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Pesquisa : D08.811.277.656.074.500.270 [Categoria DeCS]
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  1 / 889 MEDLINE  
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[PMID]:28945168
[Au] Autor:Wu CF; Lee CT; Kuo YH; Chen TH; Chang CY; Chang IW; Wang WL
[Ad] Endereço:1 Department of Internal Medicine, E-Da Hospital/I-Shou University, Kaohsiung City, Taiwan.
[Ti] Título:High endothelin-converting enzyme-1 expression independently predicts poor survival of patients with esophageal squamous cell carcinoma.
[So] Source:Tumour Biol;39(9):1010428317725922, 2017 Sep.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Patients with esophageal squamous cell carcinoma have poor survival and high recurrence rate, thus an effective prognostic biomarker is needed. Endothelin-converting enzyme-1 is responsible for biosynthesis of endothelin-1, which promotes growth and invasion of human cancers. The role of endothelin-converting enzyme-1 in esophageal squamous cell carcinoma is still unknown. Therefore, this study investigated the significance of endothelin-converting enzyme-1 expression in esophageal squamous cell carcinoma clinically. We enrolled patients with esophageal squamous cell carcinoma who provided pretreated tumor tissues. Tumor endothelin-converting enzyme-1 expression was evaluated by immunohistochemistry and was defined as either low or high expression. Then we evaluated whether tumor endothelin-converting enzyme-1 expression had any association with clinicopathological findings or predicted survival of patients with esophageal squamous cell carcinoma. Overall, 54 of 99 patients with esophageal squamous cell carcinoma had high tumor endothelin-converting enzyme-1 expression, which was significantly associated with lymph node metastasis ( p = 0.04). In addition, tumor endothelin-converting enzyme-1 expression independently predicted survival of patients with esophageal squamous cell carcinoma, and the 5-year survival was poorer in patients with high tumor endothelin-converting enzyme-1 expression ( p = 0.016). Among patients with locally advanced and potentially resectable esophageal squamous cell carcinoma (stage II and III), 5-year survival was poorer with high tumor endothelin-converting enzyme-1 expression ( p = 0.003). High tumor endothelin-converting enzyme-1 expression also significantly predicted poorer survival of patients in this population. In patients with esophageal squamous cell carcinoma, high tumor endothelin-converting enzyme-1 expression might indicate high tumor invasive property. Therefore, tumor endothelin-converting enzyme-1 expression could be a good biomarker to identify patients with worse survival and higher risks of recurrence, who might benefit from the treatment by endothelin-converting enzyme-1 inhibitor.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/análise
Carcinoma de Células Escamosas/patologia
Enzimas Conversoras de Endotelina/biossíntese
Neoplasias Esofágicas/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Carcinoma de Células Escamosas/metabolismo
Carcinoma de Células Escamosas/mortalidade
Enzimas Conversoras de Endotelina/análise
Neoplasias Esofágicas/metabolismo
Neoplasias Esofágicas/mortalidade
Feminino
Seres Humanos
Imuno-Histoquímica
Estimativa de Kaplan-Meier
Masculino
Meia-Idade
Prognóstico
Modelos de Riscos Proporcionais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); EC 3.4.24.71 (Endothelin-Converting Enzymes)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170926
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317725922


  2 / 889 MEDLINE  
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[PMID]:28171705
[Au] Autor:Miners JS; Love S
[Ad] Endereço:Dementia Research Group, University of Bristol, Bristol, UK.
[Ti] Título:Endothelin-converting enzymes degrade α-synuclein and are reduced in dementia with Lewy bodies.
[So] Source:J Neurochem;141(2):275-286, 2017 Apr.
