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[PMID]:29391192
[Au] Autor:Hadzi-Petrushev N; Bogdanov J; Krajoska J; Ilievska J; Bogdanova-Popov B; Gjorgievska E; Mitrokhin V; Sopi R; Gagov H; Kamkin A; Mladenov M
[Ad] Endereço:Faculty of Natural Sciences and Mathematics, Institute of Biology, "Ss Cyril and Methodius" University, P.O. Box 162, 1000 Skopje, Macedonia.
[Ti] Título:Comparative study of the antioxidant properties of monocarbonyl curcumin analogues C66 and B2BrBC in isoproteranol induced cardiac damage.
[So] Source:Life Sci;197:10-18, 2018 Mar 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIM: To test the antioxidant properties of the newly synthesized (2E,6E)-2,6-bis(2-bromobenzylidene)cyclohexanone (B2BrBC) in parallel with C66 in rats with cardiac hypertrophy. MATERIALS AND METHODS: The protective effects of both C66 and B2BrBC against oxidative stress in rats with cardiac hypertrophy, was studied by evaluating the activity of antioxidant enzymes, the relationship between the ratio of the activities of the antioxidant enzymes R = SOD/(GPx + CAT) and levels of thiols and lipid peroxidation in the heart. In order to gain better understanding of the antioxidant properties of the studied compounds, computational methods were utilized. The properties of selected structurally related derivatives were obtained on optimized geometries for ground states, using semi-empirical PM3 quantum mechanical calculations. KEY FINDINGS: The ratio R shows disequilibrium in rats with induced hypertrophy (p < 0.001). Coextending changes were detected in total and free sulfhydryl group content (p = 0.011 for t-SH and p = 0.008, for free SH, respectively). The results with the B2BrBC, indicated strong thiol prevention reflected in the levels of both t-SH and f-SH. Taking into account the HOMO energies of B2BrBC (-9.398 eV) and C66 (-9.667), it can be concluded that B2BrBC has lower HOMO energy, which makes it a better electron donor and a better antioxidant. SIGNIFICANCE: The obtained results indicated that the antioxidant ability of B2BrBC is positively associated with the catalytic SOD and GPx activities expressed through preserved t-SH levels. It seems plausible that for a compound to exhibit antioxidant activity, as most of the 2,6-bis(benzylidene)cyclohexanones do, they should be good electron donors. IMPACT STATEMENT: Understanding the relationship between cardiac hypertrophy induced oxidative injuries and supporters of endogenous reparatory machinery will help in establishing the beneficial role of adequate antioxidant supplementation. In this study reliable data on the preventive effects of newly synthesized symmetric monocarbonyl curcumin analogue B2BrBC and its role in the prevention of oxidative injuries on three levels (enzymatic, protein and lipid), in the heart hypertrophic onset, were obtained.
[Mh] Termos MeSH primário: Antioxidantes
Cardiomegalia
Curcumina
Isoproterenol/efeitos adversos
Peroxidação de Lipídeos/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Antioxidantes/química
Antioxidantes/farmacologia
Cardiomegalia/induzido quimicamente
Cardiomegalia/tratamento farmacológico
Cardiomegalia/metabolismo
Curcumina/análogos & derivados
Curcumina/química
Curcumina/farmacologia
Isoproterenol/farmacologia
Masculino
Miocárdio/metabolismo
Ratos
Ratos Wistar
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); IT942ZTH98 (Curcumin); L628TT009W (Isoproterenol)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE


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[PMID]:28467637
[Au] Autor:Li X; Zhou M; Huang W; Yang H
[Ad] Endereço:Drug Discovery and Design Center, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.
[Ti] Título:N-glycosylation of the ß adrenergic receptor regulates receptor function by modulating dimerization.
[So] Source:FEBS J;284(13):2004-2018, 2017 07.
