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Pesquisa : D03.633.100.759.646.138.124.070.125.195 [Categoria DeCS]
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  1 / 699 MEDLINE  
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[PMID]:28636353
[Au] Autor:Takano S; Tsuzuki T; Murayama T; Kameda T; Kumaki Y; Sakurai T; Fukuda H; Watanabe M; Arisawa M; Shuto S
[Ti] Título:Synthesis of 8-Substituted Analogues of Cyclic ADP-4-Thioribose and Their Unexpected Identification as Ca -Mobilizing Full Agonists.
[So] Source:J Med Chem;60(13):5868-5875, 2017 Jul 13.
[Is] ISSN:1520-4804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A series of 8-substituted analogues of cyclic ADP-4-thioribose (cADPtR, 3), which is a stable equivalent of Ca -mobilizing second messenger cyclic ADP-ribose (cADPR, 1), were designed as potential pharmacological tools for studies on cADPR-modulated Ca signaling pathways. These 8-amino analogue (8-NH -cADPtR, 4), 8-azido analogue (8-N -cADPtR, 5), and 8-chloro analogue (8-Cl-cADPtR, 6) were efficiently synthesized, where the stereoselective N1-ß-thioribosyladenine ring closure reaction via an α/ß-equilibrium of the 1-aminothioribose derivative and construction of the characteristic 18-membered pyrophosphate ring by Ag -promoted activation of a phenyl phosphorothioate type substrate were the two key steps. Although 8-NH -cADPR (2) is a well-known potent antagonist against cADPR-inducing Ca -release, the 4-thioribose congener 8-NH -cADPtR turned out unexpectedly to be a full agonist in sea urchin egg homogenate evaluation system. This important finding suggested that the ring-oxygen in the N1-ribose of cADPR analogues is essential for the antagonistic activity in the Ca -signaling pathway, which can contribute to clarify the structure-agonist/antagonist activity relationship.
[Mh] Termos MeSH primário: Sinalização do Cálcio/efeitos dos fármacos
ADP-Ribose Cíclica/análogos & derivados
ADP-Ribose Cíclica/farmacologia
[Mh] Termos MeSH secundário: Animais
Azidas/química
Azidas/farmacologia
Cálcio/metabolismo
ADP-Ribose Cíclica/química
Halogenação
Modelos Moleculares
Ouriços-do-Mar/efeitos dos fármacos
Ouriços-do-Mar/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Azides); 119340-53-3 (Cyclic ADP-Ribose); 151898-25-8 (8-aminoadenosine cyclic 3',5'-(hydrogen phosphate) 5'-ribofuranosyl ester); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jmedchem.7b00540


  2 / 699 MEDLINE  
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[PMID]:28539361
[Au] Autor:Lin WK; Bolton EL; Cortopassi WA; Wang Y; O'Brien F; Maciejewska M; Jacobson MP; Garnham C; Ruas M; Parrington J; Lei M; Sitsapesan R; Galione A; Terrar DA
[Ad] Endereço:From the Department of Pharmacology, University of Oxford, Mansfield Road, Oxford OX1 3QT, United Kingdom.
[Ti] Título:Synthesis of the Ca -mobilizing messengers NAADP and cADPR by intracellular CD38 enzyme in the mouse heart: Role in ß-adrenoceptor signaling.
