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[PMID]:29182509
[Au] Autor:Xie L; Lu B; Zheng Z; Miao Y; Liu Y; Zhang Y; Zheng C; Ke X; Hu Q; Wang H
[Ad] Endereço:1​CAS Key Laboratory of Special Pathogens and Biosafety, Center for Emerging Infectious Diseases, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, PR China.
[Ti] Título:The 3C protease of enterovirus A71 counteracts the activity of host zinc-finger antiviral protein (ZAP).
[So] Source:J Gen Virol;99(1):73-85, 2018 Jan.
[Is] ISSN:1465-2099
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Enterovirus A71 (EV-A71) is a positive-strand RNA virus that causes hand-foot-mouth disease and neurological complications in children and infants. Although the underlying mechanisms remain to be further defined, impaired immunity is thought to play an important role. The host zinc-finger antiviral protein (ZAP), an IFN-stimulated gene product, has been reported to specifically inhibit the replication of certain viruses. However, whether ZAP restricts the infection of enteroviruses remains unknown. Here, we report that EV-A71 infection upregulates ZAP mRNA in RD and HeLa cells. Moreover, ZAP overexpression rendered 293 T cells resistant to EV-A71 infection, whereas siRNA-mediated depletion of endogenous ZAP enhanced EV-A71 infection. The EV-A71 infection stimulated site-specific proteolysis of two ZAP isoforms, leading to the accumulation of a 40 kDa N-terminal ZAP fragment in virus-infected cells. We further revealed that the 3C protease (3Cpro) of EV-A71 mediates ZAP cleavage, which requires protease activity. Furthermore, ZAP variants with single amino acid substitutions at Gln-369 were resistant to 3Cpro cleavage, implying that Gln-369 is the sole cleavage site in ZAP. Moreover, although ZAP overexpression inhibited EV-A71 replication, the cleaved fragments did not show this effect. Our results indicate that an equilibrium between ZAP and enterovirus 3Cpro controls viral infection. The findings in this study suggest that viral 3Cpro mediated ZAP cleavage may represent a mechanism to escape host antiviral responses.
[Mh] Termos MeSH primário: Cisteína Endopeptidases/metabolismo
Enterovirus Humano A/enzimologia
Interações Hospedeiro-Patógeno
Proteínas de Ligação a RNA/metabolismo
Proteínas Virais/metabolismo
Replicação Viral
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Substituição de Aminoácidos
Animais
Linhagem Celular Tumoral
Cisteína Endopeptidases/genética
Enterovirus Humano A/genética
Regulação da Expressão Gênica
Genes Reporter
Células HEK293
Células HeLa
Seres Humanos
Luciferases/genética
Luciferases/metabolismo
Células Musculares/metabolismo
Células Musculares/virologia
Proteólise
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Proteínas de Ligação a RNA/antagonistas & inibidores
Proteínas de Ligação a RNA/genética
Células Sf9/imunologia
Células Sf9/virologia
Transdução de Sinais
Spodoptera
Proteínas Virais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Small Interfering); 0 (RNA-Binding Proteins); 0 (Viral Proteins); 0 (ZC3HAV1 protein, human); EC 1.13.12.- (Luciferases); EC 3.4.22.- (Cysteine Endopeptidases); EC 3.4.22.28 (3C proteases)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171229
[Lr] Data última revisão:
171229
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1099/jgv.0.000982


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[PMID]:28466496
[Au] Autor:Temereva EN
[Ad] Endereço:Biological Faculty, Department of Invertebrate Zoology, Moscow State University, Vorobievi Gory 1-12, Moscow, 119991, Russia.
[Ti] Título:Ultrastructure of the coelom in the brachiopod Lingula anatina.
[So] Source:J Morphol;278(7):997-1011, 2017 Jul.
