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[PMID]:28450398
[Au] Autor:Dickey DM; Otto NM; Potter LR
[Ad] Endereço:From the Department of Biochemistry, Molecular Biology, and Biophysics and.
[Ti] Título:Skeletal overgrowth-causing mutations mimic an allosterically activated conformation of guanylyl cyclase-B that is inhibited by 2,4,6,-trinitrophenyl ATP.
[So] Source:J Biol Chem;292(24):10220-10229, 2017 06 16.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Activating mutations in the receptor for C-type natriuretic peptide (CNP), guanylyl cyclase B (GC-B, also known as Npr2 or NPR-B), increase cellular cGMP and cause skeletal overgrowth, but how these mutations affect GTP catalysis is poorly understood. The A488P and R655C mutations were compared with the known mutation V883M. Neither mutation affected GC-B concentrations. The A488P mutation decreased the EC 5-fold, increased 2.6-fold, and decreased the 13-fold, whereas the R655C mutation decreased the EC 5-fold, increased the 2.1-fold, and decreased the 4.7-fold. Neither mutation affected maximum activity at saturating CNP concentrations. Activation by R655C did not require disulfide bond formation. Surprisingly, the A488P mutant only activated the receptor when it was phosphorylated. In contrast, the R655C mutation converted GC-B-7A from CNP-unresponsive to CNP-responsive. Interestingly, neither mutant was activated by ATP, and the and Hill coefficient of each mutant assayed in the absence of ATP were similar to those of wild-type GC-B assayed in the presence of ATP. Finally, 1 mm 2,4,6,-trinitrophenyl ATP inhibited all three mutants by as much as 80% but failed to inhibit WT-GC-B. We conclude that 1) the A488P and R655C missense mutations result in a GC-B conformation that mimics the allosterically activated conformation, 2) GC-B phosphorylation is required for CNP-dependent activation by the A488P mutation, 3) the R655C mutation abrogates the need for phosphorylation in receptor activation, and 4) an ATP analog selectively inhibits the GC-B mutants, indicating that a pharmacologic approach could reduce GC-B dependent human skeletal overgrowth.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/análogos & derivados
Doenças do Desenvolvimento Ósseo/genética
Inibidores Enzimáticos/farmacologia
Modelos Moleculares
Mutação
Peptídeo Natriurético Tipo C/metabolismo
Receptores do Fator Natriurético Atrial/antagonistas & inibidores
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/farmacologia
Regulação Alostérica
Substituição de Aminoácidos
Doenças do Desenvolvimento Ósseo/metabolismo
GMP Cíclico/metabolismo
Guanosina Trifosfato/metabolismo
Células HEK293
Seres Humanos
Cinética
Mutagênese Sítio-Dirigida
Mutação de Sentido Incorreto
Fosforilação
Conformação Proteica
Processamento de Proteína Pós-Traducional
Receptores do Fator Natriurético Atrial/química
Receptores do Fator Natriurético Atrial/genética
Receptores do Fator Natriurético Atrial/metabolismo
Proteínas Recombinantes/química
Proteínas Recombinantes/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Recombinant Proteins); 127869-51-6 (Natriuretic Peptide, C-Type); 61368-63-6 (2',3'-O-(2,4,6-trinitro-cyclohexadienylidine)adenosine 5'-triphosphate); 86-01-1 (Guanosine Triphosphate); 8L70Q75FXE (Adenosine Triphosphate); EC 4.6.1.2 (Receptors, Atrial Natriuretic Factor); EC 4.6.1.2 (atrial natriuretic factor receptor B); H2D2X058MU (Cyclic GMP)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171228
[Lr] Data última revisão:
171228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.780536


  2 / 1200 MEDLINE  
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[PMID]:28676526
[Au] Autor:Wilson MO; McNeill BA; Barrell GK; Prickett TCR; Espiner EA
[Ad] Endereço:Faculty of Agriculture and Life SciencesLincoln University, Christchurch, New Zealand michele.wilson@lincolnuni.ac.nz.
[Ti] Título:Dexamethasone increases production of C-type natriuretic peptide in the sheep brain.
[So] Source:J Endocrinol;235(1):15-25, 2017 Oct.