[So] Source:J Biol Chem;292(32):13243-13257, 2017 Aug 11.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nicotinic acid adenine dinucleotide phosphate (NAADP) and cyclic ADP-ribose (cADPR) are Ca -mobilizing messengers important for modulating cardiac excitation-contraction coupling and pathophysiology. CD38, which belongs to the ADP-ribosyl cyclase family, catalyzes synthesis of both NAADP and cADPR However, it remains unclear whether this is the main enzyme for their production under physiological conditions. Here we show that membrane fractions from WT but not mouse hearts supported NAADP and cADPR synthesis. Membrane permeabilization of cardiac myocytes with saponin and/or Triton X-100 increased NAADP synthesis, indicating that intracellular CD38 contributes to NAADP production. The permeabilization also permitted immunostaining of CD38, with a striated pattern in WT myocytes, whereas myocytes and nonpermeabilized WT myocytes showed little or no staining, without striation. A component of ß-adrenoreceptor signaling in the heart involves NAADP and lysosomes. Accordingly, in the presence of isoproterenol, Ca transients and contraction amplitudes were smaller in myocytes than in the WT. In addition, suppressing lysosomal function with bafilomycin A1 reduced the isoproterenol-induced increase in Ca transients in cardiac myocytes from WT but not mice. Whole hearts isolated from mice and exposed to isoproterenol showed reduced arrhythmias. SAN4825, an ADP-ribosyl cyclase inhibitor that reduces cADPR and NAADP synthesis in mouse membrane fractions, was shown to bind to CD38 in docking simulations and reduced the isoproterenol-induced arrhythmias in WT hearts. These observations support generation of NAADP and cADPR by intracellular CD38, which contributes to effects of ß-adrenoreceptor stimulation to increase both Ca transients and the tendency to disturb heart rhythm.
[Mh] Termos MeSH primário: ADP-Ribosil Ciclase 1/metabolismo
Sinalização do Cálcio
ADP-Ribose Cíclica/metabolismo
Glicoproteínas de Membrana/metabolismo
Miócitos Cardíacos/metabolismo
NADP/análogos & derivados
Retículo Sarcoplasmático/metabolismo
[Mh] Termos MeSH secundário: ADP-Ribosil Ciclase 1/antagonistas & inibidores
Agonistas Adrenérgicos beta/farmacologia
Animais
Antiarrítmicos/química
Antiarrítmicos/metabolismo
Antiarrítmicos/farmacologia
Sinalização do Cálcio/efeitos dos fármacos
Permeabilidade da Membrana Celular/efeitos dos fármacos
Células Cultivadas
Detergentes/farmacologia
Inibidores Enzimáticos/farmacologia
Coração/efeitos dos fármacos
Técnicas In Vitro
Masculino
Glicoproteínas de Membrana/antagonistas & inibidores
Camundongos Endogâmicos C57BL
Camundongos Knockout
Simulação de Acoplamento Molecular
Contração Miocárdica/efeitos dos fármacos
Miócitos Cardíacos/citologia
Miócitos Cardíacos/efeitos dos fármacos
NADP/metabolismo
Transporte Proteico/efeitos dos fármacos
Coelhos
Retículo Sarcoplasmático/efeitos dos fármacos
Retículo Sarcoplasmático/enzimologia
Análise de Célula Única
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic beta-Agonists); 0 (Anti-Arrhythmia Agents); 0 (Detergents); 0 (Enzyme Inhibitors); 0 (Membrane Glycoproteins); 119340-53-3 (Cyclic ADP-Ribose); 53-59-8 (NADP); 5502-96-5 (NAADP); EC 3.2.2.5 (Cd38 protein, mouse); EC 3.2.2.6 (ADP-ribosyl Cyclase 1)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.789347


  3 / 699 MEDLINE  
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[PMID]:28340569
[Au] Autor:Higashida H; Liang M; Yoshihara T; Akther S; Fakhrul A; Stanislav C; Nam TS; Kim UH; Kasai S; Nishimura T; Al Mahmuda N; Yokoyama S; Ishihara K; Gerasimenko M; Salmina A; Zhong J; Tsuji T; Tsuji C; Lopatina O
[Ad] Endereço:Research Centre for Child Mental Development, Kanazawa University, Kanazawa, 920-8640, Japan. haruhiro@med.kanazawa-u.ac.jp.
[Ti] Título:An immunohistochemical, enzymatic, and behavioral study of CD157/BST-1 as a neuroregulator.
[So] Source:BMC Neurosci;18(1):35, 2017 Mar 24.