[Is] ISSN:1471-4159
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We have examined the roles of the endothelin-converting enzyme-1 and -2 (ECE-1 and ECE-2) in the homeostasis of α-synuclein (α-syn) and pathogenesis of Lewy body disease. The ECEs are named for their ability to convert inactive big endothelin to the vasoactive peptide endothelin-1 (EDN1). We have found that ECE-1 and ECE-2 cleave and degrade α-syn in vitro and siRNA-mediated knockdown of ECE-1 and ECE-2 in SH-SY5Y neuroblastoma cells significantly increased α-syn both intracellularly (within the cell lysate) (p < 0.05 for both ECE-1 and -2) and extracellularly (in the surrounding medium) (p < 0.05 for ECE-1 and p = 0.07 for ECE-2). Double immunofluorescent labelling showed co-localization of ECE-1 and ECE-2 with α-syn within the endolysosomal system (confirmed by a proximity ligation assay). To assess the possible relevance of these findings to human Lewy body disease, we measured ECE-1 and ECE-2 levels by sandwich ELISA in post-mortem samples of cingulate cortex (a region with a predilection for Lewy body pathology) in dementia with Lewy bodies (DLB) and age-matched controls. ECE-1 (p < 0.001) and ECE-2 (p < 0.01) levels were significantly reduced in DLB and both enzymes correlated inversely with the severity of Lewy body pathology as indicated by the level of α-syn phosphorylated at Ser129 (r = -0.54, p < 0.01 for ECE-1 and r = -0.49, p < 0.05 for ECE-2). Our novel findings suggest a role for ECEs in the metabolism of α-syn that could contribute to the development and progression of DLB.
[Mh] Termos MeSH primário: Encéfalo/enzimologia
Enzimas Conversoras de Endotelina/metabolismo
Doença por Corpos de Lewy/enzimologia
alfa-Sinucleína/metabolismo
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Encéfalo/patologia
Linhagem Celular Tumoral
Enzimas Conversoras de Endotelina/antagonistas & inibidores
Feminino
Seres Humanos
Doença por Corpos de Lewy/patologia
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (alpha-Synuclein); EC 3.4.24.71 (ECE1 protein, human); EC 3.4.24.71 (ECE2 protein, human); EC 3.4.24.71 (Endothelin-Converting Enzymes)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170208
[St] Status:MEDLINE
[do] DOI:10.1111/jnc.13974


  3 / 889 MEDLINE  
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[PMID]:28109039
[Au] Autor:Iklé JM; Tavares AL; King M; Ding H; Colombo S; Firulli BA; Firulli AB; Targoff KL; Yelon D; Clouthier DE
[Ad] Endereço:Department of Craniofacial Biology, University of Colorado Anschutz Medical Campus, Aurora, Colorado, 80045.
[Ti] Título:Nkx2.5 regulates endothelin converting enzyme-1 during pharyngeal arch patterning.
[So] Source:Genesis;55(3), 2017 Mar.
[Is] ISSN:1526-968X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In gnathostomes, dorsoventral (D-V) patterning of neural crest cells (NCC) within the pharyngeal arches is crucial for the development of hinged jaws. One of the key signals that mediate this process is Endothelin-1 (EDN1). Loss of EDN1 binding to the Endothelin-A receptor (EDNRA) results in loss of EDNRA signaling and subsequent facial birth defects in humans, mice and zebrafish. A rate-limiting step in this crucial signaling pathway is the conversion of immature EDN1 into a mature active form by Endothelin converting enzyme-1 (ECE1). However, surprisingly little is known about how Ece1 transcription is induced or regulated. We show here that Nkx2.5 is required for proper craniofacial development in zebrafish and acts in part by upregulating ece1 expression. Disruption of nkx2.5 in zebrafish embryos results in defects in both ventral and dorsal pharyngeal arch-derived elements, with changes in ventral arch gene expression consistent with a disruption in Ednra signaling. ece1 mRNA rescues the nkx2.5 morphant phenotype, indicating that Nkx2.5 functions through modulating Ece1 expression or function. These studies illustrate a new function for Nkx2.5 in embryonic development and provide new avenues with which to pursue potential mechanisms underlying human facial disorders.