[Is] ISSN:1479-6805
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Although C-type natriuretic peptide (CNP) has high abundance in brain tissues and cerebrospinal fluid (CSF), the source and possible factors regulating its secretion within the central nervous system (CNS) are unknown. Here we report the dynamic effects of a single IV bolus of dexamethasone or saline solution on plasma, CSF, CNS and pituitary tissue content of CNP products in adult sheep, along with changes in CNP gene expression in selected tissues. Both CNP and NTproCNP (the amino-terminal product of proCNP) in plasma and CSF showed dose-responsive increases lasting 12-16 h after dexamethasone, whereas other natriuretic peptides were unaffected. CNS tissue concentrations of CNP and NTproCNP were increased by dexamethasone in all of the 12 regions examined. Abundance was highest in limbic tissues, pons and medulla oblongata. Relative to controls, CNP gene expression ( ) was upregulated by dexamethasone in 5 of 7 brain tissues examined. Patterns of responses differed in pituitary tissue. Whereas the abundance of CNP in both lobes of the pituitary gland greatly exceeded that of brain tissues, neither CNP nor NTproCNP concentration was affected by dexamethasone, despite an increase in expression. This is the first report of enhanced production and secretion of CNP in brain tissues in response to a corticosteroid. Activation of CNP secretion within CNS tissues by dexamethasone, not exhibited by other natriuretic peptides, suggests an important role for CNP in settings of acute stress. Differential findings in pituitary tissues likely relate to altered processing of proCNP storage and secretion.
[Mh] Termos MeSH primário: Encéfalo/metabolismo
Dexametasona/farmacologia
Peptídeo Natriurético Tipo C/metabolismo
[Mh] Termos MeSH secundário: Animais
Encéfalo/efeitos dos fármacos
Feminino
Ovinos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
127869-51-6 (Natriuretic Peptide, C-Type); 7S5I7G3JQL (Dexamethasone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170706
[St] Status:MEDLINE
[do] DOI:10.1530/JOE-17-0148


  3 / 1200 MEDLINE  
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[PMID]:28377431
[Au] Autor:Wong PC; Guo J; Zhang A
[Ad] Endereço:Department of Cardiology, First Affiliated Hospital of Jinan University, Guangzhou, China.
[Ti] Título:The renal and cardiovascular effects of natriuretic peptides.
[So] Source:Adv Physiol Educ;41(2):179-185, 2017 Jun 01.
[Is] ISSN:1522-1229
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The landmark report by de Bold et al. in 1981 signified the heart as one of the endocrine organs involved in fluid and salt balance (de Bold AJ, Borenstein HB, Veress AT, Sonnenberg H. 28: 89-94, 1981). Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are secreted from cardiomyocytes in response to cardiac stretch as in the case of heart failure, whereas C-type natriuretic peptide (CNP) is secreted from endothelial and renal cells in response to cytokines and endothelium-dependent agonists, such as acetylcholine. Binding ANP or BNP to natriuretic peptide receptor A induces cyclic guanylyl monophosphate as second messenger in the target cells to mediate the following: natriuresis; water diuresis; increasing glomerular filtration rate; decreasing systemic sympathetic activities; plasma volume; cardiac output and blood pressure; and curbing mitoses of heart fibroblasts and hypertrophy of cardiovascular muscle cells. ANP, BNP, and CNP are cleared from the bloodstream by natriuretic peptide receptor C and degraded by an ectoenzyme called neprilysin (NEP). The plasma levels of BNP are typically >100 pg/ml in patients with congestive heart failure. Sacubitril/valsartan is an angiotensin receptor NEP inhibitor that prevents the clinical progression of surviving patients with heart failure more effectively than enalapril, an angiotensin-converting enzyme inhibitor. A thorough understanding of the renal and cardiovascular effects of natriuretic peptides is of major importance for first-year medical students to gain insight into the significance of plasma levels of BNP in patients with heart failure.