[Is] ISSN:1471-2202
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Recent rodent and human studies provide evidence in support of the fact that CD157, well known as bone marrow stromal cell antigen-1 (BST-1) and a risk factor in Parkinson's disease, also meaningfully acts in the brain as a neuroregulator and affects social behaviors. It has been shown that social behaviors are impaired in CD157 knockout mice without severe motor dysfunction and that CD157/BST1 gene single nucleotide polymorphisms are associated with autism spectrum disorder in humans. However, it is still necessary to determine how this molecule contributes to the brain's physiological and pathophysiological functions. METHODS: To gain fresh insights about the relationship between the presence of CD157 in the brain and its enzymatic activity, and aberrant social behavior, CD157 knockout mice of various ages were tested. RESULTS: CD157 immunoreactivity colocalized with nestin-positive cells and elements in the ventricular zones in E17 embryos. Brain CD157 mRNA levels were high in neonates but low in adults. Weak but distinct immunoreactivity was detected in several areas in the adult brain, including the amygdala. CD157 has little or no base exchange activity, but some ADP-ribosyl cyclase activity, indicating that CD157 formed cyclic ADP-ribose but much less nicotinic acid adenine dinucleotide phosphate, with both mobilizing Ca from intracellular Ca pools. Social avoidance in CD157 knockout mice was rescued by a single intraperitoneal injection of oxytocin. CONCLUSIONS: CD157 may play a role in the embryonic and adult nervous systems. The functional features of CD157 can be explained in part through the production of cyclic ADP-ribose rather than nicotinic acid adenine dinucleotide phosphate. Further experiments are required to elucidate how the embryonic expression of CD157 in neural stem cells contributes to behaviors in adults or to psychiatric symptoms.
[Mh] Termos MeSH primário: ADP-Ribosil Ciclase/metabolismo
Antígenos CD/metabolismo
Encéfalo/enzimologia
Comportamento Social
[Mh] Termos MeSH secundário: ADP-Ribosil Ciclase/genética
ADP-Ribosil Ciclase 1/genética
ADP-Ribosil Ciclase 1/metabolismo
Animais
Animais Recém-Nascidos
Antígenos CD/genética
Aprendizagem da Esquiva/fisiologia
Encéfalo/embriologia
Encéfalo/crescimento & desenvolvimento
ADP-Ribose Cíclica/metabolismo
Proteínas Ligadas por GPI/genética
Proteínas Ligadas por GPI/metabolismo
Células HEK293
Seres Humanos
Imuno-Histoquímica
Masculino
Glicoproteínas de Membrana/genética
Glicoproteínas de Membrana/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Endogâmicos ICR
Camundongos Knockout
Modelos Animais
NADP/análogos & derivados
NADP/metabolismo
Nestina/metabolismo
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (GPI-Linked Proteins); 0 (Membrane Glycoproteins); 0 (Nes protein, mouse); 0 (Nestin); 0 (RNA, Messenger); 119340-53-3 (Cyclic ADP-Ribose); 53-59-8 (NADP); 5502-96-5 (NAADP); EC 3.2.2.5 (ADP-ribosyl Cyclase); EC 3.2.2.5 (ADP-ribosyl cyclase 2); EC 3.2.2.5 (Cd38 protein, mouse); EC 3.2.2.6 (ADP-ribosyl Cyclase 1)
[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:170326
[St] Status:MEDLINE
[do] DOI:10.1186/s12868-017-0350-7


  4 / 699 MEDLINE  
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[PMID]:27664703
[Au] Autor:Jiao C; Yang R; Gu Z
[Ad] Endereço:College of Food Science and Technology, Nanjing Agricultural University, Nanjing, Jiangsu 210095, People's Republic of China.
[Ti] Título:Cyclic ADP-ribose and IP3 mediate abscisic acid-induced isoflavone accumulation in soybean sprouts.
[So] Source:Biochem Biophys Res Commun;479(3):530-536, 2016 Oct 21.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In this study, the roles of ABA-cADPR-Ca and ABA-IP3-Ca signaling pathways in UV-B-induced isoflavone accumulation in soybean sprouts were investigated. Results showed that abscisic acid (ABA) up regulated cyclic ADP-ribose (cADPR) and inositol 1,4,5-trisphosphate (IP3) levels in soybean sprouts under UV-B radiation. Furthermore, cADPR and IP3, as second messengers of UV-B-triggered ABA, induced isoflavone accumulation by up-regulating proteins and genes expression and activity of isoflavone biosynthetic-enzymes (chalcone synthase, CHS; isoflavone synthase, IFS). After Ca was chelated by EGTA, isoflavone content decreased. Overall, ABA-induced cADPR and IP3 up regulated isoflavone accumulation which was mediated by Ca signaling via enhancing the expression of proteins and genes participating in isoflavone biosynthesis in soybean sprouts under UV-B radiation.