[Mh] Termos MeSH primário: Enzimas Conversoras de Endotelina/genética
Regulação da Expressão Gênica no Desenvolvimento
Proteína Homeobox Nkx-2.5/genética
Crista Neural/metabolismo
Proteínas de Peixe-Zebra/genética
[Mh] Termos MeSH secundário: Animais
Enzimas Conversoras de Endotelina/metabolismo
Proteína Homeobox Nkx-2.5/metabolismo
Camundongos
Crista Neural/embriologia
Faringe/embriologia
Faringe/metabolismo
Regulação para Cima
Peixe-Zebra
Proteínas de Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Homeobox Protein Nkx-2.5); 0 (Nkx2.5 protein, zebrafish); 0 (Zebrafish Proteins); EC 3.4.24.71 (Endothelin-Converting Enzymes)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171115
[Lr] Data última revisão:
171115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170122
[St] Status:MEDLINE
[do] DOI:10.1002/dvg.23021


  4 / 889 MEDLINE  
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[PMID]:28025386
[Au] Autor:Martínez-Miguel P; Medrano-Andrés D; Griera-Merino M; Ortiz A; Rodríguez-Puyol M; Rodríguez-Puyol D; López-Ongil S
[Ad] Endereço:Research Unit, Fundación para la Investigación Biomédica del Hospital Universitario Príncipe de Asturias, Alcalá de Henares, Madrid, Spain.
[Ti] Título:Tweak up-regulates endothelin-1 system in mouse and human endothelial cells.
[So] Source:Cardiovasc Res;113(2):207-221, 2017 Feb.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIM: To analyse the ability of TWEAK to modify the endothelin system, particularly endothelin-1 (ET-1) and endothelin-converting enzyme-1 (ECE-1), studying the intracellular mechanisms implied. TNF-like weak inducer of apoptosis (TWEAK) is a member of TNF superfamily; it has different biological functions such as inflammation, angiogenesis, proliferation, and apoptosis. TWEAK and fibroblast growth-factor-inducible 14 are expressed in different cell types, including endothelial and smooth muscle cells. Despite their presence in endothelial cells, the effect of TWEAK on endothelial function is incompletely defined. METHODS AND RESULTS: In cells, TWEAK induced protein (Western blot) and mRNA (quantitative polymerase chain reaction) expression of ECE-1. Results were related to transcriptional changes, as ECE-1 promoter activity (transfection assays) was also increased. Transfections with serial deletions of ECE-1 promoter suggest a potential role for AP-1 and NFkB, which were confirmed by electrophoretic mobility shift assays. When AP-1 or NFkB activations were inhibited by specific inhibitors of AP-1, PD-98059 (Erk1/2 inhibitor), or SP-600125 (JNK inhibitor), and also with an inhibitor of NFKB and PDTC, TWEAK effect was partially blocked in both cases, suggesting that both transcription factors are implied in ECE-1 regulation. Moreover, the endothelial changes induced by TWEAK were also tested in vivo, using 3-month-old male CD-1 mice treated with TWEAK 10 µg/kg body weight for 24 h, finding similar effects, a rise in ET-1 production (enzyme-linked immunosorbent assay), and ECE-1 expression in aorta and lung tissues. Mice showed slight hypertension after 4 h of treatment, which disappeared at 24 h. CONCLUSIONS: In pathological situations such as chronic inflammation, TWEAK could be more harmful through this effect at endothelial level. Pharmacological blockade of this cytokine could prevent the haemodynamic and structural changes related to an increased ET-1 synthesis.
