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[PMID]:28449099
[Au] Autor:Allagnat F; Dubuis C; Lambelet M; Le Gal L; Alonso F; Corpataux JM; Déglise S; Haefliger JA
[Ad] Endereço:Department of Vascular Surgery, Centre Hospitalier Universitaire Vaudois (CHUV), Lausanne, Switzerland.
[Ti] Título:Connexin37 reduces smooth muscle cell proliferation and intimal hyperplasia in a mouse model of carotid artery ligation.
[So] Source:Cardiovasc Res;113(7):805-816, 2017 Jun 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aims: Intimal hyperplasia (IH) is an abnormal response to vessel injury characterized by the dedifferentiation, migration, and proliferation of quiescent vascular smooth muscle cells (VSMC) to form a neointima layer. Vascular connexins (Cx) are involved in the pathophysiology of various vascular diseases, and Cx43, the main Cx expressed in VSMC, has been shown to promote VSMC proliferation and IH. The aim of this study was to investigate the participation of another Cx, namely Cx37, in the formation of the neointima layer. Methods and results: Wild-type (WT) and Cx37-deficient (Cx37-/-) C57BL/6J mice were subjected to carotid artery ligation (CAL), a model of vessel injury and IH. The neointima developed linearly in WT until 28 days post surgery. In contrast, the neointima layer was almost absent 14 days after surgery in Cx37-/- mice, and twice as more developed after 28 days compared to WT mice. This large neointima formation correlated with a two-fold increase in cell proliferation in the media and neointima regions between 14 and 28 days in Cx37-/- mice compared to WT mice. The CAL triggered Cx43 overexpression in the media and neointima layers of ligated carotids in WT mice, and selectively up-regulated Cx37 expression in the media layer, but not in the neointima layer. The de novo expression of Cx37 in human primary VSMC reduced cell proliferation and P-Akt levels, in association with lower Cx43 levels, whereas Cx43 overexpression increased P-Akt levels. Conclusion: The presence of Cx37 in the media layer of injured arteries restrains VSMC proliferation and limits the development of IH, presumably by interfering with the pro-proliferative effect of Cx43 and the Akt pathway.
[Mh] Termos MeSH primário: Lesões das Artérias Carótidas/metabolismo
Estenose das Carótidas/metabolismo
Proliferação Celular
Conexinas/metabolismo
Músculo Liso Vascular/metabolismo
Miócitos de Músculo Liso/metabolismo
Neointima
[Mh] Termos MeSH secundário: Idoso
Animais
Artérias Carótidas/metabolismo
Artérias Carótidas/patologia
Artérias Carótidas/cirurgia
Lesões das Artérias Carótidas/genética
Lesões das Artérias Carótidas/patologia
Estenose das Carótidas/genética
Estenose das Carótidas/patologia
Células Cultivadas
Conexina 43/metabolismo
Conexinas/deficiência
Conexinas/genética
Modelos Animais de Doenças
Feminino
Seres Humanos
Hiperplasia
Ligadura
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Músculo Liso Vascular/patologia
Miócitos de Músculo Liso/patologia
Fosforilação
Proteínas Proto-Oncogênicas c-akt/metabolismo
Transdução de Sinais
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexin 43); 0 (Connexins); 0 (connexin 37); 0 (connexin 43 protein, rat); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvx079


  2 / 4793 MEDLINE  
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[PMID]:28471544
[Au] Autor:Sarkar D; Singh SK
[Ad] Endereço:Department of Zoology, Institute of Science, Banaras Hindu University, Varanasi, India.
[Ti] Título:Neonatal hypothyroidism affects testicular glucose homeostasis through increased oxidative stress in prepubertal mice: effects on GLUT3, GLUT8 and Cx43.
[So] Source:Andrology;5(4):749-762, 2017 07.