[Mh] Termos MeSH primário: Ácido Abscísico/metabolismo
ADP-Ribose Cíclica/metabolismo
Inositol 1,4,5-Trifosfato/metabolismo
Feijão de Soja/metabolismo
[Mh] Termos MeSH secundário: ADP-Ribosil Ciclase/metabolismo
Cálcio/química
Cálcio/metabolismo
Quelantes/química
Perfilação da Expressão Gênica
Isoflavonas/química
Reação em Cadeia da Polimerase em Tempo Real
Sistemas do Segundo Mensageiro
Transdução de Sinais
Raios Ultravioleta
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chelating Agents); 0 (Isoflavones); 119340-53-3 (Cyclic ADP-Ribose); 72S9A8J5GW (Abscisic Acid); 85166-31-0 (Inositol 1,4,5-Trisphosphate); EC 3.2.2.5 (ADP-ribosyl Cyclase); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170827
[Lr] Data última revisão:
170827
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160925
[St] Status:MEDLINE


  5 / 699 MEDLINE  
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[PMID]:27466127
[Au] Autor:Hayakawa K; Esposito E; Wang X; Terasaki Y; Liu Y; Xing C; Ji X; Lo EH
[Ad] Endereço:Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA.
[Ti] Título:Transfer of mitochondria from astrocytes to neurons after stroke.
[So] Source:Nature;535(7613):551-5, 2016 07 28.
[Is] ISSN:1476-4687
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Neurons can release damaged mitochondria and transfer them to astrocytes for disposal and recycling. This ability to exchange mitochondria may represent a potential mode of cell-to-cell signalling in the central nervous system. Here we show that astrocytes in mice can also release functional mitochondria that enter neurons. Astrocytic release of extracellular mitochondrial particles was mediated by a calcium-dependent mechanism involving CD38 and cyclic ADP ribose signalling. Transient focal cerebral ischaemia in mice induced entry of astrocytic mitochondria into adjacent neurons, and this entry amplified cell survival signals. Suppression of CD38 signalling by short interfering RNA reduced extracellular mitochondria transfer and worsened neurological outcomes. These findings suggest a new mitochondrial mechanism of neuroglial crosstalk that may contribute to endogenous neuroprotective and neurorecovery mechanisms after stroke.
[Mh] Termos MeSH primário: Astrócitos/patologia
Mitocôndrias/metabolismo
Mitocôndrias/patologia
Neurônios/patologia
Acidente Vascular Cerebral/patologia
[Mh] Termos MeSH secundário: ADP-Ribosil Ciclase 1/deficiência
ADP-Ribosil Ciclase 1/genética
ADP-Ribosil Ciclase 1/metabolismo
Animais
Astrócitos/metabolismo
Isquemia Encefálica/metabolismo
Isquemia Encefálica/patologia
Cálcio/metabolismo
Sobrevivência Celular
ADP-Ribose Cíclica/metabolismo
Masculino
Glicoproteínas de Membrana/deficiência
Glicoproteínas de Membrana/genética
Glicoproteínas de Membrana/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Plasticidade Neuronal
Neurônios/metabolismo
Fatores de Proteção
RNA Interferente Pequeno/genética
Transdução de Sinais
Estresse Fisiológico
Acidente Vascular Cerebral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Membrane Glycoproteins); 0 (RNA, Small Interfering); 119340-53-3 (Cyclic ADP-Ribose); EC 3.2.2.5 (Cd38 protein, mouse); EC 3.2.2.6 (ADP-ribosyl Cyclase 1); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160729
[St] Status:MEDLINE
[do] DOI:10.1038/nature18928


  6 / 699 MEDLINE  
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[PMID]:27411462
[Au] Autor:Peng QY; Zou Y; Zhang LN; Ai ML; Liu W; Ai YH
[Ad] Endereço:Department of Critical Care Medicine, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China.
[Ti] Título:Blocking Cyclic Adenosine Diphosphate Ribose-mediated Calcium Overload Attenuates Sepsis-induced Acute Lung Injury in Rats.
