Base de dados : MEDLINE
Pesquisa : G04.325 [Categoria DeCS]
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[PMID]:29351550
[Au] Autor:Rachid TL; Silva-Veiga FM; Graus-Nunes F; Bringhenti I; Mandarim-de-Lacerda CA; Souza-Mello V
[Ad] Endereço:Laboratory of Morphometry, Metabolism, and Cardiovascular Diseases, Biomedical Center, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
[Ti] Título:Differential actions of PPAR-α and PPAR-ß/δ on beige adipocyte formation: A study in the subcutaneous white adipose tissue of obese male mice.
[So] Source:PLoS One;13(1):e0191365, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND AIMS: Obesity compromises adipocyte physiology. PPARs are essential to adipocyte plasticity, but its isolated role in the browning phenomenon is not clear. This study aimed to examine whether activation of PPAR-α or PPAR-ß/δ could induce beige cell depots in the subcutaneous white adipose tissue of diet-induced obese mice. MATERIAL AND METHODS: Sixty animals were randomly assigned to receive a control diet (C, 10% lipids) or a high-fat diet (HF, 50% lipids) for ten weeks. Then each group was re-divided to begin the treatments that lasted 4 weeks, totalizing six groups: C, C-α (C plus PPAR-α agonist, 2.5 mg/kg BM), C-ß (C plus PPAR-ß/δ agonist, 1 mg/kg BM), HF, HF-α (HF plus PPAR-α agonist), HF-ß (HF plus PPAR-ß/δ agonist). RESULTS: HF animals presented with overweight, glucose intolerance and subcutaneous white adipocyte hypertrophy. Both treatments significantly attenuated these parameters. Browning, verified by UCP1 positive beige cells and enhanced body temperature, was just observed in PPAR-α treated groups. PPAR-α agonism also elicited an enhanced gene expression of the thermogenesis effector UCP1, the beige-selective gene TMEM26 and the PRDM16, an essential gene for brown-like phenotype maintenance in the beige adipocytes when compared to their counterparts. The enhanced CIDEA and the reduced UCP1 gene levels might justify the white phenotype predominance after the treatment with the PPAR-ß/δ agonist. CONCLUSIONS: This work provides evidence that the PPAR-ß/δ agonist ameliorated metabolic disorders through enhanced beta-oxidation and better tolerance to glucose, whereas the PPAR-α agonism was confirmed as a promising therapeutic target for treating metabolic diseases via beige cell induction and enhanced thermogenesis.
[Mh] Termos MeSH primário: Adipócitos Bege/efeitos dos fármacos
Obesidade/tratamento farmacológico
PPAR alfa/agonistas
PPAR delta/agonistas
PPAR beta/agonistas
[Mh] Termos MeSH secundário: Adipócitos Bege/metabolismo
Adipócitos Bege/patologia
Tecido Adiposo Branco/efeitos dos fármacos
Tecido Adiposo Branco/metabolismo
Tecido Adiposo Branco/patologia
Adiposidade/efeitos dos fármacos
Animais
Glicemia/metabolismo
Peso Corporal/efeitos dos fármacos
Tamanho Celular/efeitos dos fármacos
Dieta Hiperlipídica/efeitos adversos
Ingestão de Energia/efeitos dos fármacos
Expressão Gênica/efeitos dos fármacos
Intolerância à Glucose/tratamento farmacológico
Hiperinsulinismo/tratamento farmacológico
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Obesidade/metabolismo
Obesidade/patologia
Termogênese/efeitos dos fármacos
Proteína Desacopladora 1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Blood Glucose); 0 (PPAR alpha); 0 (PPAR delta); 0 (PPAR-beta); 0 (Ucp1 protein, mouse); 0 (Uncoupling Protein 1)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180120
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191365