[Mh] Termos MeSH primário: Células Endoteliais/efeitos dos fármacos
Endotelina-1/metabolismo
Enzimas Conversoras de Endotelina/metabolismo
Fatores de Necrose Tumoral/farmacologia
[Mh] Termos MeSH secundário: Animais
Pressão Sanguínea/efeitos dos fármacos
Linhagem Celular
Células Endoteliais/enzimologia
Endotelina-1/genética
Enzimas Conversoras de Endotelina/genética
Seres Humanos
Hipertensão/induzido quimicamente
Hipertensão/metabolismo
Hipertensão/fisiopatologia
Técnicas In Vitro
Masculino
Camundongos
NF-kappa B/metabolismo
Regiões Promotoras Genéticas
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Fatores de Tempo
Fator de Transcrição AP-1/metabolismo
Transcrição Genética
Transfecção
Fatores de Necrose Tumoral/toxicidade
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelin-1); 0 (NF-kappa B); 0 (RNA, Messenger); 0 (Transcription Factor AP-1); 0 (Tumor Necrosis Factors); EC 3.4.24.71 (ECE1 protein, human); EC 3.4.24.71 (Ece1 protein, mouse); EC 3.4.24.71 (Endothelin-Converting Enzymes)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161228
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvw239


  5 / 889 MEDLINE  
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[PMID]:27941335
[Au] Autor:Sun L; Gao Y; Zhang W; Liu X; Li B; Cui X; Sun D
[Ad] Endereço:Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University; Key Lab of Etiology and Epidemiology, Education Bureau of Heilongjiang Province & Ministry of Health (23618504), Harbin, China.
[Ti] Título:Mechanisms Underlying Endothelin-1 Level Elevations Caused by Excessive Fluoride Exposure.
[So] Source:Cell Physiol Biochem;40(5):861-873, 2016.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To explore the mechanisms underlying endothelin-1 (ET-1) elevations induced by excessive fluoride exposure. METHODS: We measured serum and bone fluoride ion content and plasma ET-1 levels and compared these parameters among different groups in an animal model. We also observed morphological changes in the aorta and endothelium of rabbits. In cell experiments, human umbilical vein endothelial cells (HUVECs) were treated with varying concentrations of NaF for 24h, with or without 10 µM U0126 pretreatment for 1 h. ET-1 levels in culture fluid and intracellular reactive oxygen species (ROS) levels, as well as ET1 gene, endothelin-converting enzyme-1 (ECE-1), extracellular signal-regulating kinase 1/2 (ERK1/2), pERK1/2 expression levels and RAS activation were measured and compared among the groups. RESULTS: Plasma ET-1 levels of rabbits increased significantly in fluorinated groups compared with those in the control group. The rabbit thoracic aortas became slightly hardened in fluorinated groups compared with those in the control group, and some vacuoles were present in the endothelial cell cytoplasm of the rabbits in fluorinated groups. In our cell experiments, ET1 gene and ECE-1 expression levels in HUVECs and ET-1 expression levels in the cell culture supernatants increased significantly in some experimental groups compared with those in the control group. These trends paralleled the changes in intracellular ROS levels, RAS activation, and the pERK1/2-to-ERK1/2 ratio. After U0126 was added, ECE-1 expression and ET-1 levels decreased significantly. CONCLUSION: Excessive fluoride exposure leads to characteristic endothelial damage (vacuoles), thoracic aorta hardening, and plasma ET-1 level elevations in rabbits. In addition, the ROS-RAS-MEK1/2-pERK1/2/ERK1/2 pathway plays a crucial-and at least partial-role in ET-1 over-expression, which is promoted by excessive fluoride exposure.