[Is] ISSN:2047-2927
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Thyroid hormones (THs) play an important role in maintaining the link between metabolism and reproduction and the altered THs status is associated with induction of oxidative stress in various organs like brain, heart, liver and testis. Further, reactive oxygen species play a pivotal role in regulation of glucose homeostasis in several organs, and glucose utilization by Leydig cells is essential for testosterone biosynthesis and thus is largely dependent on glucose transporter 8 (GLUT8). Glucose uptake by Sertoli cells is mediated through glucose transporter 3 (GLUT3) under the influence of THs to meet energy requirement of developing germ cells. THs also modulate level of gap junctional protein such as connexin 43 (Cx43), a potential regulator of cell proliferation and apoptosis in the seminiferous epithelium. Although the role of transient neonatal hypothyroidism in adult testis in terms of testosterone production is well documented, the effect of THs deficiency in early developmental period and its role in testicular glucose homeostasis and oxidative stress with reference to Cx43 in immature mice remain unknown. Therefore, the present study was conducted to evaluate the effect of neonatal hypothyroidism on testicular glucose homeostasis and oxidative stress at postnatal days (PND) 21 and 28 in relation to GLUT3, GLUT8 and Cx43. Hypothyroidism induced by 6-propyl-2-thiouracil (PTU) markedly decreased testicular glucose level with considerable reduction in expression level of GLUT3 and GLUT8. Likewise, lactate dehydrogenase (LDH) activity and intratesticular concentration of lactate were also decreased in hypothyroid mice. There was also a rise in germ cell apoptosis with increased expression of caspase-3 in PTU-treated mice. Further, neonatal hypothyroidism affected germ cell proliferation with decreased expression of proliferating cell nuclear antigen (PCNA) and Cx43. In conclusion, our results suggest that neonatal hypothyroidism alters testicular glucose homeostasis via increased oxidative stress in prepubertal mice, thereby affecting germ cell survival and proliferation.
[Mh] Termos MeSH primário: Conexina 43/metabolismo
Proteínas Facilitadoras de Transporte de Glucose/metabolismo
Transportador de Glucose Tipo 3/metabolismo
Glucose/metabolismo
Hipotireoidismo/metabolismo
Estresse Oxidativo
Testículo/metabolismo
[Mh] Termos MeSH secundário: Fatores Etários
Animais
Animais Recém-Nascidos
Antioxidantes/metabolismo
Apoptose
Proliferação Celular
Conexina 43/genética
Modelos Animais de Doenças
Regulação para Baixo
Homeostase
Hipotireoidismo/induzido quimicamente
Hipotireoidismo/genética
Hipotireoidismo/patologia
L-Lactato Desidrogenase/metabolismo
Ácido Láctico/metabolismo
Peroxidação de Lipídeos
Masculino
Camundongos
Antígeno Nuclear de Célula em Proliferação/metabolismo
Propiltiouracila
Testículo/patologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antioxidants); 0 (Connexin 43); 0 (GJA1 protein, mouse); 0 (Glucose Transport Proteins, Facilitative); 0 (Glucose Transporter Type 3); 0 (Proliferating Cell Nuclear Antigen); 0 (Slc2a3 protein, mouse); 0 (Slc2a8 protein, mouse); 33X04XA5AT (Lactic Acid); 721M9407IY (Propylthiouracil); EC 1.1.1.27 (L-Lactate Dehydrogenase); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1111/andr.12363


  3 / 4793 MEDLINE  
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[PMID]:29197877
[Au] Autor:Gerbino A; Bottillo I; Milano S; Lipari M; Zio R; Morlino S; Mola MG; Procino G; Re F; Zachara E; Grammatico P; Svelto M; Carmosino M
[Ad] Endereço:Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, Bari, Italy.
[Ti] Título:Functional Characterization of a Novel Truncating Mutation in Lamin A/C Gene in a Family with a Severe Cardiomyopathy with Conduction Defects.