[Is] ISSN:1742-4658
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:N-glycosylation is a common post-translational modification of G-protein-coupled receptors (GPCRs). However, it remains unknown how N-glycosylation affects GPCR signaling. ß adrenergic receptor (ß AR) has three N-glycosylation sites: Asn6, Asn15 at the N-terminus, and Asn187 at the second extracellular loop (ECL2). Here, we show that deletion of the N-glycan did not affect receptor expression and ligand binding. Deletion of the N-glycan at the N-terminus rather than Asn187 showed decreased effects on isoproterenol-promoted G-protein-dependent signaling, ß-arrestin2 recruitment, and receptor internalization. Both N6Q and N15Q showed decreased receptor dimerization, while N187Q did not influence receptor dimerization. As decreased ß AR homodimer accompanied with reduced efficiency for receptor function, we proposed that the N-glycosylation of ß AR regulated receptor function by influencing receptor dimerization. To verify this hypothesis, we further paid attention to the residues at the dimerization interface. Studies of Lys60 and Glu338, two residues at the receptor dimerization interface, exhibited that the K60A/E338A showed decreased ß AR dimerization and its effects on receptor signaling were similar to N6Q and N15Q, which further supported the importance of receptor dimerization for receptor function. This work provides new insights into the relationship among glycosylation, dimerization, and function of GPCRs. ENZYMES: Peptide-N-glycosidase F (PNGase F, EC 3.2.2.11); endo-ß-N-acetylglucosaminidase A (Endo-A, EC 3.2.1.96).
[Mh] Termos MeSH primário: Multimerização Proteica
Receptores Adrenérgicos beta 2/química
Receptores Adrenérgicos beta 2/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Agonistas Adrenérgicos beta/farmacologia
Sítios de Ligação/genética
Western Blotting
Endocitose/efeitos dos fármacos
Glicosilação
Células HEK293
Seres Humanos
Isoproterenol/farmacologia
Microscopia Confocal
Mutação
Polissacarídeos/metabolismo
Processamento de Proteína Pós-Traducional
Receptores Adrenérgicos beta 2/genética
beta-Arrestinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adrenergic beta-Agonists); 0 (Polysaccharides); 0 (Receptors, Adrenergic, beta-2); 0 (beta-Arrestins); L628TT009W (Isoproterenol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1111/febs.14098


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[PMID]:29355689
[Au] Autor:Gryshkova V; Fleming A; McGhan P; De Ron P; Fleurance R; Valentin JP; Nogueira da Costa A
[Ad] Endereço:Investigative Toxicology, Non-Clinical Development, UCB Biopharma SPRL, Belgium.
[Ti] Título:miR-21-5p as a potential biomarker of inflammatory infiltration in the heart upon acute drug-induced cardiac injury in rats.
[So] Source:Toxicol Lett;286:31-38, 2018 Apr.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Investigation of genomic changes in cardiotoxicity can provide novel biomarkers and insights into molecular mechanisms of drug-induced cardiac injury (DICI). The main objective of this study was to identify and characterize dysregulated microRNAs (miRNAs) in the heart associated with cardiotoxicity. Wistar rats were dosed once with either isoproterenol (1.5 mg/kg, i.p), allylamine (100 mg/kg, p.o.) or the respective vehicle controls. Heart tissue was collected at 24 h, 48 h and 72 h post-drug administration and used for histopathological assessment, miRNA profiling, immunohistochemical analysis and in situ hybridization. Multiplex analysis of 68 miRNAs in the heart revealed a significant upregulation of several miRNAs (miR-19a-3p, miR-142-3p, miR-155-5p, miR-208b-3p, miR-21-5p) after isoproterenol and one miRNA (miR-21-5p) after allylamine administration. Localization of miR-21-5p was specific to inflammatory cell infiltrates in the heart after both treatments. Immunohistochemical analysis of Stat3, a known miR-21-5p regulator, also confirmed its upregulation in cardiomyocytes and inflammatory cell infiltrates. The toxicity signatures based on miRNA networks, identified in vivo, can potentially be used as mechanistic biomarkers as well as to study cardiotoxicity in vitro in order to develop sensitive tools for early hazard identification and risk assessment.