[So] Source:Chin Med J (Engl);129(14):1725-30, 2016 Jul 20.
[Is] ISSN:0366-6999
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Acute lung injury (ALI) is a common complication of sepsis that is associated with high mortality. Intracellular Ca2+ overload plays an important role in the pathophysiology of sepsis-induced ALI, and cyclic adenosine diphosphate ribose (cADPR) is an important regulator of intracellular Ca2+ mobilization. The cluster of differentiation 38 (CD38)/cADPR pathway has been found to play roles in multiple inflammatory processes but its role in sepsis-induced ALI is still unknown. This study aimed to investigate whether the CD38/cADPR signaling pathway is activated in sepsis-induced ALI and whether blocking cADPR-mediated calcium overload attenuates ALI. METHODS: Septic rat models were established by cecal ligation and puncture (CLP). Rats were divided into the sham group, the CLP group, and the CLP+ 8-bromo-cyclic adenosine diphosphate ribose (8-Br-cADPR) group. Nicotinamide adenine dinucleotide (NAD+), cADPR, CD38, and intracellular Ca2+ levels in the lung tissues were measured at 6, 12, 24, and 48 h after CLP surgery. Lung histologic injury, tumor necrosis factor (TNF)-µ, malondialdehyde (MDA) levels, and superoxide dismutase (SOD) activities were measured. RESULTS: NAD+, cADPR, CD38, and intracellular Ca2+ levels in the lungs of septic rats increased significantly at 24 h after CLP surgery. Treatment with 8-Br-cADPR, a specific inhibitor of cADPR, significantly reduced intracellular Ca2+ levels (P = 0.007), attenuated lung histological injury (P = 0.023), reduced TNF-µ and MDA levels (P < 0.001 and P = 0.002, respectively) and recovered SOD activity (P = 0.031) in the lungs of septic rats. CONCLUSIONS: The CD38/cADPR pathway is activated in the lungs of septic rats, and blocking cADPR-mediated calcium overload with 8-Br-cADPR protects against sepsis-induced ALI.
[Mh] Termos MeSH primário: Lesão Pulmonar Aguda/induzido quimicamente
Lesão Pulmonar Aguda/tratamento farmacológico
Cálcio/metabolismo
ADP-Ribose Cíclica/antagonistas & inibidores
Sepse/complicações
[Mh] Termos MeSH secundário: ADP-Ribosil Ciclase 1/metabolismo
Animais
ADP-Ribose Cíclica/análogos & derivados
ADP-Ribose Cíclica/metabolismo
ADP-Ribose Cíclica/uso terapêutico
Masculino
Malondialdeído/metabolismo
Ratos
Ratos Sprague-Dawley
Superóxido Dismutase/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (8-bromo-cyclic-ADP-ribose); 0 (Tumor Necrosis Factor-alpha); 119340-53-3 (Cyclic ADP-Ribose); 4Y8F71G49Q (Malondialdehyde); EC 1.15.1.1 (Superoxide Dismutase); EC 3.2.2.6 (ADP-ribosyl Cyclase 1); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160715
[St] Status:MEDLINE
[do] DOI:10.4103/0366-6999.185854


  7 / 699 MEDLINE  
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[PMID]:27345368
[Au] Autor:Igarashi M; Guarente L
[Ad] Endereço:Department of Biology, Glenn Labs for the Science of Aging and Koch Institute, MIT, Cambridge, MA 02139, USA.
[Ti] Título:mTORC1 and SIRT1 Cooperate to Foster Expansion of Gut Adult Stem Cells during Calorie Restriction.
[So] Source:Cell;166(2):436-450, 2016 Jul 14.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Longevity-promoting caloric restriction is thought to trigger downregulation of mammalian target of rapamycin complex 1 (mTORC1) signaling and upregulation of SIRT1 activity with associated health benefits. Here, we show that mTORC1 signaling in intestinal stem cells (ISCs) is instead upregulated during calorie restriction (CR). SIRT1 deacetylates S6K1, thereby enhancing its phosphorylation by mTORC1, which leads to an increase in protein synthesis and an increase in ISC number. Paneth cells in the ISC niche secrete cyclic ADP ribose that triggers SIRT1 activity and mTORC1 signaling in neighboring ISCs. Notably, the mTOR inhibitor rapamycin, previously reported to mimic effects of CR, abolishes this expansion of ISCs. We suggest that Paneth cell signaling overrides any direct nutrient sensing in ISCs to sculpt the observed response to CR. Moreover, drugs that modulate pathways important in CR may exert opposing effects on different cell types.