[So] Source:Cell Physiol Biochem;44(4):1559-1577, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Truncating LMNA gene mutations occur in many inherited cardiomyopathy cases, but the molecular mechanisms involved in the disease they cause have not yet been systematically investigated. Here, we studied a novel frameshift LMNA variant (p.D243Gfs*4) identified in three members of an Italian family co-segregating with a severe form of cardiomyopathy with conduction defects. METHODS: HEK293 cells and HL-1 cardiomyocytes were transiently transfected with either Lamin A or D243Gfs*4 tagged with GFP (or mCherry). D243Gfs*4 expression, cellular localization and its effects on diverse cellular mechanisms were evaluated with western blotting, laser-scanning confocal microscopy and video-imaging analysis in single cells. RESULTS: When expressed in HEK293 cells, GFP- (or mCherry)-tagged LMNA D243Gfs*4 colocalized with calnexin within the ER. ER mislocalization of LMNA D243Gfs*4 did not significantly induce ER stress response, abnormal Ca2+ handling and apoptosis when compared with HEK293 cells expressing another truncated mutant of LMNA (R321X) which similarly accumulates within the ER. Of note, HEK293-LMNA D243Gfs*4 cells showed a significant reduction of connexin 43 (CX43) expression level, which was completely rescued by activation of the WNT/ß-catenin signaling pathway. When expressed in HL-1 cardiomyocytes, D243Gfs*4 significantly impaired the spontaneous Ca2+ oscillations recorded in these cells as result of propagation of the depolarizing waves through the gap junctions between non-transfected cells surrounding a cell harboring the mutation. Furthermore, mCh-D243Gfs*4 HL-1 cardiomyocytes showed reduced CX43-dependent Lucifer Yellow (LY) loading and propagation. Of note, activation of ß-catenin rescued both LY loading and LMNA D243Gfs*4 -HL-1 cells spontaneous activity propagation. CONCLUSION: Overall, the present results clearly indicate the involvement of the aberrant CX43 expression/activity as a pathogenic mechanism for the conduction defects associated to this LMNA truncating alteration.
[Mh] Termos MeSH primário: Doença do Sistema de Condução Cardíaco/genética
Cardiomiopatias/genética
Lamina Tipo A/genética
[Mh] Termos MeSH secundário: Apoptose
Sequência de Bases
Cálcio/metabolismo
Calnexina/metabolismo
Doença do Sistema de Condução Cardíaco/complicações
Doença do Sistema de Condução Cardíaco/patologia
Cardiomiopatias/complicações
Cardiomiopatias/patologia
Linhagem Celular
Conexina 43
Retículo Endoplasmático/metabolismo
Feminino
Junções Comunicantes/metabolismo
Células HEK293
Seres Humanos
Lamina Tipo A/metabolismo
Repetições de Microssatélites/genética
Microscopia Confocal
Meia-Idade
Mutagênese Sítio-Dirigida
Miócitos Cardíacos/citologia
Miócitos Cardíacos/metabolismo
Linhagem
Polimorfismo de Nucleotídeo Único
Imagem com Lapso de Tempo
Via de Sinalização Wnt
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexin 43); 0 (LMNA protein, human); 0 (Lamin Type A); 139873-08-8 (Calnexin); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171204
[St] Status:MEDLINE
[do] DOI:10.1159/000485651


  4 / 4793 MEDLINE  
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[PMID]:29180066
[Au] Autor:Tsai CF; Cheng YK; Lu DY; Wang SL; Chang CN; Chang PC; Yeh WL
[Ad] Endereço:Department of Biotechnology, Asia University, No.500 Lioufeng Road, Taichung 41354, Taiwan. Electronic address: tsaicf@asia.edu.tw.
[Ti] Título:Inhibition of estrogen receptor reduces connexin 43 expression in breast cancers.
[So] Source:Toxicol Appl Pharmacol;338:182-190, 2018 01 01.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Connexins are widely supported as tumor suppressors due to their downregulation in cancers, nevertheless, more recent evidence suggests roles for connexins in facilitating tumor progression in later stages, including metastasis. One of the key factors regulating the expression, modification, stability, and localization of connexins is hormone receptors in hormone-dependent cancers. It is reasonable to consider that hormones/hormone receptors may modulate connexins expression and play critical roles in the cellular control of connexins during breast cancer progression. In estrogen receptor (ER)-positive breast cancers, tamoxifen and fulvestrant are widely used therapeutic agents and are considered to alter ER signaling. In this present study, we investigated the effects of fulvestrant and tamoxifen in Cx43 expression, and we also explored the role of Cx43 in ER-positive breast cancer migration and the relationship between Cx43 and ER. The involvement of estrogen/ER in Cx43 modulation was further verified by administering tyrosine kinase inhibitors and chemotherapeutic agents. We found that inhibition of ER promoted the binding of E3 ligase Nedd4 to Cx43, leading to Cx43 ubiquitination. Furthermore, inhibition of ER by fulvestrant and tamoxifen phosphorylated p38 MAPK, and inhibition of Rac, MKK3/6, and p38 reversed fulvestrant-reduced Cx43 expression. These findings suggest that Cx43 expression which may positively regulate cell migration is ER-dependent in ER-positive breast cancer cells.