[Mh] Termos MeSH primário: Cardiopatias/induzido quimicamente
Inflamação/induzido quimicamente
MicroRNAs/genética
Miocárdio/metabolismo
[Mh] Termos MeSH secundário: Alilamina
Animais
Cardiotoxicidade
Modelos Animais de Doenças
Perfilação da Expressão Gênica/métodos
Regulação da Expressão Gênica
Marcadores Genéticos
Cardiopatias/genética
Cardiopatias/metabolismo
Cardiopatias/patologia
Hibridização In Situ
Inflamação/genética
Inflamação/metabolismo
Inflamação/patologia
Isoproterenol
Masculino
MicroRNAs/metabolismo
Reação em Cadeia da Polimerase Multiplex
Miocárdio/patologia
Análise de Sequência com Séries de Oligonucleotídeos
Ratos Wistar
Medição de Risco
Fator de Transcrição STAT3/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Genetic Markers); 0 (MicroRNAs); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, rat); 0 (mirn21 microRNA, rat); 48G762T011 (Allylamine); L628TT009W (Isoproterenol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180123
[St] Status:MEDLINE


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[PMID]:29406244
[Au] Autor:Ashokkumar R; Jamuna S; Sakeena Sadullah MS; Niranjali Devaraj S
[Ad] Endereço:Department of Biochemistry, University of Madras, Guindy Campus, Chennai 600 025, India.
[Ti] Título:Vitexin protects isoproterenol induced post myocardial injury by modulating hipposignaling and ER stress responses.
[So] Source:Biochem Biophys Res Commun;496(2):731-737, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The molecular mechanisms involved in ER stress-induced post myocardial injury remain elusive. In this study, we have investigated the molecular mechanism of ER stress-mediated myocyte death in Isoproterenol (ISO) induced myocardial infarction and its inhibition by a potent anti oxidant and anti-apoptotic bioflavonoid, Vitexin. ISO mediated apoptosis was found to be associated with ER permeabilization and characterized by enhanced production of ROS, activation of caspase-3, modulation of Bcl2 family proteins and activation of bnip3. Moreover, post treatment with Vitexin inhibits the ISO induced translocation of CHOP to nucleus during MI. Further results have demonstrated that, activation of Mst1 through ER stress was diminished upon treatment with Vitexin. In addition to this, Vitexin treatment significantly downregulated the expression of p-Yap and p-Mst1 which were enhanced during post myocardial injury. Taken together, our data indicate that co-ordinated activation of ER stress and hipposignaling by ISO was ameliorated by the potent cardioprotective effects of Vitexin.
[Mh] Termos MeSH primário: Antioxidantes/uso terapêutico
Apigenina/uso terapêutico
Cardiotônicos/uso terapêutico
Estresse do Retículo Endoplasmático/efeitos dos fármacos
Infarto do Miocárdio/tratamento farmacológico
Miócitos Cardíacos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Caspase 3/metabolismo
Isoproterenol
Masculino
Infarto do Miocárdio/induzido quimicamente
Infarto do Miocárdio/patologia
Miócitos Cardíacos/patologia
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Ratos Wistar
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antioxidants); 0 (Cardiotonic Agents); 0 (Proto-Oncogene Proteins c-bcl-2); 7V515PI7F6 (Apigenin); 9VP70K75OK (vitexin); EC 3.4.22.- (Caspase 3); L628TT009W (Isoproterenol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE


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[PMID]:29225109
[Au] Autor:Khan V; Sharma S; Bhandari U; Ali SM; Haque SE
[Ad] Endereço:Department of Pharmacology, School of Pharmaceutical Education & Research (SPER), Jamia Hamdard, New Delhi 110062, India.
[Ti] Título:Raspberry ketone protects against isoproterenol-induced myocardial infarction in rats.
[So] Source:Life Sci;194:205-212, 2018 Feb 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIM: The cardioprotective role of raspberry ketone (RK) against isoproterenol (ISO)-induced myocardial infarction (MI) in rats was assessed. MATERIALS AND METHODS: Rats were randomly divided into Group I - Vehicle control; Group II - Toxic control ISO (85mg/kg, s.c.); Group III, IV and V - RK (50, 100 and 200mg/kg, respectively) with ISO; Group VI- RK (200mg/kg) alone; Group VII - Propranolol (10mg/kg) with ISO; and Group VIII - Propranolol (10mg/kg) alone. After twenty-four hours of the last dose, animals were sacrificed and creatine kinase-MB, lactate dehydrogenase, total cholesterol, triglycerides, high-density-lipoprotein, low-density-lipoprotein, very-low-density-lipoprotein, malondialdehyde, reduced glutathione, superoxide dismutase, catalase, Na , K -ATPase, nitric oxide, histopathological and immunohistochemical analysis (tumor necrosis factor-α and inducible nitric oxide synthase) were performed. KEY FINDINGS: Treatment with ISO significantly deviated the biochemical parameters from the normal levels, which were considerably restored by RK at 100 and 200mg/kg doses. 50mg/kg dose, however, did not demonstrate any significant cardioprotective action. The histopathological and immunohistochemical analysis further substantiated these findings. SIGNIFICANCE: Our study showed a dose-dependent reduction in oxidative stress, inflammation and dyslipidemia by RK in ISO-intoxicated rats, which signifies that RK from the European red raspberry plant might be a valuable entity for the management of MI.