[Mh] Termos MeSH primário: Células-Tronco Adultas/metabolismo
Restrição Calórica
Complexos Multiproteicos/metabolismo
Transdução de Sinais
Sirtuína 1/metabolismo
Serina-Treonina Quinases TOR/metabolismo
[Mh] Termos MeSH secundário: Animais
Proliferação Celular
ADP-Ribose Cíclica/metabolismo
Dieta
Intestinos/citologia
Intestinos/metabolismo
Alvo Mecanístico do Complexo 1 de Rapamicina
Camundongos
Camundongos Endogâmicos C57BL
NAD/metabolismo
Organoides/metabolismo
Fosforilação
Proteínas Quinases S6 Ribossômicas 90-kDa/metabolismo
Sirtuína 2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Multiprotein Complexes); 0U46U6E8UK (NAD); 119340-53-3 (Cyclic ADP-Ribose); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1); EC 2.7.11.1 (Ribosomal Protein S6 Kinases, 90-kDa); EC 2.7.11.1 (Rps6ka1 protein, mouse); EC 3.5.1.- (Sirt1 protein, mouse); EC 3.5.1.- (Sirtuin 1); EC 3.5.1.- (Sirtuin 2)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:171124
[Lr] Data última revisão:
171124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160628
[St] Status:MEDLINE


  8 / 699 MEDLINE  
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[PMID]:27325083
[Au] Autor:Khalaf A; Babiker F
[Ad] Endereço:Department of Physiology, Faculty of Medicine, Health Science Center, Kuwait University, P.O. Box 24923, Safat, 13110, Kuwait.
[Ti] Título:Discrepancy in calcium release from the sarcoplasmic reticulum and intracellular acidic stores for the protection of the heart against ischemia/reperfusion injury.
[So] Source:J Physiol Biochem;72(3):495-508, 2016 Sep.
[Is] ISSN:1877-8755
[Cp] País de publicação:Spain
[La] Idioma:eng
[Ab] Resumo:We and others have demonstrated a protective effect of pacing postconditioning (PPC) against ischemia/reperfusion (I/R) injury. However, the mechanisms underlying this protection are not completely clear. In the present study, we evaluated the effects of calcium release from the sarcoplasmic reticulum (SR) and the novel intracellular acidic stores (AS). Isolated rat hearts (n = 6 per group) were subjected to coronary occlusion followed by reperfusion using a modified Langendorff system. Cardiac hemodynamics and contractility were assessed using a data acquisition program, and cardiac injury was evaluated by creatine kinase (CK) and lactate dehydrogenase (LDH) levels. Hearts were subjected to 30 min of regional ischemia, produced by ligation of the left anterior descending (LAD) coronary artery, followed by 30 min of reperfusion. The hearts were also subjected to PPC (3 cycles of 30 s of left ventricle (LV) pacing alternated with 30 s of right atrium (RA) pacing) and/or were treated during reperfusion with agonists or antagonists of release of calcium from SR or AS. PPC significantly (P < 0.05) normalized LV, contractility, and coronary vascular dynamics and significantly (P < 0.001) decreased heart enzyme levels compared to the control treatments. The blockade of SR calcium release resulted in a significant (P < 0.01) recovery in LV function and contractility and a significant reduction in CK and LDH levels (P < 0.01) when applied alone or in combination with PPC. Interestingly, the release of calcium from AS alone or in combination with PPC significantly improved LV function and contractility (P < 0.05) and significantly decreased the CK and LDH levels (P < 0.01) compared to the control treatments. An additive effect was produced when agonism of calcium release from AS or blockade of calcium release from the SR was combined with PPC. Calcium release from AS and blockade of calcium release from the SR protect the heart against I/R. Combining calcium release from acidic stores or blockade of calcium release from the SR with PPC produced a synergistic protective effect.
