patologia
Camundongos Endogâmicos BALB C
Camundongos Nus
Terapia de Alvo Molecular
Mutação
Inibidores de Proteínas Quinases/farmacologia
Quinazolinas/farmacologia
Receptor do Fator de Crescimento Epidérmico/antagonistas & inibidores
Carga Tumoral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Bacterial Proteins); 0 (Heparin-binding EGF-like Growth Factor); 0 (Protein Kinase Inhibitors); 0 (Quinazolines); 08VC9WC084 (CRM197 (non-toxic variant of diphtheria toxin)); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); S65743JHBS (gefitinib)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170703
[St] Status:MEDLINE


  8 / 1323 MEDLINE  
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[PMID]:28611210
[Au] Autor:Liu J; Gao F; Liu YF; Dou HT; Yan JQ; Fan ZM; Yang ZM
[Ad] Endereço:College of Veterinary MedicineSouth China Agricultural University, Guangzhou, China.
[Ti] Título:HB-EGF regulates Prss56 expression during mouse decidualization via EGFR/ERK/EGR2 signaling pathway.
[So] Source:J Endocrinol;234(3):247-254, 2017 Sep.
[Is] ISSN:1479-6805
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Embryo implantation and decidualization are key steps for successful reproduction. Although numerous factors have been identified to be involved in embryo implantation and decidualization, the mechanisms underlying these processes are still unclear. Based on our preliminary data, Prss56, a trypsin-like serine protease, is strongly expressed at implantation site in mouse uterus. However, the expression, regulation and function of Prss56 during early pregnancy are still unknown. In mouse uterus, is strongly expressed in the subluminal stromal cells at implantation site on day 5 of pregnancy compared to inter-implantation site. Under delayed implantation, expression is undetected. After delayed implantation is activated by estrogen, Prss56 is obviously induced at implantation site. Under artificial decidualization, Prss56 signal is seen at the primary decidual zone at the initial stage of artificial decidualization. When stromal cells are induced for decidualization, expression is significantly elevated. expression under decidualization is suppressed by siRNA. In cultured stromal cells, HB-EGF markedly stimulates expression through EGFR/ERK pathway. Based on promoter analysis, we also showed that Egr2 is involved in Prss56 regulation by HB-EGF. Collectively, expression at implantation site is modulated by HB-EGF/EGFR/ERK signaling pathway and involved in mouse decidualization.
[Mh] Termos MeSH primário: Proteína 2 de Resposta de Crescimento Precoce/metabolismo
Fator de Crescimento Semelhante a EGF de Ligação à Heparina/metabolismo
Serina Proteases/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteína 2 de Resposta de Crescimento Precoce/genética
Implantação do Embrião
Estrogênios/metabolismo
Feminino
Fator de Crescimento Semelhante a EGF de Ligação à Heparina/genética
Sistema de Sinalização das MAP Quinases
Camundongos
Gravidez
Receptor do Fator de Crescimento Epidérmico/genética
Receptor do Fator de Crescimento Epidérmico/metabolismo
Serina Proteases/genética
Transdução de Sinais
Útero/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Early Growth Response Protein 2); 0 (Egr2 protein, mouse); 0 (Estrogens); 0 (Heparin-binding EGF-like Growth Factor); EC 2.7.10.1 (EGFR protein, mouse); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 3.4.- (Prss56 protein, mouse); EC 3.4.- (Serine Proteases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170615
[St] Status:MEDLINE
[do] DOI:10.1530/JOE-16-0636


  9 / 1323 MEDLINE  
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[PMID]:28588064
[Au] Autor:Aikawa S; Kano K; Inoue A; Wang J; Saigusa D; Nagamatsu T; Hirota Y; Fujii T; Tsuchiya S; Taketomi Y; Sugimoto Y; Murakami M; Arita M; Kurano M; Ikeda H; Yatomi Y; Chun J; Aoki J
[Ad] Endereço:Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Miyagi, Japan.
[Ti] Título:Autotaxin-lysophosphatidic acid-LPA signaling at the embryo-epithelial boundary controls decidualization pathways.
[So] Source:EMBO J;36(14):2146-2160, 2017 Jul 14.
[Is] ISSN:1460-2075
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:During pregnancy, up-regulation of heparin-binding (HB-) EGF and cyclooxygenase-2 (COX-2) in the uterine epithelium contributes to decidualization, a series of uterine morphological changes required for placental formation and fetal development. Here, we report a key role for the lipid mediator lysophosphatidic acid (LPA) in decidualization, acting through its G-protein-coupled receptor LPA in the uterine epithelium. Knockout of or inhibition of the LPA-producing enzyme autotaxin (ATX) in pregnant mice leads to HB-EGF and COX-2 down-regulation near embryos and attenuates decidual reactions. Conversely, selective pharmacological activation of LPA induces decidualization via up-regulation of HB-EGF and COX-2. ATX and its substrate lysophosphatidylcholine can be detected in the uterine epithelium and in pre-implantation-stage embryos, respectively. Our results indicate that ATX-LPA-LPA signaling at the embryo-epithelial boundary induces decidualization via the canonical HB-EGF and COX-2 pathways.
[Mh] Termos MeSH primário: Decídua/crescimento & desenvolvimento
Embrião de Mamíferos/fisiologia
Lisofosfolipídeos/metabolismo
Diester Fosfórico Hidrolases/metabolismo
Receptores de Ácidos Lisofosfatídicos/metabolismo
Transdução de Sinais
Útero/fisiologia
[Mh] Termos MeSH secundário: Animais
Ciclo-Oxigenase 2/metabolismo
Desenvolvimento Embrionário
Feminino
Técnicas de Inativação de Genes
Fator de Crescimento Semelhante a EGF de Ligação à Heparina/metabolismo
Camundongos
Camundongos Knockout
Receptores de Ácidos Lisofosfatídicos/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hbegf protein, mouse); 0 (Heparin-binding EGF-like Growth Factor); 0 (Lpar3 protein, mouse); 0 (Lysophospholipids); 0 (Receptors, Lysophosphatidic Acid); EC 1.14.99.- (Ptgs2 protein, mouse); EC 1.14.99.1 (Cyclooxygenase 2); EC 3.1.4.- (Phosphoric Diester Hydrolases); EC 3.1.4.39 (alkylglycerophosphoethanolamine phosphodiesterase); PG6M3969SG (lysophosphatidic acid)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170727
[Lr] Data última revisão:
170727
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170608
[St] Status:MEDLINE
[do] DOI:10.15252/embj.201696290