[Mh] Termos MeSH primário: Anti-Inflamatórios/uso terapêutico
Antioxidantes/uso terapêutico
Butanonas/uso terapêutico
Cardiotônicos/uso terapêutico
Infarto do Miocárdio/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Butanonas/química
Isoproterenol
Infarto do Miocárdio/induzido quimicamente
Infarto do Miocárdio/patologia
Miocárdio/patologia
Estresse Oxidativo/efeitos dos fármacos
PPAR alfa/agonistas
Ratos
Ratos Wistar
Rubus/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antioxidants); 0 (Butanones); 0 (Cardiotonic Agents); 0 (PPAR alpha); 7QY1MH15BG (raspberry ketone); L628TT009W (Isoproterenol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE


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[PMID]:28743500
[Au] Autor:Manivasagam S; Vellaichamy E
[Ad] Endereço:Department of Biochemistry, University of Madras, Guindy Campus, Chennai, 600025, India.
[Ti] Título:Suppression of Npr1, not Npr2 gene function induces hypertrophic growth in H9c2 cells in vitro.
[So] Source:Biochem Biophys Res Commun;491(2):250-256, 2017 09 16.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Npr1 gene (coding for NPR-A) and Npr2 gene (coding for NPR-B) are identified as intrinsic anti-hypertrophic genes that opposes abnormal cardiac remodeling. However, the functional role of Npr1 and Npr2 genes during cardiac hypertrophic growth is not well understood. Hence, the present investigation was aimed to study the effect of Npr1 and Npr2 gene silencing, respectively on ß-AR activation induced cardiac hypertrophic growth in H9c2 cells in vitro. The control, Npr1, and Npr2 gene suppressed H9c2 cells, respectively were treated with ISO (10 M) for 48 h. The mRNA and protein expression profile of NPR-A, NPR-B, PKG-I and cGMP were analyzed by qPCR, Western blotting, ELISA, and immunofluorescence methods, respectively. A marked increase in cell size (30.10 ± 0.51 µm vs 61.83 ± 0.43 µm, 2-fold) accompanied by elevated hypertrophic marker genes (α-sk and ß-MHC 3-fold, respectively) expression was observed in Npr1 gene suppressed H9c2 cells as compared with control cells. In contrast, the Npr2 gene suppression in H9c2 cells neither altered the cell size nor the level of hypertrophic marker genes expression. Upon exposure to Isoproterenol, the Npr1 suppressed H9c2 cells exhibited further increase in cell size (1.5 fold), whereas, no significant increase in cell size or marker genes expression was noticed in Npr2 suppressed cells. Moreover, the intracellular cGMP level was down-regulated by 2-fold in Npr1 suppressed cells, while, no significant change was observed in Npr2 suppressed cells. Together, these results suggest that Npr1, not Npr2 gene function is positively associated with the initiation of cardiac fetal gene program and development of cardiac hypertrophic growth.