[Mh] Termos MeSH primário: Sinalização do Cálcio
Vasos Coronários/fisiopatologia
Coração/fisiopatologia
Lisossomos/metabolismo
Traumatismo por Reperfusão Miocárdica/metabolismo
Miocárdio/metabolismo
Retículo Sarcoplasmático/metabolismo
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Sinalização do Cálcio/efeitos dos fármacos
Carbolinas/farmacologia
Estimulação Cardíaca Artificial
Vasos Coronários/efeitos dos fármacos
ADP-Ribose Cíclica/farmacologia
Dantroleno/farmacologia
Coração/efeitos dos fármacos
Técnicas In Vitro
Pós-Condicionamento Isquêmico
Lisossomos/efeitos dos fármacos
Masculino
Relaxantes Musculares Centrais/farmacologia
Traumatismo por Reperfusão Miocárdica/fisiopatologia
Traumatismo por Reperfusão Miocárdica/terapia
Miocárdio/enzimologia
NADP/análogos & derivados
NADP/antagonistas & inibidores
NADP/farmacologia
Piperazinas/farmacologia
Ratos Wistar
Retículo Sarcoplasmático/efeitos dos fármacos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Carbolines); 0 (Muscle Relaxants, Central); 0 (Ned-19 compound); 0 (Piperazines); 119340-53-3 (Cyclic ADP-Ribose); 53-59-8 (NADP); 5502-96-5 (NAADP); F64QU97QCR (Dantrolene)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160622
[St] Status:MEDLINE
[do] DOI:10.1007/s13105-016-0498-0


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[PMID]:27020835
[Au] Autor:Peng QY; Ai ML; Zhang LN; Zou Y; Ma XH; Ai YH
[Ad] Endereço:Department of Critical Care Medicine, Xiang-Ya Hospital, Central South University, Changsha, Hunan Province, China.
[Ti] Título:Blocking NAD(+)/CD38/cADPR/Ca(2+) pathway in sepsis prevents organ damage.
[So] Source:J Surg Res;201(2):480-9, 2016 Apr.
[Is] ISSN:1095-8673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Although the nicotinamide adenine dinucleotide (NAD(+))/CD38/cyclic ADP ribose (cADPR)/Ca(2+) signaling pathway has been shown to regulate intracellular calcium homeostasis and functions in multiple inflammatory processes, its role in sepsis remains unknown. The aim of this study was to determine whether the NAD(+)/CD38/cADPR/Ca(2+) signaling pathway is activated during sepsis and whether an inhibitor of this pathway, 8-Br-cADPR, protects the organs from sepsis-induced damage. MATERIALS AND METHODS: Male Sprague-Dawley rats were subjected to cecal ligation and puncture (CLP) or sham laparotomies. NAD(+), cADPR, CD38, and intracellular Ca(2+) levels were measured in the hearts, livers, and kidneys of septic rats at 0, 6, 12, 24, and 48 h after CLP surgery. Rats were also divided into sham, CLP, and CLP+8-Br-cADPR groups, and the hearts, livers, and kidneys were hematoxylin-eosin-stained and assayed for malondialdehyde and superoxide dismutase activities. RESULTS: NAD(+), cADPR, CD38, and intracellular Ca(2+) levels increased in the hearts, livers, and kidneys of septic rats as early as 6-24 h after CLP surgery. Treatment with 8-Br-cADPR inhibited sepsis-induced intracellular Ca(2+) mobilization, attenuated tissue injury, reduced malondialdehyde levels, and increased superoxide dismutase activity in septic rats. CONCLUSIONS: The NAD(+)/CD38/cADPR/Ca(2+) signaling pathway was activated during sepsis in the CLP rat model. Blocking this pathway with 8-Br-cADPR protected hearts, livers, and kidneys from sepsis-induced damage.