[Mh] Termos MeSH primário: Insuficiência Cardíaca/sangue
Peptídeos Natriuréticos/sangue
Peptídeos Natriuréticos/metabolismo
[Mh] Termos MeSH secundário: Aminobutiratos/uso terapêutico
Fator Natriurético Atrial/sangue
Fator Natriurético Atrial/metabolismo
Progressão da Doença
Enalapril/uso terapêutico
Insuficiência Cardíaca/tratamento farmacológico
Seres Humanos
Rim/fisiopatologia
Peptídeo Natriurético Encefálico/sangue
Peptídeo Natriurético Encefálico/metabolismo
Peptídeo Natriurético Tipo C/sangue
Peptídeo Natriurético Tipo C/metabolismo
Tetrazóis/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminobutyrates); 0 (LCZ 696); 0 (Natriuretic Peptides); 0 (Tetrazoles); 114471-18-0 (Natriuretic Peptide, Brain); 127869-51-6 (Natriuretic Peptide, C-Type); 69PN84IO1A (Enalapril); 85637-73-6 (Atrial Natriuretic Factor)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170406
[St] Status:MEDLINE
[do] DOI:10.1152/advan.00177.2016


  4 / 1200 MEDLINE  
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[PMID]:28277543
[Au] Autor:Liu W; Xin Q; Wang X; Wang S; Wang H; Zhang W; Yang Y; Zhang Y; Zhang Z; Wang C; Xu Y; Duan E; Xia G
[Ad] Endereço:State Key Laboratory of Agrobiotechnology, College of Biological Sciences, China Agricultural University, No. 2 Yuanmingyuan West Road, Beijing 100193, China.
[Ti] Título:Estrogen receptors in granulosa cells govern meiotic resumption of pre-ovulatory oocytes in mammals.
[So] Source:Cell Death Dis;8(3):e2662, 2017 Mar 09.
[Is] ISSN:2041-4889
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In mammals, oocytes are arrested at the diplotene stage of meiosis I until the pre-ovulatory luteinizing hormone (LH) surge triggers meiotic resumption through the signals in follicular granulosa cells. In this study, we show that the estradiol (E2)-estrogen receptors (ERs) system in follicular granulosa cells has a dominant role in controlling oocyte meiotic resumption in mammals. We found that the expression of ERs was controlled by gonadotropins under physiological conditions. E2-ERs system was functional in maintaining oocyte meiotic arrest by regulating the expression of natriuretic peptide C and natriuretic peptide receptor 2 (NPPC/NPR2), which was achieved through binding to the promoter regions of Nppc and Npr2 genes directly. In ER knockout mice, meiotic arrest was not sustained by E2 in most cumulus-oocyte complexes in vitro and meiosis resumed precociously in pre-ovulatory follicles in vivo. In human granulosa cells, similar conclusions are reached that ER levels were controlled by gonadotropins and E2-ERs regulated the expression of NPPC/NPR2 levels. In addition, our results revealed that the different regulating patterns of follicle-stimulating hormone and LH on ER levels in vivo versus in vitro determined their distinct actions on oocyte maturation. Taken together, these findings suggest a critical role of E2-ERs system during oocyte meiotic progression and may propose a novel approach for oocyte in vitro maturation treatment in clinical practice.
[Mh] Termos MeSH primário: Meiose/genética
Peptídeo Natriurético Tipo C/genética
Receptores do Fator Natriurético Atrial/genética
Receptores de Estradiol/genética
Receptores Estrogênicos/genética
[Mh] Termos MeSH secundário: Animais
Feminino
Regulação da Expressão Gênica no Desenvolvimento
Células da Granulosa/metabolismo
Seres Humanos
Técnicas de Maturação in Vitro de Oócitos
Hormônio Luteinizante/genética
Camundongos Knockout
Oócitos/crescimento & desenvolvimento
Oogênese/genética
Folículo Ovariano/crescimento & desenvolvimento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Estradiol); 0 (Receptors, Estrogen); 127869-51-6 (Natriuretic Peptide, C-Type); 9002-67-9 (Luteinizing Hormone); EC 4.6.1.2 (Receptors, Atrial Natriuretic Factor); EC 4.6.1.2 (atrial natriuretic factor receptor B)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE
[do] DOI:10.1038/cddis.2017.82


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[PMID]:28101584
[Au] Autor:Zenitani M; Nojiri T; Kimura T; Hosoda H; Miura K; Hino J; Nakahata K; Uehara S; Miyazato M; Oue T; Okuyama H; Kangawa K
[Ad] Endereço:Department of Biochemistry, National Cerebral and Cardiovascular Center Research Institute, 5-7-1, Fujishirodai, Suita, Osaka, 565-8565, Japan.
[Ti] Título:Myeloprotective effects of C-type natriuretic peptide on cisplatin-induced bone marrow granulocytopenia in mice.
[So] Source:Cancer Chemother Pharmacol;79(2):363-368, 2017 Feb.