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[PMID]:28471109
[Au] Autor:Ye SF; Yang Y; Wu L; Ma WW; Zeng HH
[Ad] Endereço:State Key Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, China.
[Ti] Título:Ethaselen: a novel organoselenium anticancer agent targeting thioredoxin reductase 1 reverses cisplatin resistance in drug-resistant K562 cells by inducing apoptosis.
[So] Source:J Zhejiang Univ Sci B;18(5):373-382, 2017 May.
[Is] ISSN:1862-1783
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:It has been reported that Ethaselen shows inhibitory effects on thioredoxin reductase (TrxR) activity and human tumor cell growth. In order to find an efficient way to reverse cisplatin resistance, we investigated the reversal effects of Ethaselen on cisplatin resistance in K562/cisplatin (CDDP) cells that were established by pulse-inducing human erythrocyte leukemic cell line K562, which are fivefold more resistant to cisplatin compared to K562 cells. The morphology and growth showed that the adhesion of K562/CDDP further decreased while the cell volume increased. The proliferation of K562/CDDP is strengthened. The antitumor activities in vitro were assessed by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and combination index (CI), showing the significant synergic effects of cisplatin and Ethaselen. Focusing on apoptosis, a series of comparisons was made between K562 and K562/CDDP. Cisplatin induced higher reactive oxygen species (ROS) generation in K562 and subsequently induced the formation of mitochondrial permeability transition pores (PTPs). In addition, cisplatin increased the ratio of Bax to Bcl-2 in K562, which can influence the mitochondrial membrane permeability. PTP formation and mitochondrial membrane permeabilization eventually resulted in the release of cytochrome c and activation of the Caspase pathway. However, these effects were not clearly seen in K562/CDDP, which may be the reason for the acquired CDDP resistance. However, Ethaselen can induce a high level of ROS in K562/CDDP by TrxR activity inhibition and increased ratio of Bax to Bcl-2 in K562/CDDP by nuclear factor κB (NF-κB) suppression, which subsequently induces the release of cytochrome c in K562/CDDP. This response is partly responsible for the reversal of the cisplatin resistance in K562/CDDP cells.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Compostos Bicíclicos Heterocíclicos com Pontes/administração & dosagem
Cisplatino/administração & dosagem
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Compostos Organosselênicos/administração & dosagem
Tiorredoxina Redutase 1/antagonistas & inibidores
Tiorredoxina Redutase 1/metabolismo
[Mh] Termos MeSH secundário: Antineoplásicos/administração & dosagem
Proliferação Celular/efeitos dos fármacos
Tamanho Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Ativação Enzimática/efeitos dos fármacos
Seres Humanos
Células K562
Terapia de Alvo Molecular/métodos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 ((1,2-bis(1,2-benzisoselenazolone-3(2H)-ketone))ethane); 0 (Antineoplastic Agents); 0 (Bridged Bicyclo Compounds, Heterocyclic); 0 (Organoselenium Compounds); EC 1.8.1.9 (TXNRD1 protein, human); EC 1.8.1.9 (Thioredoxin Reductase 1); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1631/jzus.B1600073


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[PMID]:29381029
[Au] Autor:Yoo J; Chang Y; Kim H; Baek S; Choi H; Jeong GJ; Shin J; Kim H; Kim BS; Kim J
[Ti] Título:Efficient Direct Lineage Reprogramming of Fibroblasts into Induced Cardiomyocytes Using Nanotopographical Cues.
[So] Source:J Biomed Nanotechnol;13(3):269-79, 2017 Mar.
[Is] ISSN:1550-7033
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Induced cardiomyocytes (iCMs) generated via direct lineage reprogramming offer a novel therapeutic target for the study and treatment of cardiac diseases. However, the efficiency of iCM generation is significantly low for therapeutic applications. Here, we show an efficient direct conversion of somatic fibroblasts into iCMs using nanotopographic cues. Compared with flat substrates, the direct conversion of fibroblasts into iCMs on nanopatterned substrates resulted in a dramatic increase in the reprogramming efficiency and maturation of iCM phenotypes. Additionally, enhanced reprogramming by substrate nanotopography was due to changes in the activation of focal adhesion kinase and specific histone modifications. Taken together, these results suggest that nanotopographic cues can serve as an efficient stimulant for direct lineage reprogramming into iCMs.
[Mh] Termos MeSH primário: Técnicas de Reprogramação Celular/métodos
Fibroblastos/citologia
Fibroblastos/fisiologia
Miócitos Cardíacos/citologia
Miócitos Cardíacos/fisiologia
Nanopartículas/química
Nanopartículas/ultraestrutura
[Mh] Termos MeSH secundário: Animais
Técnicas de Cultura Celular por Lotes/métodos
Adesão Celular/fisiologia
Diferenciação Celular/fisiologia
Linhagem da Célula/fisiologia
Polaridade Celular/fisiologia
Proliferação Celular/fisiologia
Tamanho Celular
Células Cultivadas
Camundongos
Propriedades de Superfície
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180131
[St] Status:MEDLINE