[Mh] Termos MeSH primário: Sinalização do Cálcio/efeitos dos fármacos
ADP-Ribose Cíclica/análogos & derivados
Insuficiência de Múltiplos Órgãos/prevenção & controle
Sepse/complicações
[Mh] Termos MeSH secundário: ADP-Ribosil Ciclase/metabolismo
ADP-Ribosil Ciclase 1/metabolismo
Animais
Cálcio/metabolismo
ADP-Ribose Cíclica/metabolismo
ADP-Ribose Cíclica/farmacologia
ADP-Ribose Cíclica/uso terapêutico
Modelos Animais de Doenças
Avaliação Pré-Clínica de Medicamentos
Masculino
Malondialdeído/metabolismo
Glicoproteínas de Membrana/metabolismo
Insuficiência de Múltiplos Órgãos/etiologia
NAD/metabolismo
Distribuição Aleatória
Ratos Sprague-Dawley
Sepse/metabolismo
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (8-bromo-cyclic-ADP-ribose); 0 (Membrane Glycoproteins); 0U46U6E8UK (NAD); 119340-53-3 (Cyclic ADP-Ribose); 4Y8F71G49Q (Malondialdehyde); EC 1.15.1.1 (Superoxide Dismutase); EC 3.2.2.5 (ADP-ribosyl Cyclase); EC 3.2.2.5 (Cd38 protein, rat); EC 3.2.2.6 (ADP-ribosyl Cyclase 1); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160330
[St] Status:MEDLINE


  10 / 699 MEDLINE  
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[PMID]:26959359
[Au] Autor:Gul R; Park DR; Shawl AI; Im SY; Nam TS; Lee SH; Ko JK; Jang KY; Kim D; Kim UH
[Ad] Endereço:Department of Biochemistry, Chonbuk National University Medical School, Jeonju, Korea.
[Ti] Título:Nicotinic Acid Adenine Dinucleotide Phosphate (NAADP) and Cyclic ADP-Ribose (cADPR) Mediate Ca2+ Signaling in Cardiac Hypertrophy Induced by ß-Adrenergic Stimulation.
[So] Source:PLoS One;11(3):e0149125, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ca2+ signaling plays a fundamental role in cardiac hypertrophic remodeling, but the underlying mechanisms remain poorly understood. We investigated the role of Ca2+-mobilizing second messengers, NAADP and cADPR, in the cardiac hypertrophy induced by ß-adrenergic stimulation by isoproterenol. Isoproterenol induced an initial Ca2+ transients followed by sustained Ca2+ rises. Inhibition of the cADPR pathway with 8-Br-cADPR abolished only the sustained Ca2+ increase, whereas inhibition of the NAADP pathway with bafilomycin-A1 abolished both rapid and sustained phases of the isoproterenol-mediated signal, indicating that the Ca2+ signal is mediated by a sequential action of NAADP and cADPR. The sequential production of NAADP and cADPR was confirmed biochemically. The isoproterenol-mediated Ca2+ increase and cADPR production, but not NAADP production, were markedly reduced in cardiomyocytes obtained from CD38 knockout mice. CD38 knockout mice were rescued from chronic isoproterenol infusion-induced myocardial hypertrophy, interstitial fibrosis, and decrease in fractional shortening and ejection fraction. Thus, our findings indicate that ß-adrenergic stimulation contributes to the development of maladaptive cardiac hypertrophy via Ca2+ signaling mediated by NAADP-synthesizing enzyme and CD38 that produce NAADP and cADPR, respectively.
[Mh] Termos MeSH primário: Sinalização do Cálcio/efeitos dos fármacos
Cardiomegalia/metabolismo
ADP-Ribose Cíclica/farmacologia
NADP/análogos & derivados
Receptores Adrenérgicos beta/metabolismo
[Mh] Termos MeSH secundário: ADP-Ribosil Ciclase 1/metabolismo
Animais
Cardiomegalia/diagnóstico por imagem
Cardiomegalia/fisiopatologia
Isoproterenol
Masculino
Camundongos Knockout
Modelos Biológicos
Miócitos Cardíacos/efeitos dos fármacos
Miócitos Cardíacos/metabolismo
NADP/farmacologia
Ratos Sprague-Dawley
Ultrassonografia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptors, Adrenergic, beta); 119340-53-3 (Cyclic ADP-Ribose); 53-59-8 (NADP); 5502-96-5 (NAADP); EC 3.2.2.6 (ADP-ribosyl Cyclase 1); L628TT009W (Isoproterenol)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160310
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0149125



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