[Is] ISSN:1432-0843
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Cisplatin is an effective chemotherapeutic agent used to treat a variety of malignant tumors. The major toxicity associated with cisplatin treatment is granulocytopenia. C-type natriuretic peptide (CNP), a member of the natriuretic peptide family, protects against toxicity in many organs, including the heart, blood vessels, lung, and kidney. The objective of this study was to investigate the myeloprotective effects of CNP in a mouse model of cisplatin-induced granulocytopenia. METHODS: The mice were divided into two groups: cisplatin with vehicle and cisplatin with CNP. CNP (2.5 µg/kg/min via osmotic pump, subcutaneously) or vehicle administration was started two day before cisplatin injection, and continued until the mice were killed. At 0, 2, 4, 8, and 14 days after cisplatin injection (16 mg/kg, intraperitoneally as a single dose), we counted total and living cells and granulocyte/macrophage colony-forming units (CFU-GM) in bone marrow. In addition, at 0, 1, 2, and 4 days after cisplatin injection, we measured mRNA levels of CXC chemokine receptor 4 (CXCR4) and chemokine CXC ligand 12 (CXCL12) in bone marrow. RESULTS: CNP significantly attenuated the reduction in bone marrow nucleated cell count and CFU-GM in bone marrow at 4 days after cisplatin injection. Four days after cisplatin injection, CNP significantly decreased the CXCR4 mRNA level in bone marrow, but had no effect on the level of CXCL12 mRNA. CONCLUSIONS: CNP exerts myeloprotective effects in cisplatin-induced granulocytopenia and decreases CXCR4 expression.
[Mh] Termos MeSH primário: Agranulocitose/prevenção & controle
Medula Óssea/efeitos dos fármacos
Cisplatino/toxicidade
Peptídeo Natriurético Tipo C/farmacologia
[Mh] Termos MeSH secundário: Animais
Quimiocina CXCL12/genética
Camundongos
Camundongos Endogâmicos C57BL
Substâncias Protetoras/farmacologia
RNA Mensageiro/análise
Receptores CXCR4/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCR4 protein, mouse); 0 (Chemokine CXCL12); 0 (Cxcl12 protein, mouse); 0 (Protective Agents); 0 (RNA, Messenger); 0 (Receptors, CXCR4); 127869-51-6 (Natriuretic Peptide, C-Type); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170606
[Lr] Data última revisão:
170606
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170120
[St] Status:MEDLINE
[do] DOI:10.1007/s00280-016-3221-5


  6 / 1200 MEDLINE  
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[PMID]:28062626
[Au] Autor:Prickett TC; Doughty RN; Troughton RW; Frampton CM; Whalley GA; Ellis CJ; Espiner EA; Richards AM
[Ad] Endereço:Department of Medicine, University of Otago, Christchurch, New Zealand; tim.prickett@otago.ac.nz.
[Ti] Título:C-Type Natriuretic Peptides in Coronary Disease.
[So] Source:Clin Chem;63(1):316-324, 2017 Jan.
[Is] ISSN:1530-8561
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIMS: C-type natriuretic peptide (CNP) is a paracrine growth factor expressed in the vascular endothelium. Although upregulated in atheromatous arteries, the predictive value of plasma CNP products for outcome in coronary disease is unknown. This study aimed to compare the prognostic value of plasma CNP products with those of other natriuretic peptides in individuals with coronary artery disease, and investigate their associations with cardiac and renal function. METHODS AND RESULTS: Plasma concentrations of CNP and amino-terminal proCNP (NT-proCNP) were measured at baseline in 2129 individuals after an index acute coronary syndrome admission and related to cardiac and renal function, other natriuretic peptides [atrial NP (ANP) and B-type NP (BNP)] and prognosis (primary end point, mortality; secondary end point, cardiac readmission). Median follow-up was 4 years. At baseline, and in contrast to CNP, ANP, and BNP, plasma NT-proCNP was higher in males and weakly related to cardiac function but strongly correlated to plasma creatinine. All NPs were univariately associated with mortality. Resampling at 4 and 12 months in survivors showed stable concentrations of NT-proCNP whereas all other peptides declined. When studied by diagnosis (myocardial infarction, unstable angina) at index admission using a multivariate model, NT-proBNP predicted mortality and readmission in myocardial infarction. In unstable angina, only NT-proCNP predicted both mortality and cardiac readmission. CONCLUSIONS: In contrast to the close association of NT-proBNP with cardiac function, and predictive value for outcome after myocardial infarction, plasma NT-proCNP is highly correlated with renal function and is an independent predictor of mortality and cardiac readmission in individuals with unstable angina.