[Mh] Termos MeSH primário: Miócitos Cardíacos/metabolismo
Receptores Adrenérgicos beta 1/genética
Receptores do Fator Natriurético Atrial/genética
[Mh] Termos MeSH secundário: Agonistas Adrenérgicos beta/farmacologia
Animais
Linhagem Celular
Proliferação Celular/efeitos dos fármacos
Tamanho Celular/efeitos dos fármacos
GMP Cíclico/metabolismo
Proteína Quinase Dependente de GMP Cíclico Tipo I/genética
Proteína Quinase Dependente de GMP Cíclico Tipo I/metabolismo
Regulação da Expressão Gênica
Isoproterenol/farmacologia
Miócitos Cardíacos/efeitos dos fármacos
Miócitos Cardíacos/patologia
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Ratos
Receptores Adrenérgicos beta 1/metabolismo
Receptores do Fator Natriurético Atrial/antagonistas & inibidores
Receptores do Fator Natriurético Atrial/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adrenergic beta-Agonists); 0 (RNA, Small Interfering); 0 (Receptors, Adrenergic, beta-1); EC 2.7.11.12 (Cyclic GMP-Dependent Protein Kinase Type I); EC 4.6.1.2 (Receptors, Atrial Natriuretic Factor); EC 4.6.1.2 (atrial natriuretic factor receptor A); EC 4.6.1.2 (atrial natriuretic factor receptor B); H2D2X058MU (Cyclic GMP); L628TT009W (Isoproterenol)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171129
[Lr] Data última revisão:
171129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE


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[PMID]:28957413
[Au] Autor:Markussen LK; Isidor MS; Breining P; Andersen ES; Rasmussen NE; Petersen LI; Pedersen SB; Richelsen B; Hansen JB
[Ad] Endereço:Department of Biology, University of Copenhagen, Copenhagen, Denmark.
[Ti] Título:Characterization of immortalized human brown and white pre-adipocyte cell models from a single donor.
[So] Source:PLoS One;12(9):e0185624, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Brown adipose tissue with its constituent brown adipocytes is a promising therapeutic target in metabolic disorders due to its ability to dissipate energy and improve systemic insulin sensitivity and glucose homeostasis. The molecular control of brown adipocyte differentiation and function has been extensively studied in mice, but relatively little is known about such regulatory mechanisms in humans, which in part is due to lack of human brown adipose tissue derived cell models. Here, we used retrovirus-mediated overexpression to stably integrate human telomerase reverse transcriptase (TERT) into stromal-vascular cell fractions from deep and superficial human neck adipose tissue biopsies from the same donor. The brown and white pre-adipocyte cell models (TERT-hBA and TERT-hWA, respectively) displayed a stable proliferation rate and differentiation until at least passage 20. Mature TERT-hBA adipocytes expressed higher levels of thermogenic marker genes and displayed a higher maximal respiratory capacity than mature TERT-hWA adipocytes. TERT-hBA adipocytes were UCP1-positive and responded to ß-adrenergic stimulation by activating the PKA-MKK3/6-p38 MAPK signaling module and increasing thermogenic gene expression and oxygen consumption. Mature TERT-hWA adipocytes underwent efficient rosiglitazone-induced 'browning', as demonstrated by strongly increased expression of UCP1 and other brown adipocyte-enriched genes. In summary, the TERT-hBA and TERT-hWA cell models represent useful tools to obtain a better understanding of the molecular control of human brown and white adipocyte differentiation and function as well as of browning of human white adipocytes.
[Mh] Termos MeSH primário: Adipócitos/citologia
Tecido Adiposo Marrom/citologia
Tecido Adiposo Branco/citologia
Doadores de Tecidos
[Mh] Termos MeSH secundário: Adipócitos/efeitos dos fármacos
Biópsia
Linhagem Celular Transformada
Colforsina/farmacologia
Seres Humanos
Isoproterenol/farmacologia
Pescoço
Retroviridae/genética
Telomerase/genética
Termogênese
Tiazolidinedionas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Thiazolidinediones); 05V02F2KDG (rosiglitazone); 1F7A44V6OU (Colforsin); EC 2.7.7.49 (Telomerase); L628TT009W (Isoproterenol)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170929
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185624


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[PMID]:28863192
[Au] Autor:Tsai CY; Kuo WW; Shibu MA; Lin YM; Liu CN; Chen YH; Day CH; Shen CY; Viswanadha VP; Huang CY
[Ad] Endereço:Department of Pediatrics, China Medical University Beigang Hospital, Yunlin, Taiwan, ROC.
[Ti] Título:E2/ER ß inhibit ISO-induced cardiac cellular hypertrophy by suppressing Ca2+-calcineurin signaling.