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[PMID]:28476642
[Au] Autor:Braz BY; Belforte JE; Murer MG; Galiñanes GL
[Ad] Endereço:Universidad de Buenos Aires, Facultad de Medicina, Departamento de Ciencias Fisiológicas, Grupo de Neurociencia de Sistemas, Buenos Aires, Argentina; Universidad de Buenos Aires, CONICET, Instituto de Fisiología y Biofísica (IFIBIO) Houssay, Buenos Aires, Argentina. Electronic address: barbybraz@gma
[Ti] Título:Properties of the corticostriatal long term depression induced by medial prefrontal cortex high frequency stimulation in vivo.
[So] Source:Neuropharmacology;121:278-286, 2017 Jul 15.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Repetitive stimulation of cognitive forebrain circuits at frequencies capable of inducing corticostriatal long term plasticity is increasingly being used with therapeutic purposes in patients with neuropsychiatric disorders. However, corticostriatal plasticity is rarely studied in the intact brain. Our aim was to study the mechanisms of corticostriatal long term depression (LTD) induced by high frequency stimulation (HFS) of the medial prefrontal cortex in vivo. Our main finding is that the LTD induced in the dorsomedial striatum by medial prefrontal cortex HFS in vivo (prefrontostriatal LTD) is not affected by manipulations that block or reduce the LTD induced in the dorsolateral striatum by motor cortex HFS in brain slices, including pharmacological dopamine receptor and CB1 receptor blockade, chronic nigrostriatal dopamine depletion, CB1 receptor genetic deletion and selective striatal cholinergic interneuron (SCIN) ablation. Conversely, like in the hippocampus and other brain areas, prefrontostriatal LTD is NMDA receptor dependent. Thus, we describe a novel form of corticostriatal LTD that operates in brain circuits involved in reward and cognition and could be relevant for understanding the therapeutic effects of deep brain stimulation.
[Mh] Termos MeSH primário: Corpo Estriado/citologia
Corpo Estriado/fisiologia
Depressão Sináptica de Longo Prazo/fisiologia
Neurônios/fisiologia
Córtex Pré-Frontal/fisiologia
[Mh] Termos MeSH secundário: Adrenérgicos/toxicidade
Animais
Animais Recém-Nascidos
Benzazepinas/farmacologia
Colina O-Acetiltransferase/genética
Colina O-Acetiltransferase/metabolismo
Corpo Estriado/lesões
Maleato de Dizocilpina/farmacologia
Antagonistas de Dopamina/farmacologia
Antagonistas de Aminoácidos Excitatórios/farmacologia
Fator de Crescimento Semelhante a EGF de Ligação à Heparina/genética
Fator de Crescimento Semelhante a EGF de Ligação à Heparina/metabolismo
Depressão Sináptica de Longo Prazo/efeitos dos fármacos
Depressão Sináptica de Longo Prazo/genética
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Vias Neurais/fisiologia
Neurônios/efeitos dos fármacos
Oxidopamina/toxicidade
Piperidinas/farmacologia
Pirazóis/farmacologia
Receptor CB1 de Canabinoide/antagonistas & inibidores
Receptor CB1 de Canabinoide/genética
Receptor CB1 de Canabinoide/metabolismo
Tirosina 3-Mono-Oxigenase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic Agents); 0 (Benzazepines); 0 (Dopamine Antagonists); 0 (Excitatory Amino Acid Antagonists); 0 (Heparin-binding EGF-like Growth Factor); 0 (Piperidines); 0 (Pyrazoles); 0 (Receptor, Cannabinoid, CB1); 0 (SCH 23390); 3I4FA44MAI (AM 251); 6LR8C1B66Q (Dizocilpine Maleate); 8HW4YBZ748 (Oxidopamine); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); EC 2.3.1.6 (Choline O-Acetyltransferase)
[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:170507
[St] Status:MEDLINE



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