[Is] ISSN:1097-4687
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The organization of the coelomic system and the ultrastructure of the coelomic lining are used in phylogenetic analysis to establish the relationships between major taxa. Investigation of the anatomy and ultrastructure of the coelomic system in brachiopods, which are poorly studied, can provide answers to fundamental questions about the evolution of the coelom in coelomic bilaterians. In the current study, the organization of the coelom of the lophophore in the brachiopod Lingula anatina was investigated using semithin sectioning, 3D reconstruction, and transmission electron microscopy. The lophophore of L. anatina contains two main compartments: the preoral coelom and the lophophoral coelom. The lining of the preoral coelom consists of ciliated cells. The lophophoral coelom is subdivided into paired coelomic sacs: the large and small sinuses (= canals). The lining of the lophophoral coelom varies in structure and includes monociliate myoepithelium, alternating epithelial and myoepithelial cells, specialized peritoneum and muscle cells, and podocyte-like cells. Connections between cells of the coelomic lining are provided by adherens junctions, tight-like junctions, septate junctions, adhesive junctions, and direct cytoplasmic bridges. The structure of the coelomic lining varies greatly in both of the main stems of the Bilateria, that is, in the Protostomia and Deuterostomia. Because of this great variety, the structure of the coelomic lining cannot by itself be used in phylogenetic analysis. At the same time, the ciliated myoepithelium can be considered as the ancestral type of coelomic lining. The many different kinds of junctions between cells of the coelomic lining may help coordinate the functioning of epithelial cells and muscle cells.
[Mh] Termos MeSH primário: Invertebrados/anatomia & histologia
Invertebrados/ultraestrutura
[Mh] Termos MeSH secundário: Animais
Evolução Biológica
Esôfago/anatomia & histologia
Esôfago/ultraestrutura
Junções Intercelulares/ultraestrutura
Invertebrados/fisiologia
Células Musculares/ultraestrutura
[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:170504
[St] Status:MEDLINE
[do] DOI:10.1002/jmor.20693


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[PMID]:28942920
[Au] Autor:Ying W; Riopel M; Bandyopadhyay G; Dong Y; Birmingham A; Seo JB; Ofrecio JM; Wollam J; Hernandez-Carretero A; Fu W; Li P; Olefsky JM
[Ad] Endereço:Division of Endocrinology and Metabolism, Department of Medicine, UC San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
[Ti] Título:Adipose Tissue Macrophage-Derived Exosomal miRNAs Can Modulate In Vivo and In Vitro Insulin Sensitivity.
[So] Source:Cell;171(2):372-384.e12, 2017 Oct 05.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:MiRNAs are regulatory molecules that can be packaged into exosomes and secreted from cells. Here, we show that adipose tissue macrophages (ATMs) in obese mice secrete miRNA-containing exosomes (Exos), which cause glucose intolerance and insulin resistance when administered to lean mice. Conversely, ATM Exos obtained from lean mice improve glucose tolerance and insulin sensitivity when administered to obese recipients. miR-155 is one of the miRNAs overexpressed in obese ATM Exos, and earlier studies have shown that PPARγ is a miR-155 target. Our results show that miR-155KO animals are insulin sensitive and glucose tolerant compared to controls. Furthermore, transplantation of WT bone marrow into miR-155KO mice mitigated this phenotype. Taken together, these studies show that ATMs secrete exosomes containing miRNA cargo. These miRNAs can be transferred to insulin target cell types through mechanisms of paracrine or endocrine regulation with robust effects on cellular insulin action, in vivo insulin sensitivity, and overall glucose homeostasis.