[Mh] Termos MeSH primário: Endotelina-1/metabolismo
Fluoretos/farmacologia
[Mh] Termos MeSH secundário: Animais
Aorta/efeitos dos fármacos
Aorta/patologia
Aorta/ultraestrutura
Peso Corporal/efeitos dos fármacos
Butadienos/farmacologia
Proliferação Celular/efeitos dos fármacos
Dieta
Água Potável
Endotelina-1/genética
Enzimas Conversoras de Endotelina/metabolismo
Endotélio Vascular/efeitos dos fármacos
Endotélio Vascular/patologia
Endotélio Vascular/ultraestrutura
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Células Endoteliais da Veia Umbilical Humana/metabolismo
Espaço Intracelular/metabolismo
Íons
Masculino
Nitrilos/farmacologia
Fosforilação/efeitos dos fármacos
Coelhos
Espécies Reativas de Oxigênio/metabolismo
Vacúolos/efeitos dos fármacos
Vacúolos/metabolismo
Proteínas ras/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Butadienes); 0 (Drinking Water); 0 (Endothelin-1); 0 (Ions); 0 (Nitriles); 0 (Reactive Oxygen Species); 0 (U 0126); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 3.4.24.71 (Endothelin-Converting Enzymes); EC 3.6.5.2 (ras Proteins); Q80VPU408O (Fluorides)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170206
[Lr] Data última revisão:
170206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161213
[St] Status:MEDLINE


  6 / 889 MEDLINE  
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[PMID]:27794420
[Au] Autor:HogenEsch H; Sola M; Stearns TM; Silva KA; Kennedy VE; Sundberg JP
[Ad] Endereço:Department of Comparative Pathobiology, College of Veterinary Medicine, Purdue University, West Lafayette, IN 47907, United States; Purdue Institute for Immunology, Inflammation and Infectious Diseases, Purdue University, West Lafayette, IN 47907, United States; The Jackson Laboratory, Bar Harbor, M
[Ti] Título:Angiogenesis in the skin of SHARPIN-deficient mice with chronic proliferative dermatitis.
[So] Source:Exp Mol Pathol;101(3):303-307, 2016 Dec.
[Is] ISSN:1096-0945
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Angiogenesis is a common feature of pathological processes including wound healing, tumor formation, and chronic inflammation. Chronic inflammation can also be associated with dilation or proliferation of lymph vessels. We examined blood vessels and lymphatics and the expression of pro- and anti-angiogenic genes in the skin of SHARPIN-deficient mice which spontaneously develop a chronic proliferative dermatitis (cpdm). The number of blood vessels in the dermis of cpdm mice increased with age as the inflammation progressed. Lymphatics identified by labeling for LYVE1 and podoplanin were moderately dilated, but they were not increased in number. The expression of proangiogenic Vegfa, Flt1 and anti-angiogenic Sema3a mRNA was increased. VEGFA was primarily localized in keratinocytes of cpdm skin. There was also increased expression of Ece1 and Pdpn mRNA. Podoplanin was restricted to lymphatic endothelial cells in normal skin, but fibroblasts in cpdm skin also reacted with anti-podoplanin antibodies indicating that they were activated. The expression of other angiogenic and lymphangiogenic factors was not altered or decreased. These results indicate that cpdm mice may be a useful model to study the pathogenesis of angiogenesis in chronic inflammation.
[Mh] Termos MeSH primário: Proteínas de Transporte/genética
Dermatite/metabolismo
Neovascularização Patológica/metabolismo
Pele/irrigação sanguínea
[Mh] Termos MeSH secundário: Animais
Dermatite/patologia
Células Endoteliais/metabolismo
Enzimas Conversoras de Endotelina/genética
Enzimas Conversoras de Endotelina/metabolismo
Feminino
Fibroblastos/metabolismo
Glicoproteínas/genética
Glicoproteínas/metabolismo
Queratinócitos/metabolismo
Vasos Linfáticos/patologia
Glicoproteínas de Membrana/genética
Glicoproteínas de Membrana/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Semaforina-3A/genética
Semaforina-3A/metabolismo
Pele/citologia
Pele/metabolismo
Fator A de Crescimento do Endotélio Vascular/genética
Fator A de Crescimento do Endotélio Vascular/metabolismo
Receptor 1 de Fatores de Crescimento do Endotélio Vascular/genética
Receptor 1 de Fatores de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (Glycoproteins); 0 (Gp38 protein, mouse); 0 (Membrane Glycoproteins); 0 (Sema3a protein, mouse); 0 (Semaphorin-3A); 0 (Sipl1 protein, mouse); 0 (Vascular Endothelial Growth Factor A); 0 (Xlkd1 protein, mouse); EC 2.7.10.1 (Flt1 protein, mouse); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-1); EC 3.4.24.71 (Ece1 protein, mouse); EC 3.4.24.71 (Endothelin-Converting Enzymes)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170428
[Lr] Data última revisão:
170428
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161031
[St] Status:MEDLINE


  7 / 889 MEDLINE  
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[PMID]:27644077
[Au] Autor:Pacheco-Quinto J; Eckman CB; Eckman EA
[Ad] Endereço:Atlantic Health System, Morristown, NJ, USA; Biomedical Research Institute of New Jersey, Cedar Knolls, NJ, USA.