[Mh] Termos MeSH primário: Doença da Artéria Coronariana/sangue
Peptídeo Natriurético Tipo C/sangue
[Mh] Termos MeSH secundário: Idoso
Biomarcadores/sangue
Doença da Artéria Coronariana/diagnóstico
Doença da Artéria Coronariana/mortalidade
Feminino
Seres Humanos
Masculino
Meia-Idade
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 127869-51-6 (Natriuretic Peptide, C-Type)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170606
[Lr] Data última revisão:
170606
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170108
[St] Status:MEDLINE
[do] DOI:10.1373/clinchem.2016.257816


  7 / 1200 MEDLINE  
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[PMID]:28049696
[Au] Autor:Nakao K; Kuwahara K; Nishikimi T; Nakagawa Y; Kinoshita H; Minami T; Kuwabara Y; Yamada C; Yamada Y; Tokudome T; Nagai-Okatani C; Minamino N; Nakao YM; Yasuno S; Ueshima K; Sone M; Kimura T; Kangawa K; Nakao K
[Ad] Endereço:From the Department of Medicine and Clinical Science (Kazuhiro Nakao, K. Kuwahara, T.N., Y.N., H.K., T.M., Y.K., C.Y., Y.Y., M.S., Kazuwa Nakao), Department of Peptide Research (Kazuhiro Nakao, Y.Y., K. Kangawa), Medical Innovation Center (Kazuwa Nakao), and Department of Cardiovascular Medicine (K.
[Ti] Título:Endothelium-Derived C-Type Natriuretic Peptide Contributes to Blood Pressure Regulation by Maintaining Endothelial Integrity.
[So] Source:Hypertension;69(2):286-296, 2017 Feb.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We previously reported the secretion of C-type natriuretic peptide (CNP) from vascular endothelial cells and proposed the existence of a vascular natriuretic peptide system composed of endothelial CNP and smooth muscle guanylyl cyclase-B (GC-B), the CNP receptor, and involved in the regulation of vascular tone, remodeling, and regeneration. In this study, we assessed the functional significance of this system in the regulation of blood pressure in vivo using vascular endothelial cell-specific CNP knockout and vascular smooth muscle cell-specific GC-B knockout mice. These mice showed neither the skeletal abnormality nor the early mortality observed in systemic CNP or GC-B knockout mice. Endothelial cell-specific CNP knockout mice exhibited significantly increased blood pressures and an enhanced acute hypertensive response to nitric oxide synthetase inhibition. Acetylcholine-induced, endothelium-dependent vasorelaxation was impaired in rings of mesenteric artery isolated from endothelial cell-specific CNP knockout mice. In addition, endothelin-1 gene expression was enhanced in pulmonary vascular endothelial cells from endothelial cell-specific CNP knockout mice, which also showed significantly higher plasma endothelin-1 concentrations and a greater reduction in blood pressure in response to an endothelin receptor antagonist than their control littermates. By contrast, vascular smooth muscle cell-specific GC-B knockout mice exhibited blood pressures similar to control mice, and acetylcholine-induced vasorelaxation was preserved in their isolated mesenteric arteries. Nonetheless, CNP-induced acute vasorelaxation was nearly completely abolished in mesenteric arteries from vascular smooth muscle cell-specific GC-B knockout mice. These results demonstrate that endothelium-derived CNP contributes to the chronic regulation of vascular tone and systemic blood pressure by maintaining endothelial function independently of vascular smooth muscle GC-B.
[Mh] Termos MeSH primário: Pressão Sanguínea/fisiologia
Endotélio Vascular/metabolismo
Hipertensão/sangue
Músculo Liso Vascular/fisiopatologia
Peptídeo Natriurético Tipo C/sangue
Vasoconstrição/fisiologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Endotélio Vascular/fisiopatologia
Hipertensão/fisiopatologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Músculo Liso Vascular/metabolismo
Vasodilatação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
127869-51-6 (Natriuretic Peptide, C-Type)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170809
[Lr] Data última revisão:
170809
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170105
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.116.08219


  8 / 1200 MEDLINE  
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[PMID]:27780485
[Au] Autor:Caixeta FM; Sousa RV; Guimarães AL; Leme LO; Sprícigo JF; Netto SB; Pivato I; Dode MA
[Ad] Endereço:School of Agriculture and Veterinary Medicine,University of Brasilia,Brasília-DF,Brazil.