[Mh] Termos MeSH primário: Tecido Adiposo/citologia
Resistência à Insulina
Macrófagos/metabolismo
MicroRNAs/metabolismo
[Mh] Termos MeSH secundário: Adipócitos/metabolismo
Animais
Células Cultivadas
Glucose/metabolismo
Hepatócitos/metabolismo
Fígado/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Células Musculares/metabolismo
Músculo Esquelético/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MicroRNAs); 0 (Mirn155 microRNA, mouse); IY9XDZ35W2 (Glucose)
[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:170926
[St] Status:MEDLINE


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[PMID]:28867488
[Au] Autor:Bonnet A; Lambert G; Ernest S; Dutrieux FX; Coulpier F; Lemoine S; Lobbardi R; Rosa FM
[Ad] Endereço:IBENS, Institut de Biologie de l'Ecole Normale Supérieure, 75005 Paris, France; INSERM U1024, 75005 Paris, France; CNRS UMR 8197, 75005 Paris, France. Electronic address: bonnet.aline@gmail.com.
[Ti] Título:Quaking RNA-Binding Proteins Control Early Myofibril Formation by Modulating Tropomyosin.
[So] Source:Dev Cell;42(5):527-541.e4, 2017 Sep 11.
[Is] ISSN:1878-1551
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Skeletal muscle contraction is mediated by myofibrils, complex multi-molecular scaffolds structured into repeated units, the sarcomeres. Myofibril structure and function have been extensively studied, but the molecular processes regulating its formation within the differentiating muscle cell remain largely unknown. Here we show in zebrafish that genetic interference with the Quaking RNA-binding proteins disrupts the initial steps of myofibril assembly without affecting early muscle differentiation. Using RNA sequencing, we demonstrate that Quaking is required for accumulation of the muscle-specific tropomyosin-3 transcript, tpm3.12. Further functional analyses reveal that Tpm3.12 mediates Quaking control of myofibril formation. Moreover, we identified a Quaking-binding site in the 3' UTR of tpm3.12 transcript, which is required in vivo for tpm3.12 accumulation and myofibril formation. Our work uncovers a Quaking/Tpm3 pathway controlling de novo myofibril assembly. This unexpected developmental role for Tpm3 could be at the origin of muscle defects observed in human congenital myopathies associated with tpm3 mutation.
[Mh] Termos MeSH primário: Miofibrilas/metabolismo
Proteínas de Ligação a RNA/metabolismo
Tropomiosina/metabolismo
Proteínas de Peixe-Zebra/metabolismo
Peixe-Zebra/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas/genética
Animais
Sítios de Ligação
Diferenciação Celular/genética
Desenvolvimento Embrionário/genética
Regulação da Expressão Gênica no Desenvolvimento
Células Musculares/citologia
Células Musculares/metabolismo
Desenvolvimento Muscular/genética
Miosinas/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Sarcômeros/metabolismo
Somitos/embriologia
Somitos/metabolismo
Peixe-Zebra/embriologia
Peixe-Zebra/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (RNA, Messenger); 0 (RNA-Binding Proteins); 0 (Tropomyosin); 0 (Zebrafish Proteins); 0 (qk protein, zebrafish); EC 3.6.4.1 (Myosins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170905
[St] Status: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


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[PMID]:28834713
[Au] Autor:Rickert C; Proenza C
[Ad] Endereço:Department of Physiology and Biophysics, University of Colorado-Anschutz Medical Campus, Aurora, Colorado.
[Ti] Título:ParamAP: Standardized Parameterization of Sinoatrial Node Myocyte Action Potentials.
[So] Source:Biophys J;113(4):765-769, 2017 Aug 22.
[Is] ISSN:1542-0086
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sinoatrial node myocytes act as cardiac pacemaker cells by generating spontaneous action potentials (APs). Much information is encoded in sinoatrial AP waveforms, but both the analysis and the comparison of AP parameters between studies is hindered by the lack of standardized parameter definitions and the absence of automated analysis tools. Here we introduce ParamAP, a standalone cross-platform computational tool that uses a template-free detection algorithm to automatically identify and parameterize APs from text input files. ParamAP employs a graphic user interface with automatic and user-customizable input modes, and it outputs data files in text and PDF formats. ParamAP returns a total of 16 AP waveform parameters including time intervals such as the AP duration, membrane potentials such as the maximum diastolic potential, and rates of change of the membrane potential such as the diastolic depolarization rate. ParamAP provides a robust AP detection algorithm in combination with a standardized AP parameter analysis over a wide range of AP waveforms and firing rates, owing in part to the use of an iterative algorithm for the determination of the threshold potential and the diastolic depolarization rate that is independent of the maximum upstroke velocity, a parameter that can vary significantly among sinoatrial APs. Because ParamAP is implemented in Python 3, it is also highly customizable and extensible. In conclusion, ParamAP is a powerful computational tool that facilitates quantitative analysis and enables comparison of sinoatrial APs by standardizing parameter definitions and providing an automated work flow.