[Ti] Título:Major amyloid-ß-degrading enzymes, endothelin-converting enzyme-2 and neprilysin, are expressed by distinct populations of GABAergic interneurons in hippocampus and neocortex.
[So] Source:Neurobiol Aging;48:83-92, 2016 Dec.
[Is] ISSN:1558-1497
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Impaired clearance of amyloid-ß peptide (Aß) has been postulated to significantly contribute to the amyloid accumulation typical of Alzheimer's disease. Among the enzymes known to degrade Aß in vivo are endothelin-converting enzyme (ECE)-1, ECE-2, and neprilysin (NEP), and evidence suggests that they regulate independent pools of Aß that may be functionally significant. To better understand the differential regulation of Aß concentration by its physiological degrading enzymes, we characterized the cell and region-specific expression pattern of ECE-1, ECE-2, and NEP by in situ hybridization and immunohistochemistry in brain areas relevant to Alzheimer's disease. In contrast to the broader distribution of ECE-1, ECE-2 and NEP were found enriched in GABAergic neurons. ECE-2 was majorly expressed by somatostatin-expressing interneurons and was active in isolated synaptosomes. NEP messenger RNA was found mainly in parvalbumin-expressing interneurons, with NEP protein localized to perisomatic parvalbuminergic synapses. The identification of somatostatinergic and parvalbuminergic synapses as hubs for Aß degradation is consistent with the possibility that Aß may have a physiological function related to the regulation of inhibitory signaling.
[Mh] Termos MeSH primário: Peptídeos beta-Amiloides/metabolismo
Enzimas Conversoras de Endotelina/metabolismo
Neurônios GABAérgicos/enzimologia
Hipocampo/citologia
Hipocampo/enzimologia
Neocórtex/citologia
Neocórtex/enzimologia
Neprilisina/metabolismo
[Mh] Termos MeSH secundário: Doença de Alzheimer/etiologia
Doença de Alzheimer/metabolismo
Peptídeos beta-Amiloides/fisiologia
Animais
Enzimas Conversoras de Endotelina/genética
Enzimas Conversoras de Endotelina/fisiologia
Expressão Gênica
Camundongos Transgênicos
Neprilisina/genética
Neprilisina/fisiologia
RNA Mensageiro/metabolismo
Sinapses/enzimologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (RNA, Messenger); EC 3.4.24.11 (Neprilysin); EC 3.4.24.71 (Ece2 protein, mouse); EC 3.4.24.71 (Endothelin-Converting Enzymes)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160920
[St] Status:MEDLINE


  8 / 889 MEDLINE  
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[PMID]:27036146
[Au] Autor:Zeng Y; Ma M; Liu B; Xia J; Xu H; Liu Y; Du X; Hu Z; Yang Q; Zhang L
[Ad] Endereço:Department of Geriatrics, Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China.
[Ti] Título:Association between ECE1 gene polymorphisms and risk of intracerebral haemorrhage.
[So] Source:J Int Med Res;44(3):444-52, 2016 Jun.