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[PMID]:28470533
[Au] Autor:Öz S; Breiling A; Maercker C
[Ad] Endereço:German Cancer Research Center (DKFZ), Epigenomics and Cancer Risk Factors, Heidelberg, Germany.
[Ti] Título:Measurement of Cellular Behavior by Electrochemical Impedance Sensing.
[So] Source:Methods Mol Biol;1601:267-273, 2017.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:There is a great demand for label-free in vitro assays in a high-throughput context, in order to measure cell viability and analyze cellular functions like cell migration or cell differentiation under noninvasive conditions. Here, we describe impedance measurement to quantify dynamic changes on cell morphology in real time. In order to monitor physiological changes, cells are grown in tissue culture vessels where gold electrodes are incorporated at the bottom. An alternating current signal of several kHz is applied to the electrodes and the resulting voltage is measured to calculate the cellular impedance. Since impedance is closely related to the area of the electrodes covered by the growing cells, parameters such as cell number, size of the cells attached to the electrodes, and cell-cell and cell-substrate/extracellular matrix interactions contribute to the overall impedance values.
[Mh] Termos MeSH primário: Diferenciação Celular/fisiologia
Movimento Celular/fisiologia
Sobrevivência Celular/fisiologia
Impedância Elétrica
[Mh] Termos MeSH secundário: Adesão Celular/fisiologia
Comunicação Celular/fisiologia
Contagem de Células
Tamanho Celular
Eletrodos
Células-Tronco de Carcinoma Embrionário/química
Matriz Extracelular/química
Ouro/química
Ensaios de Triagem em Larga Escala
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
7440-57-5 (Gold)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1007/978-1-4939-6960-9_21


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[PMID]:29337054
[Au] Autor:Han SJ; Jung JK; Im SS; Lee SR; Jang BC; Park KM; Kim JI
[Ad] Endereço:Department of Anatomy and BK21 Plus, Kyungpook National University School of Medicine, Daegu, 700-422, Republic of Korea.
[Ti] Título:Deficiency of primary cilia in kidney epithelial cells induces epithelial to mesenchymal transition.
[So] Source:Biochem Biophys Res Commun;496(2):450-454, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Primary cilium is a microtubule-based non-motile organelle that plays critical roles in kidney pathophysiology. Our previous studies revealed that the lengths of primary cilia decreased upon renal ischemia/reperfusion injury and oxidative stress, and restored with recovery. Here, we tested the hypothesis that lack of primary cilium causes epithelial to mesenchymal transition (EMT) of kidney tubule cells. We investigated the alteration of length of primary cilia in TGF-ß-induced EMT via visualization of primary cilia by fluorescence staining against acetylated α-tubulin. EMT was determined by measuring mesenchymal protein expression using quantitative PCR and indirect fluorescence staining. As a result, TGF-ß treatment decreased ciliary length along with EMT. To test whether defect of primary cilia trigger onset of EMT, cilia formation was disturbed by knock down of ciliary protein using siRNA along with/without TGF-ß treatment. Knock down of Arl13b and Ift20 reduced cilia elongation and increased expression of EMT markers such as fibronectin, α-SMA, and collagen III. TGF-ß-induced EMT was greater as well in Arl13b and Ift20-knock down cells compared to control cells. Taken together, deficiency of primary cilia trigger EMT and exacerbates it under pro-fibrotic signals.
[Mh] Termos MeSH primário: Cílios/efeitos dos fármacos
Transição Epitelial-Mesenquimal/efeitos dos fármacos
Fator de Crescimento Transformador beta/farmacologia
Tubulina (Proteína)/genética
[Mh] Termos MeSH secundário: Fatores de Ribosilação do ADP/antagonistas & inibidores
Fatores de Ribosilação do ADP/genética
Fatores de Ribosilação do ADP/metabolismo
Actinas/genética
Actinas/metabolismo
Animais
Proteínas de Transporte/antagonistas & inibidores
Proteínas de Transporte/genética
Proteínas de Transporte/metabolismo
Tamanho Celular
Cílios/metabolismo
Cílios/ultraestrutura
Colágeno Tipo III/genética
Colágeno Tipo III/metabolismo
Cães
Transição Epitelial-Mesenquimal/genética
Fibronectinas/genética
Fibronectinas/metabolismo
Regulação da Expressão Gênica
Células Madin Darby de Rim Canino
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Transdução de Sinais
Tubulina (Proteína)/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Actins); 0 (Carrier Proteins); 0 (Collagen Type III); 0 (Fibronectins); 0 (RNA, Small Interfering); 0 (Transforming Growth Factor beta); 0 (Tubulin); EC 3.6.5.2 (ADP-Ribosylation Factors)
[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:180117
[St] Status:MEDLINE