[Mh] Termos MeSH primário: Potenciais de Ação
Biologia Computacional/métodos
Células Musculares/citologia
Nó Sinoatrial/citologia
Estatística como Assunto/normas
[Mh] Termos MeSH secundário: Padrões de Referência
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170824
[St] Status:MEDLINE


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[PMID]:28696251
[Au] Autor:Zhai X; Leo MD; Jaggar JH
[Ad] Endereço:From the Department of Physiology, University of Tennessee Health Science Center, Memphis.
[Ti] Título:Endothelin-1 Stimulates Vasoconstriction Through Rab11A Serine 177 Phosphorylation.
[So] Source:Circ Res;121(6):650-661, 2017 Sep 01.
[Is] ISSN:1524-4571
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Large-conductance calcium-activated potassium channels (BK) are composed of pore-forming BKα and auxiliary ß1 subunits in arterial smooth muscle cells (myocytes). Vasoconstrictors, including endothelin-1 (ET-1), inhibit myocyte BK channels, leading to contraction, but mechanisms involved are unclear. Recent evidence indicates that BKα is primarily plasma membrane localized, whereas the cellular location of ß1 can be rapidly altered by Rab11A-positive recycling endosomes. Whether vasoconstrictors regulate the multisubunit composition of surface BK channels to stimulate contraction is unclear. OBJECTIVE: Test the hypothesis that ET-1 inhibits BK channels by altering BKα and ß1 surface trafficking in myocytes, identify mechanisms involved, and determine functional significance in myocytes of small cerebral arteries. METHODS AND RESULTS: ET-1, through activation of PKC (protein kinase C), reduced surface ß1 abundance and the proximity of ß1 to surface BKα in myocytes. In contrast, ET-1 did not alter surface BKα, total ß1, or total BKα proteins. ET-1 stimulated Rab11A phosphorylation, which reduced Rab11A activity. Rab11A serine 177 was identified as a high-probability PKC phosphorylation site. Expression of a phosphorylation-incapable Rab11A construct (Rab11A S177A) blocked the ET-1-induced Rab11A phosphorylation, reduction in Rab11A activity, and decrease in surface ß1 protein. ET-1 inhibited single BK channels and transient BK currents in myocytes and stimulated vasoconstriction via a PKC-dependent mechanism that required Rab11A S177. In contrast, NO-induced Rab11A activation, surface trafficking of ß1 subunits, BK channel and transient BK current activation, and vasodilation did not involve Rab11A S177. CONCLUSIONS: ET-1 stimulates PKC-mediated phosphorylation of Rab11A at serine 177, which inhibits Rab11A and Rab11A-dependent surface trafficking of ß1 subunits. The decrease in surface ß1 subunits leads to a reduction in BK channel calcium-sensitivity, inhibition of transient BK currents, and vasoconstriction. We describe a unique mechanism by which a vasoconstrictor inhibits BK channels and identify Rab11A serine 177 as a modulator of arterial contractility.