[Ti] Título:Meiotic arrest as an alternative to increase the production of bovine embryos by somatic cell nuclear transfer.
[So] Source:Zygote;25(1):32-40, 2017 Feb.
[Is] ISSN:1469-8730
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:This study aimed to evaluate the effect of meiotic arrest using phosphodiesterase type 3A (PDE 3A) inhibitors, cilostamide and C-type natriuretic peptide (NPPC), on pre-maturation (PM) of oocytes to be used in the production of cloned embryos. Nuclear maturation, in vitro embryo production (IVP), somatic cell nuclear transfer (SCNT) and parthenogenetic activation (PA), and total cells number of cloned embryos were evaluated. The results were analysed by chi-squared and Kruskal-Wallis test with a P-value 0.05) between control and PM, both for cleavage (78.2% and 76.9%) and blastocyst (35.5% and 29.3%) rates. After SCNT, cleavage rate was also similar (P > 0.05) between control and PM (66% and 51.9%) however, blastocyst rate was lower (P < 0.05) in the PM group than in the control group (7.4% and 30.2%). After 6 h of PM with 100 nM of NPPC, approximately 84.9% of the oocytes remained at GV. No difference was found between control and PM in cleavage (69.2% and 76.1%) and blastocyst rates (37,4% and 35%) after IVP. Similarly, no differences between PM and control groups were observed for cleavage (69.2% and 68.4%) and blastocyst (24.4% and 21.5%) rates. SCNT and PA embryos from control or PM oocytes had similar total cell number. It can be concluded that PM for 6 h with 100 nM NPPC is feasible for cloned embryo production without affecting embryo outcome.
[Mh] Termos MeSH primário: Clonagem de Organismos/métodos
Meiose/efeitos dos fármacos
Técnicas de Transferência Nuclear
Oócitos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Bovinos
Nucleotídeo Cíclico Fosfodiesterase do Tipo 3/metabolismo
Técnicas de Cultura Embrionária
Embrião de Mamíferos/citologia
Feminino
Peptídeo Natriurético Tipo C/farmacologia
Oócitos/citologia
Oócitos/fisiologia
Partenogênese
Inibidores da Fosfodiesterase 3/farmacologia
Quinolonas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Phosphodiesterase 3 Inhibitors); 0 (Quinolones); 127869-51-6 (Natriuretic Peptide, C-Type); 45S5605Q18 (cilostamide); EC 3.1.4.17 (Cyclic Nucleotide Phosphodiesterases, Type 3)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170411
[Lr] Data última revisão:
170411
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161027
[St] Status:MEDLINE
[do] DOI:10.1017/S0967199416000289


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[PMID]:27761784
[Au] Autor:Zhang T; Zhang C; Fan X; Li R; Zhang J
[Ad] Endereço:Key Laboratory of Animal Genetics, Breeding and Reproduction, College of Animal Science, Inner Mongolia Agricultural University, 306 Zhaowuda Road, Hohhot, Inner Mongolia, 010018, China.
[Ti] Título:Effect of C-type natriuretic peptide pretreatment on in vitro bovine oocyte maturation.
[So] Source:In Vitro Cell Dev Biol Anim;53(3):199-206, 2017 Mar.
[Is] ISSN:1543-706X
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:C-type natriuretic peptide (CNP) has been considered as a physiological meiotic inhibitor that stimulates the cGMP production by cumulus cell natriuretic peptide receptor 2 (NPR2), which inhibits oocyte phosphodiesterase type 3 activity and increases cAMP. In this study, we explored the effect of CNP pretreatment on the in vitro maturation (IVM) of bovine oocytes by examining changes in cleavage rate, blastocyst formation, mitochondrial DNA (mtDNA) copy number, reactive oxygen species (ROS) level, glutathione (GSH) content, and redox state. Our results showed that 200 nM CNP could effectively maintain meiotic arrest of bovine oocytes in vitro within 6 h. The two-step IVM system in which oocytes were pretreated with 200 nM CNP for 6 h and then cultured IVM for 28 h yielded a significantly (P < 0.05) increased blastocyst rate and cell number after in vitro fertilization (IVF) while compared to the conventional one-step IVM method. In addition, in comparison with the conventional 24-h matured oocyte, oocytes pretreated with 200 nM CNP for 6 h followed by 28 h IVM resulted in significantly (P < 0.05) higher mtDNA copy number and ROS levels in oocytes, while GSH level significantly (P < 0.05) decreased. Remarkably, regardless of treatment, no changes were observed in FAD++, NAD(P)H autofluorescence intensity, and redox ratio (FAD++/NAD(P)H) within the oocytes, maintaining a healthy metabolic equilibrium of redox throughout the two-step IVM. In conclusion, these results indicate that CNP pretreatment could dramatically improve the quality of bovine oocytes during in vitro maturation.