[Is] ISSN:1473-2300
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To determine whether endothelin converting enzyme-1 (ECE1) gene polymorphisms contribute to susceptibility to intracerebral haemorrhage (ICH) by influencing blood pressure. METHODS: This case-control study enrolled patients with ICH and healthy control subjects from a Southern Han Chinese population. The ECE1 gene polymorphisms rs212528 and rs213045 were genotyped. The association between the genotypes and the risk of ICH was assessed. The effects of these two ECE1 gene polymorphisms on blood pressure were also analysed. RESULTS: A total of 389 patients with ICH and 404 healthy control subjects participated in the study. There was no significant association between the ECE1 rs212528 and rs213045 polymorphisms and ICH even after adjusting for different confounding variables. In patients with ICH, the systolic blood pressure of patients with the rs212528 AA genotype was significantly lower than that of patients with the AG/GG genotypes. CONCLUSIONS: These results indicated that the ECE1 rs212528 and rs213045 polymorphisms had no major role to play in the genetic susceptibility to ICH, although rs212528 might influence blood pressure in patients with ICH.
[Mh] Termos MeSH primário: Hemorragia Cerebral/genética
Hemorragia Cerebral/fisiopatologia
Enzimas Conversoras de Endotelina/genética
Estudos de Associação Genética
Predisposição Genética para Doença
Polimorfismo de Nucleotídeo Único/genética
[Mh] Termos MeSH secundário: Estudos de Casos e Controles
Demografia
Feminino
Seres Humanos
Masculino
Meia-Idade
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.4.24.71 (ECE1 protein, human); EC 3.4.24.71 (Endothelin-Converting Enzymes)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160403
[St] Status:MEDLINE
[do] DOI:10.1177/0300060516635385


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[PMID]:26931059
[Au] Autor:Smith AI; Rajapakse NW; Kleifeld O; Lomonte B; Sikanyika NL; Spicer AJ; Hodgson WC; Conroy PJ; Small DH; Kaye DM; Parkington HC; Whisstock JC; Kuruppu S
[Ad] Endereço:Department of Biochemistry &Molecular Biology, Biomedical Discovery Institute, Monash University, Clayton, Vic 3800, Australia.
[Ti] Título:N-terminal domain of Bothrops asper Myotoxin II Enhances the Activity of Endothelin Converting Enzyme-1 and Neprilysin.
[So] Source:Sci Rep;6:22413, 2016 Mar 02.
[Is] ISSN:2045-2322
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Neprilysin (NEP) and endothelin converting enzyme-1 (ECE-1) are two enzymes that degrade amyloid beta in the brain. Currently there are no molecules to stimulate the activity of these enzymes. Here we report, the discovery and characterisation of a peptide referred to as K49-P1-20, from the venom of Bothrops asper which directly enhances the activity of both ECE-1 and NEP. This is evidenced by a 2- and 5-fold increase in the Vmax of ECE-1 and NEP respectively. The K49-P1-20 concentration required to achieve 50% of maximal stimulation (AC50) of ECE-1 and NEP was 1.92 ± 0.07 and 1.33 ± 0.12 µM respectively. Using BLITZ biolayer interferometry we have shown that K49-P1-20 interacts directly with each enzyme. Intrinsic fluorescence of the enzymes change in the presence of K49-P1-20 suggesting a change in conformation. ECE-1 mediated reduction in the level of endogenous soluble amyloid beta 42 in cerebrospinal fluid is significantly higher in the presence of K49-P1-20 (31 ± 4% of initial) compared with enzyme alone (11 ± 5% of initial; N = 8, P = 0.005, unpaired t-test). K49-P1-20 could be an excellent research tool to study mechanism(s) of enzyme stimulation, and a potential novel drug lead in the fight against Alzheimer's disease.