[So] Source:PLoS One;12(9):e0184153, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cardiovascular incidences are markedly higher in men than in pre-menstrual women. However, this advantage in women declines with aging and therefore can be correlated with the sex hormone 17ß-Estradiol (E2) which is reported to protect heart cells by acting though estrogen receptors (ERs). In this study we have determined the effect of E2/ERß against ISO induced cellular hypertrophy in H9c2 cardiomyoblast cells. The results confirm that ISO induced cardiac-hypertrophy by elevating the levels of hypertrophy associated proteins, ANP and BNP and further by upregulating p-CaMKII, calcineurin, p-GATA4 and NFATc3 which was correlated with a significant enlargement of the H9c2 cardiomyoblast. However, overexpression of ERß and/or administration of E2 inhibited ISO-induced hypertrophy in H9c2 cells. In addition, E2/ERß also inhibited ISO-induced NFATc3 translocation, and reduced the protein level of downstream marker, BNP. Furthermore, by testing with the calcineurin inhibitor (CsA), it was confirmed that calcineurin acted as a key mediator for the anti-hypertrophic effect of E2/ERß. In cells treated with calcium blocker (BATPA), the inhibitory effect of E2/ERß on ISO-induced Ca2+ influx and hypertrophic effects were totally blocked suggesting that E2/ERß inhibited calcineurin activity to activate I-1 protein and suppress PP1, then induce PLB protein phosphorylation and activation, resulting in Ca2+ reuptake into sarcoplasmic reticulum through SR Ca2+ cycling modification. In conclusion, E2/ERß suppresses the Ca2+ influx and calcineurin activity induced by ISO to enhance the PLB protein activity and SR Ca2+ cycling.
[Mh] Termos MeSH primário: Calcineurina/metabolismo
Cálcio/metabolismo
Cardiomegalia/metabolismo
Receptor beta de Estrogênio/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Inibidores de Calcineurina/farmacologia
Proteína Quinase Tipo 2 Dependente de Cálcio-Calmodulina/metabolismo
Cardiomegalia/induzido quimicamente
Núcleo Celular/metabolismo
Estradiol/metabolismo
Feminino
Isoproterenol/efeitos adversos
Miócitos Cardíacos/metabolismo
Fatores de Transcrição NFATC/metabolismo
Neurônios/metabolismo
Fosforilação
Ratos
Retículo Sarcoplasmático/metabolismo
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcineurin Inhibitors); 0 (Estrogen Receptor beta); 0 (NFATC Transcription Factors); 0 (transcription factor NF-AT c3); 4TI98Z838E (Estradiol); EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 2); EC 3.1.3.16 (Calcineurin); L628TT009W (Isoproterenol); SY7Q814VUP (Calcium)
[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:170902
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184153


  9 / 28688 MEDLINE  
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[PMID]:28859158
[Au] Autor:Kanaporis G; Treinys R; Fischmeister R; Jurevicius J
[Ad] Endereço:Institute of Cardiology, Lithuanian University of Health Sciences, Kaunas, Lithuania.
[Ti] Título:Metabolic inhibition reduces cardiac L-type Ca2+ channel current due to acidification caused by ATP hydrolysis.
[So] Source:PLoS One;12(8):e0184246, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Metabolic stress evoked by myocardial ischemia leads to impairment of cardiac excitation and contractility. We studied the mechanisms by which metabolic inhibition affects the activity of L-type Ca2+ channels (LTCCs) in frog ventricular myocytes. Metabolic inhibition induced by the protonophore FCCP (as well as by 2,4- dinitrophenol, sodium azide or antimycin A) resulted in a dose-dependent reduction of LTCC current (ICa,L) which was more pronounced during ß-adrenergic stimulation with isoprenaline. ICa,L was still reduced by metabolic inhibition even in the presence of 3 mM intracellular ATP, or when the cell was dialysed with cAMP or ATP-γ-S to induce irreversible thiophosphorylation of LTCCs, indicating that reduction in ICa,L is not due to ATP depletion and/or reduced phosphorylation of the channels. However, the effect of metabolic inhibition on ICa,L was strongly attenuated when the mitochondrial F1F0-ATP-synthase was blocked by oligomycin or when the cells were dialysed with the non-hydrolysable ATP analogue AMP-PCP. Moreover, increasing the intracellular pH buffering capacity or intracellular dialysis of the myocytes with an alkaline solution strongly attenuated the inhibitory effect of FCCP on ICa,L. Thus, our data demonstrate that metabolic inhibition leads to excessive ATP hydrolysis by the mitochondrial F1F0-ATP-synthase operating in the reverse mode and this results in intracellular acidosis causing the suppression of ICa,L. Limiting ATP break-down by F1F0-ATP-synthase and the consecutive development of intracellular acidosis might thus represent a potential therapeutic approach for maintaining a normal cardiac function during ischemia.