[Mh] Termos MeSH primário: Técnicas de Maturação in Vitro de Oócitos/métodos
Peptídeo Natriurético Tipo C/farmacologia
Oócitos/crescimento & desenvolvimento
Oogênese/genética
[Mh] Termos MeSH secundário: Animais
Blastocisto/citologia
Blastocisto/efeitos dos fármacos
Bovinos
Desenvolvimento Embrionário/efeitos dos fármacos
Feminino
Fertilização In Vitro/métodos
Meiose/efeitos dos fármacos
Oócitos/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
127869-51-6 (Natriuretic Peptide, C-Type)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171105
[Lr] Data última revisão:
171105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161021
[St] Status:MEDLINE
[do] DOI:10.1007/s11626-016-0101-6


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[PMID]:27406184
[Au] Autor:Lobo MD; Sobotka PA; Pathak A
[Ad] Endereço:Barts BP Centre of Excellence, Barts Heart Centre, St Bartholomew's Hospital, Barts Health NHS Trust, London, UK.
[Ti] Título:Interventional procedures and future drug therapy for hypertension.
[So] Source:Eur Heart J;38(15):1101-1111, 2017 Apr 14.
[Is] ISSN:1522-9645
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Hypertension management poses a major challenge to clinicians globally once non-drug (lifestyle) measures have failed to control blood pressure (BP). Although drug treatment strategies to lower BP are well described, poor control rates of hypertension, even in the first world, suggest that more needs to be done to surmount the problem. A major issue is non-adherence to antihypertensive drugs, which is caused in part by drug intolerance due to side effects. More effective antihypertensive drugs are therefore required which have excellent tolerability and safety profiles in addition to being efficacious. For those patients who either do not tolerate or wish to take medication for hypertension or in whom BP control is not attained despite multiple antihypertensives, a novel class of interventional procedures to manage hypertension has emerged. While most of these target various aspects of the sympathetic nervous system regulation of BP, an additional procedure is now available, which addresses mechanical aspects of the circulation. Most of these new devices are supported by early and encouraging evidence for both safety and efficacy, although it is clear that more rigorous randomized controlled trial data will be essential before any of the technologies can be adopted as a standard of care.
[Mh] Termos MeSH primário: Hipertensão/terapia
[Mh] Termos MeSH secundário: Antagonistas de Receptores de Angiotensina/uso terapêutico
Anti-Hipertensivos/uso terapêutico
Derivação Arteriovenosa Cirúrgica/métodos
Derivação Arteriovenosa Cirúrgica/tendências
Barorreflexo/fisiologia
Ablação por Cateter/tendências
Ensaios Clínicos como Assunto
Estimulação Encefálica Profunda/métodos
Estimulação Encefálica Profunda/tendências
Venenos Elapídicos/agonistas
Medicina Baseada em Evidências
Previsões
Seres Humanos
Hipertensão/genética
Hipertensão/imunologia
Antagonistas de Receptores de Mineralocorticoides/uso terapêutico
Peptídeo Natriurético Tipo C/agonistas
Neprilisina/antagonistas & inibidores
Regeneração Nervosa/fisiologia
Norepinefrina/antagonistas & inibidores
Peptídeos/uso terapêutico
Sistema Renina-Angiotensina/fisiologia
Simpatectomia/métodos
Simpatectomia/tendências
Estimulação Elétrica Nervosa Transcutânea/métodos
Estimulação Elétrica Nervosa Transcutânea/tendências
Peptídeo Intestinal Vasoativo/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Angiotensin Receptor Antagonists); 0 (Antihypertensive Agents); 0 (CD-NP natriuretic peptide); 0 (Elapid Venoms); 0 (Mineralocorticoid Receptor Antagonists); 0 (Peptides); 0 (serum sodium transport inhibitor); 127869-51-6 (Natriuretic Peptide, C-Type); 37221-79-7 (Vasoactive Intestinal Peptide); EC 3.4.24.11 (Neprilysin); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160714
[St] Status:MEDLINE
[do] DOI:10.1093/eurheartj/ehw303



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