  6 / 16572 MEDLINE  
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[PMID]:29227596
[Au] Autor:Veklich TO
[Ti] Título:The inhibitory influence of calix[4]Arene of C-90 on the activity of Ca2+,Mg2+-ATPases in plasma membrane and sarcoplasmic reticulum in myometrium cells.
[So] Source:Ukr Biochem J;88(2):5-15, 2016 Mar-Apr.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:Our study on the plasma membrane vesicles and myometrium cells treated with 0.1% digitonin showed that inhibitory effect of calix[4]arene C-90 (5,11,17,23-tetra(trifluoro)methyl(phenylsulphonylimino)-methylamino- 25,26,27,28-tetrapropoxy-calix[4]arene) on the plasma membrane Ca2+,Mg2+-ATPase was more significant than on the Ca2+,Mg2+-ATPase in sarcoplasmic reticulum (the inhibition coefficient I0.5 values were 20.2 ± 0.5 µM and 57.0 ± 1.4 µM for the plasma membrane Ca2+,Mg2+-ATPase and Ca2+,Mg2+-ATPase in sarcoplasmic reticulum, respectively (n = 5)). Inhibition kinetics of calix[4]arene C-90 effect on the Ca2+,Mg2+- ATPase activities in plasma membrane and sarcoplasmic reticulum were studied. This substance inhibited both pumps as complete noncompetitive inhibitor. Calix[4]arene C-90 caused the increase of intracellular Ca2+ concentration and decrease of hydrodynamic diameter in smooth muscle cells similar to the action of uterotonic drug oxytocin.
[Mh] Termos MeSH primário: ATPase de Ca(2+) e Mg(2+)/antagonistas & inibidores
Calixarenos/farmacologia
Membrana Celular/efeitos dos fármacos
Inibidores Enzimáticos/farmacologia
Miócitos de Músculo Liso/efeitos dos fármacos
Fenóis/farmacologia
Retículo Sarcoplasmático/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
ATPase de Ca(2+) e Mg(2+)/metabolismo
Cálcio/metabolismo
Membrana Celular/enzimologia
Tamanho Celular
Feminino
Transporte de Íons/efeitos dos fármacos
Cinética
Miócitos de Músculo Liso/enzimologia
Miométrio/efeitos dos fármacos
Miométrio/enzimologia
Ocitocina/farmacologia
Ligação Proteica
Retículo Sarcoplasmático/enzimologia
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Phenols); 0 (calix(4)arene); 130036-26-9 (Calixarenes); 50-56-6 (Oxytocin); EC 3.6.1.- (Ca(2+) Mg(2+)-ATPase); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.02.005