[Mh] Termos MeSH primário: Neoplasias da Mama/patologia
Conexina 43/fisiologia
Antagonistas de Estrogênios/farmacologia
[Mh] Termos MeSH secundário: Neoplasias da Mama/química
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Conexina 43/análise
Feminino
Seres Humanos
Ubiquitina-Proteína Ligases Nedd4/metabolismo
Receptores Estrogênicos/fisiologia
Tamoxifeno/análogos & derivados
Tamoxifeno/farmacologia
Proteínas Quinases p38 Ativadas por Mitógeno/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Connexin 43); 0 (Estrogen Antagonists); 0 (GJA1 protein, human); 0 (Receptors, Estrogen); 094ZI81Y45 (Tamoxifen); 17197F0KYM (afimoxifene); EC 2.3.2.26 (Nedd4 Ubiquitin Protein Ligases); EC 2.3.2.26 (Nedd4 protein, human); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE


  5 / 4793 MEDLINE  
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[PMID]:29197784
[Au] Autor:Banerjee S; Chaturvedi CM
[Ad] Endereço:Department of Zoology, Banaras Hindu University, Varanasi 221005, India.
[Ti] Título:Simulated photoperiod influences testicular activity in quail via modulating local GnRHR-GnIHR, GH-R, Cnx-43 and 14-3-3.
[So] Source:J Photochem Photobiol B;178:412-423, 2018 Jan.
[Is] ISSN:1873-2682
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The hypothalamo-hypophyseal-gonadal axis mediated differential photosexual responses in quail kept under different simulated photoperiodic conditions have been studied in details. Local testicular GnRH-GnIH and their receptor system has been hypothesized to be modulated in quail showing different photo-sexual responses and thus influence the testicular activity and steroidogenesis through local (paracrine and autocrine) action. To validate this hypothesis, we studied the expression of gonadotropin releasing hormone receptor (GnRH-R), gonadotropin inhibiting hormone receptor (GnIH-R) mRNA, growth hormone receptor (GH-R), proliferating cell nuclear antigen (PCNA), 14-3-3, Connexin-43 (Cnx-43), steroidogenic factor-1 (SF-1), Steroidogenic Acute Regulatory protein (StAR), steroidogenic enzyme (3ß HSD) in testis as well as androgen receptor (AR) in testis and epididymis of photosensitive (PS), scotorefractory (SR), photorefractory (PR) and scotosensitive (SS) quail. Experimental findings clearly indicate the increased expression of GnIH-R mRNA and suppression of GnRH-R, GH-R, PCNA, 14-3-3, Connexin-43, SF-1, StAR, 3ß HSD in testis as well as AR in testis and epididymis of PR and SS quail, while PS and SR quail exhibited the opposite results i.e., significantly decreased expression of GnIH-R mRNA and increased expression of GnRH-R, GH-R, PCNA, 14-3-3, Cnx-43, SF-1, StAR, 3ß HSD in testis as well as AR in testis and epididymis. The significantly increased intra-testicular testosterone has been observed in the PS and SR quail while, PR and SS quail showed opposite results. Hence, we conclude that PS and SR quail showed significantly increased testicular activity and steroidogenesis while opposite pattern was observed in PR and SS quail.