[Mh] Termos MeSH primário: Enzimas Conversoras de Endotelina/metabolismo
Fosfolipases A2 do Grupo II/química
Fosfolipases A2 do Grupo II/farmacologia
Neprilisina/metabolismo
Proteínas de Répteis/química
Proteínas de Répteis/farmacologia
[Mh] Termos MeSH secundário: Alanina/metabolismo
Sequência de Aminoácidos
Ativação Enzimática/efeitos dos fármacos
Ensaios Enzimáticos
Células HEK293
Seres Humanos
Cinética
Peptídeos/química
Peptídeos/metabolismo
Domínios Proteicos
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Peptides); 0 (Reptilian Proteins); EC 3.1.1.4 (Group II Phospholipases A2); EC 3.1.1.4 (myotoxin II, Bothrops asper); EC 3.4.24.11 (Neprilysin); EC 3.4.24.71 (Endothelin-Converting Enzymes); OF5P57N2ZX (Alanine)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170420
[Lr] Data última revisão:
170420
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160303
[St] Status:MEDLINE
[do] DOI:10.1038/srep22413


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[PMID]:26806547
[Au] Autor:Boratkó A; Veréb Z; Petrovski G; Csortos C
[Ad] Endereço:Department of Medical Chemistry, Faculty of Medicine, University of Debrecen, Egyetem tér 1, Debrecen H-4032, Hungary.
[Ti] Título:TIMAP-protein phosphatase 1-complex controls endothelin-1 production via ECE-1 dephosphorylation.
[So] Source:Int J Biochem Cell Biol;73:11-18, 2016 Apr.
[Is] ISSN:1878-5875
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Endothelin induced signaling pathways can affect blood pressure and vascular tone, but the influence of endothelins on tumor cells is also significant. We have detected elevated endothelin-1 secretion from TIMAP (TGF-ß inhibited membrane associated protein) depleted vascular endothelial cells. The autocrine signaling activated by the elevated endothelin-1 level through the ETB receptors evoked an angiogenic-like phenotype, the cells assumed an elongated morphology, and enhanced tube formation and wound healing abilities. The depleted protein, TIMAP, is a highly specific and abundant protein in the endothelial cells, and it is a regulatory/targeting subunit for the catalytic subunit of protein phosphatase 1 (PP1c). Protein-protein interaction between the TIMAP-PP1c complex and the endothelin converting enzyme-1 (ECE-1) was detected, the latter of which is a transmembrane protein that produces the biologically active 21-amino acid form of endothelin-1 from proendothelin. The results indicate that silencing of TIMAP induces a reduction in TIMAP-PP1c activity connected to ECE-1. This leads to an increase in the amount of ECE-1 protein in the plasma membrane and a consequent increase in endothelin-1 secretion. Similarly, activation of PKC, the kinase responsible for ECE-1 phosphorylation increased ECE-1 protein level in the membrane fraction of the endothelial cells. The elevated ECE-1 level was mitigated in time in normal cells, but was clearly preserved in TIMAP-depleted cells. Overall, our results indicate that PKC-phosphorylated ECE-1 is a TIMAP-PP1c substrate and this phosphatase complex has an important role in endothelin-1 production of EC through the regulation of ECE-1 activity.
[Mh] Termos MeSH primário: Células Endoteliais/metabolismo
Endotelina-1/metabolismo
Enzimas Conversoras de Endotelina/metabolismo
Proteínas de Membrana/metabolismo
[Mh] Termos MeSH secundário: Western Blotting
Linhagem Celular
Endotelina-1/genética
Enzimas Conversoras de Endotelina/genética
Imunofluorescência
Seres Humanos
Imunoprecipitação
Proteínas de Membrana/genética
Modelos Biológicos
Fosforilação
RNA Interferente Pequeno/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Endothelin-1); 0 (Membrane Proteins); 0 (PPP1R16B protein, human); 0 (RNA, Small Interfering); EC 3.4.24.71 (ECE1 protein, human); EC 3.4.24.71 (Endothelin-Converting Enzymes)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170728
[Lr] Data última revisão:
170728
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160126
[St] Status:MEDLINE



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