[Mh] Termos MeSH primário: Endotelina-1/farmacologia
Vasoconstrição
Proteínas rab de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Endotelina-1/metabolismo
Células HEK293
Seres Humanos
Canais de Potássio Ativados por Cálcio de Condutância Alta/metabolismo
Masculino
Células Musculares/efeitos dos fármacos
Células Musculares/metabolismo
Células Musculares/fisiologia
Músculo Liso Vascular/metabolismo
Músculo Liso Vascular/fisiologia
Fosforilação
Proteína Quinase C/metabolismo
Processamento de Proteína Pós-Traducional
Transporte Proteico
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelin-1); 0 (Large-Conductance Calcium-Activated Potassium Channels); EC 2.7.11.13 (Protein Kinase C); EC 3.6.1.- (rab11 protein); EC 3.6.5.2 (rab GTP-Binding Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170712
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCRESAHA.117.311102


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[PMID]:28658296
[Au] Autor:Castellanos N; Martínez LC; Silva EH; Teodoro AV; Serrão JE; Oliveira EE
[Ad] Endereço:Departamento de Entomologia, Universidade Federal de Viçosa, Viçosa-MG, Brasil.
[Ti] Título:Ultrastructural analysis of salivary glands in a phytophagous stink bug revealed the presence of unexpected muscles.
[So] Source:PLoS One;12(6):e0179478, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The exceptional abilities of stink bugs (Hemiptera: Pentatomidae) to colonize a diverse group of plants have been attributed to the feeding behaviors and the functions of the salivary complex of these insects. Here, we describe the ultrastructure of the salivary glands of the Neotropical brown stink bug, Euschistus heros, which is a major component of the pentatomid pest complex on soybeans, Glycine max, in the neotropics. Our results revealed a salivary gland complex consisting of two lobes (i.e., anterior and posterior), with a constriction between them (i.e., the hilum), in which the salivary and accessory gland ducts are inserted. The principal gland epithelium has a single layer of cells lining an enlarged lumen filled with saliva, and these cells are cuboidal, rich in rough endoplasmic reticulum and secretory vesicles, with well-developed nuclei, all of which are typical features of protein-secreting cells. We report, for the first time in insects, the presence of a layer of muscle cells surrounding the columnar hilum epithelium. The accessory salivary gland cells are cuboidal with nuclei containing condensed chromatin and cytoplasm rich in vacuoles and rough endoplasmic reticulum, indicating the potential involvement of these glands in water transport/secretion. The lumen content of each lobe of the principal gland suggests that the lobes produce different compounds. Thus, our results suggest that the E. heros salivary complex might have unconventional mechanisms to mix/release saliva, which might help explain the polyphagous abilities of these insects.
[Mh] Termos MeSH primário: Retículo Endoplasmático Rugoso/ultraestrutura
Heterópteros/ultraestrutura
Células Musculares/ultraestrutura
Glândulas Salivares/ultraestrutura
Vacúolos/ultraestrutura
[Mh] Termos MeSH secundário: Animais
Comportamento Alimentar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170629
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179478


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[PMID]:28637196
[Au] Autor:Cho HJ; Heo W; Han JW; Lee YH; Park JM; Kang MJ; Yoon JH; Lee MG; Kim CH; Kim JY
[Ad] Endereço:Department of Otorhinolaryngology, Yonsei University College of Medicine, Seoul, Korea.
[Ti] Título:Chronological Change of Right Ventricle by Chronic Intermittent Hypoxia in Mice.
[So] Source:Sleep;40(8), 2017 Aug 01.
[Is] ISSN:1550-9109
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Study Objective: No studies have investigated sequential changes in the heart on magnetic resonance imaging (MRI), along with observation of functional lung phenotypes and genetics, over the duration of chronic intermittent hypoxia (CIH). We investigated chronological changes in heart and lung phenotypes after CIH using a mouse model to provide new insights into the pathophysiology of sleep apnea-induced cardiovascular disease. Methods: C57BL/6J adult male mice were randomized to 4 or 8 weeks of CIH. Cardiac cine-MRI images were analyzed to assess functional parameters of right ventricle (RV). Histopathological features of myocytes and pulmonary vessels, as well as genes involved in the endothelin (ET) system, were investigated. Results: Function of the RV reduced significantly at 4 weeks and continuously decreased following another 4 weeks of CIH, although the rate of decrease was attenuated. Notably, persistence of reduced ejection fraction and end-systole RV wall thickness (WT) and increases in the ET system of the lungs and blood strongly implied the development of pulmonary hypertension after 8 weeks of CIH. Conclusions: RV dysfunction with reduced end-systole RV WT could be a late phenotype in long-standing CIH and possibly also in obstructive sleep apnea.