[Mh] Termos MeSH primário: Canais de Cálcio Tipo L/metabolismo
ATPases Mitocondriais Próton-Translocadoras/metabolismo
Contração Miocárdica/genética
Isquemia Miocárdica/metabolismo
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Animais
Canais de Cálcio Tipo L/genética
Carbonil Cianeto p-Trifluormetoxifenil Hidrazona/administração & dosagem
Ventrículos do Coração/metabolismo
Ventrículos do Coração/fisiopatologia
Isoproterenol/administração & dosagem
Mitocôndrias/enzimologia
Células Musculares/efeitos dos fármacos
Células Musculares/metabolismo
Contração Miocárdica/efeitos dos fármacos
Isquemia Miocárdica/genética
Isquemia Miocárdica/fisiopatologia
Miócitos Cardíacos/efeitos dos fármacos
Miócitos Cardíacos/metabolismo
Miócitos Cardíacos/patologia
Rana esculenta
Estresse Fisiológico/efeitos dos fármacos
Estresse Fisiológico/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channels, L-Type); 370-86-5 (Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone); 8L70Q75FXE (Adenosine Triphosphate); EC 3.6.1.- (F1F0-ATP synthase); EC 3.6.3.- (Mitochondrial Proton-Translocating ATPases); L628TT009W (Isoproterenol)
[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:170901
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184246


  10 / 28688 MEDLINE  
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[PMID]:28793220
[Au] Autor:Shiferaw Y; Aistrup GL; Wasserstrom JA
[Ad] Endereço:Department of Physics and Astronomy, California State University, Northridge, California. Electronic address: yshiferaw@csun.edu.
[Ti] Título:Mechanism for Triggered Waves in Atrial Myocytes.
[So] Source:Biophys J;113(3):656-670, 2017 Aug 08.
[Is] ISSN:1542-0086
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Excitation-contraction coupling in atrial cells is mediated by calcium (Ca) signaling between L-type Ca channels and Ryanodine receptors that occurs mainly at the cell boundary. This unique architecture dictates essential aspects of Ca signaling under both normal and diseased conditions. In this study we apply laser scanning confocal microscopy, along with an experimentally based computational model, to understand the Ca cycling dynamics of an atrial cell subjected to rapid pacing. Our main finding is that when an atrial cell is paced under Ca overload conditions, Ca waves can then nucleate on the cell boundary and propagate to the cell interior. These propagating Ca waves are referred to as "triggered waves" because they are initiated by L-type Ca channel openings during the action potential. These excitations are distinct from spontaneous Ca waves originating from random fluctuations of Ryanodine receptor channels, and which occur after much longer waiting times. Furthermore, we argue that the onset of these triggered waves is a highly nonlinear function of the sarcoplasmic reticulum Ca load. This strong nonlinearity leads to aperiodic response of Ca at rapid pacing rates that is caused by the complex interplay between paced Ca release and triggered waves. We argue further that this feature of atrial cells leads to dynamic instabilities that may underlie atrial arrhythmias. These studies will serve as a starting point to explore the nonlinear dynamics of atrial cells and will yield insights into the trigger and maintenance of atrial fibrillation.
[Mh] Termos MeSH primário: Sinalização do Cálcio
Átrios do Coração/citologia
Miócitos Cardíacos/citologia
[Mh] Termos MeSH secundário: Animais
Fibrilação Atrial/patologia
Sinalização do Cálcio/efeitos dos fármacos
Cães
Isoproterenol/farmacologia
Modelos Biológicos
Miócitos Cardíacos/efeitos dos fármacos
Miócitos Cardíacos/patologia
Dinâmica não Linear
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
L628TT009W (Isoproterenol)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170831
[Lr] Data última revisão:
170831
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE



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