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[PMID]:28743797
[Au] Autor:Castillo-Azofeifa D; Losacco JT; Salcedo E; Golden EJ; Finger TE; Barlow LA
[Ad] Endereço:Department of Cell and Developmental Biology and the Rocky Mountain Taste and Smell Center University of Colorado, Anschutz Medical Campus, Aurora, CO 80045, USA.
[Ti] Título:Sonic hedgehog from both nerves and epithelium is a key trophic factor for taste bud maintenance.
[So] Source:Development;144(17):3054-3065, 2017 09 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The integrity of taste buds is intimately dependent on an intact gustatory innervation, yet the molecular nature of this dependency is unknown. Here, we show that differentiation of new taste bud cells, but not progenitor proliferation, is interrupted in mice treated with a hedgehog (Hh) pathway inhibitor (HPI), and that gustatory nerves are a source of sonic hedgehog (Shh) for taste bud renewal. Additionally, epithelial taste precursor cells express Shh transiently, and provide a local supply of Hh ligand that supports taste cell renewal. Taste buds are minimally affected when Shh is lost from either tissue source. However, when both the epithelial and neural supply of Shh are removed, taste buds largely disappear. We conclude Shh supplied by taste nerves and local taste epithelium act in concert to support continued taste bud differentiation. However, although neurally derived Shh is in part responsible for the dependence of taste cell renewal on gustatory innervation, neurotrophic support of taste buds likely involves a complex set of factors.
[Mh] Termos MeSH primário: Epitélio/inervação
Epitélio/metabolismo
Proteínas Hedgehog/metabolismo
Papilas Gustativas/metabolismo
[Mh] Termos MeSH secundário: Animais
Proliferação Celular
Tamanho Celular
Feminino
Deleção de Genes
Masculino
Camundongos
Células Receptoras Sensoriais/metabolismo
Transdução de Sinais
Células-Tronco/citologia
Células-Tronco/metabolismo
Paladar
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Hedgehog Proteins); 0 (Shh protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180109
[Lr] Data última revisão:
180109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1242/dev.150342


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[PMID]:29183944
[Au] Autor:Tsugawa S; Hervieux N; Kierzkowski D; Routier-Kierzkowska AL; Sapala A; Hamant O; Smith RS; Roeder AHK; Boudaoud A; Li CB
[Ad] Endereço:Theoretical Biology Laboratory, RIKEN, Wako 351-0198, Japan.
[Ti] Título:Clones of cells switch from reduction to enhancement of size variability in sepals.
[So] Source:Development;144(23):4398-4405, 2017 Dec 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Organs form with remarkably consistent sizes and shapes during development, whereas a high variability in growth is observed at the cell level. Given this contrast, it is unclear how such consistency in organ scale can emerge from cellular behavior. Here, we examine an intermediate scale, the growth of clones of cells in sepals. Each clone consists of the progeny of a single progenitor cell. At early stages, we find that clones derived from a small progenitor cell grow faster than those derived from a large progenitor cell. This results in a reduction in clone size variability, a phenomenon we refer to as size uniformization. By contrast, at later stages of clone growth, clones change their growth pattern to enhance size variability, when clones derived from larger progenitor cells grow faster than those derived from smaller progenitor cells. Finally, we find that, at early stages, fast growing clones exhibit greater cell growth heterogeneity. Thus, cellular variability in growth might contribute to a decrease in the variability of clones throughout the sepal.
[Mh] Termos MeSH primário: Arabidopsis/citologia
Arabidopsis/crescimento & desenvolvimento
[Mh] Termos MeSH secundário: Diferenciação Celular
Divisão Celular
Tamanho Celular
Células Clonais/citologia
Flores/citologia
Flores/crescimento & desenvolvimento
Modelos Biológicos
Desenvolvimento Vegetal/fisiologia
Células-Tronco/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171204
[Lr] Data última revisão:
171204
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE
[do] DOI:10.1242/dev.153999


  9 / 16572 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]:28743850
[Au] Autor:Shibata Y; Miyazaki T
[Ad] Endereço:Department of Conservative Dentistry, Division of Biomaterials & Engineering, Showa University School of Dentistry, Tokyo, Japan.
[Ti] Título:[New methods for the evaluation of bone quality. Nanoindentation protocol for measurement of bone mechanical properties of material level.]
[So] Source:Clin Calcium;27(8):1139-1145, 2017.
[Is] ISSN:0917-5857
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:Bone is an inhomogeneous, anisotropic natural biomaterial with complex, multiscale structural variations. Thus, experiments on the bulk scale using a universal testing machine are not applicable for localized precision mechanical testing of bone. Nanoscale mechanical testing technologies such as nanoindentation enables to assess the intrinsic toughening mechanism of bone, which is a function of the highly-organized matrix proteins within the mineralized nanostructure. Understanding the basic nanomechanical properties of calcified tissues will help us to appreciate general concepts associated with the excellent design of advanced engineering materials and engineered tissues.
[Mh] Termos MeSH primário: Osso e Ossos/citologia
[Mh] Termos MeSH secundário: Fenômenos Biomecânicos
Densidade Óssea
Osso e Ossos/fisiologia
Tamanho Celular
Seres Humanos
Nanoestruturas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:CliCa170811391145



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