[Mh] Termos MeSH primário: Ventrículos do Coração/patologia
Hipóxia/patologia
[Mh] Termos MeSH secundário: Animais
Doença Crônica
Modelos Animais de Doenças
Endotelinas/metabolismo
Pulmão/irrigação sanguínea
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Células Musculares/metabolismo
Células Musculares/patologia
Apneia Obstrutiva do Sono/metabolismo
Apneia Obstrutiva do Sono/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1093/sleep/zsx103


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[PMID]:28618254
[Au] Autor:Piñol-Jurado P; Gallardo E; de Luna N; Suárez-Calvet X; Sánchez-Riera C; Fernández-Simón E; Gomis C; Illa I; Díaz-Manera J
[Ad] Endereço:Neuromuscular Disorders Unit, Department of Neurology, Universitat Autònoma de Barcelona, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain; Network Research Center in Rare Diseases, Barcelona, Spain.
[Ti] Título:Platelet-Derived Growth Factor BB Influences Muscle Regeneration in Duchenne Muscle Dystrophy.
[So] Source:Am J Pathol;187(8):1814-1827, 2017 Aug.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Duchenne muscular dystrophy (DMD) is characterized by a progressive loss of muscle fibers, and their substitution by fibrotic and adipose tissue. Many factors contribute to this process, but the molecular pathways related to regeneration and degeneration of muscle are not completely known. Platelet-derived growth factor (PDGF)-BB belongs to a family of growth factors that regulate proliferation, migration, and differentiation of mesenchymal cells. The role of PDGF-BB in muscle regeneration in humans has not been studied. We analyzed the expression of PDGF-BB in muscle biopsy samples from controls and patients with DMD. We performed in vitro experiments to understand the effects of PDGF-BB on myoblasts involved in the pathophysiology of muscular dystrophies and confirmed our results in vivo by treating the mdx murine model of DMD with repeated i.m. injections of PDGF-BB. We observed that regenerating and necrotic muscle fibers in muscle biopsy samples from DMD patients expressed PDGF-BB. In vitro, PDGF-BB attracted myoblasts and activated their proliferation. Analysis of muscles from the animals treated with PDGF-BB showed an increased population of satellite cells and an increase in the number of regenerative fibers, with a reduction in inflammatory infiltrates, compared with those in vehicle-treated mice. Based on our results, PDGF-BB may play a protective role in muscular dystrophies by enhancing muscle regeneration through activation of satellite cell proliferation and migration.
[Mh] Termos MeSH primário: Proliferação Celular/efeitos dos fármacos
Células Musculares/efeitos dos fármacos
Músculo Esquelético/metabolismo
Distrofia Muscular de Duchenne/metabolismo
Proteínas Proto-Oncogênicas c-sis/metabolismo
Regeneração/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/efeitos dos fármacos
Movimento Celular/efeitos dos fármacos
Distrofina/genética
Distrofina/metabolismo
Seres Humanos
Camundongos
Camundongos Endogâmicos mdx
Células Musculares/metabolismo
Músculo Esquelético/efeitos dos fármacos
Músculo Esquelético/patologia
Distrofia Muscular de Duchenne/genética
Distrofia Muscular de Duchenne/patologia
Proteínas Proto-Oncogênicas c-sis/genética
Proteínas Proto-Oncogênicas c-sis/farmacologia
Regeneração/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dystrophin); 0 (Proto-Oncogene Proteins c-sis); 1B56C968OA (becaplermin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170616
[St] Status:MEDLINE



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