[Mh] Termos MeSH primário: Proteínas 14-3-3/metabolismo
Conexina 43/metabolismo
Hormônio Liberador de Gonadotropina/metabolismo
Receptores LHRH/metabolismo
Testículo/metabolismo
[Mh] Termos MeSH secundário: Proteínas 14-3-3/genética
Animais
Conexina 43/genética
Epididimo/metabolismo
Epididimo/patologia
Hormônio Liberador de Gonadotropina/genética
Masculino
Microscopia Confocal
Fotoperíodo
Antígeno Nuclear de Célula em Proliferação/genética
Antígeno Nuclear de Célula em Proliferação/metabolismo
Codorniz
Receptores Androgênicos/genética
Receptores Androgênicos/metabolismo
Receptores LHRH/genética
Fator Esteroidogênico 1/genética
Fator Esteroidogênico 1/metabolismo
Testículo/patologia
Testosterona/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (14-3-3 Proteins); 0 (Connexin 43); 0 (Proliferating Cell Nuclear Antigen); 0 (Receptors, Androgen); 0 (Receptors, LHRH); 0 (Steroidogenic Factor 1); 33515-09-2 (Gonadotropin-Releasing Hormone); 3XMK78S47O (Testosterone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171204
[St] Status:MEDLINE


  6 / 4793 MEDLINE  
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[PMID]:29179175
[Au] Autor:Tu RH; Li QJ; Huang Z; He Y; Meng JJ; Zheng HL; Zeng ZY; Zhong GQ
[Ad] Endereço:Department of Geriatric Cardiology, Nanning, China.
[Ti] Título:Novel Functional Role of Heat Shock Protein 90 in Mitochondrial Connexin 43-Mediated Hypoxic Postconditioning.
[So] Source:Cell Physiol Biochem;44(3):982-997, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Previous studies have shown that heat shock protein 90 (HSP90)-mediated mitochondrial import of connexin 43 (Cx43) is critical in preconditioning cardioprotection. The present study was designed to test whether postconditioning has the same effect as preconditioning in promoting Cx43 translocation to mitochondria and whether mitochondrial HSP90 modulates this effect. METHODS: Cellular models of hypoxic postconditioning (HPC) from rat heart-derived H9c2 cells and neonatal rat cardiomyocytes were employed. The effects of HPC on cardiomyocytes apoptosis were examined by flow cytometry and Hoechst 33342 fluorescent staining. Reactive oxidative species (ROS) production was assessed with the peroxide-sensitive fluorescent probe 2',7'-dichlorofluorescin in diacetate (DCFH-DA). The anti- and pro-apoptotic markers Bcl-2 and Bax, HSP90 and Cx43 protein levels were studied by Western blot analysis in total cell homogenate and sarcolemmal and mitochondrial fractions. The effects on HPC of the HSP90 inhibitor geldanamycin (GA), ROS scavengers superoxide dismutase (SOD) and catalase (CAT), and small interfering RNA (siRNA) targeting Cx43 and HSP90 were also investigated. RESULTS: HPC significantly reduced hypoxia/reoxygenation (H/R)-induced cardiomyocyte apoptosis. These beneficial effects were accompanied by an increase in Bcl-2 levels and a decrease in Bax levels in both sarcolemmal and mitochondrial fractions. HPC with siRNA targeting Cx43 or the ROS scavengers SOD plus CAT significantly prevented ROS generation and HPC cardioprotection, but HPC with either SOD or CAT did not. These data strongly supported the involvement of Cx43 in HPC cardioprotection, likely via modulation of the ROS balance which plays a central role in HPC protection. Furthermore, HPC increased total and mitochondrial levels of HSP90 and the mitochondria-to-sarcolemma ratio of Cx43; blocking the function of HSP90 with the HSP90 inhibitor geldanamycin (GA) or siRNA targeting HSP90 prevented the protection of HPC and the HPC-induced association of Cx43, indicating that mitochondrial HSP90 was important for mitochondrial translocation of Cx43 during HPC. CONCLUSION: Mitochondrial HSP90 played a central role in HPC cardioprotection, and its activity was linked to the mitochondrial targeting of Cx43, the activation of which triggered ROS signaling and the subsequent reduction of redox stress. Consequently, its target gene, Bcl-2, was upregulated, and proapoptotic Bax was inhibited in the sarcolemma and mitochondria, ultimately attenuating H/R-induced cardiomyocyte apoptosis. These data reveal a novel mechanism of HPC protection.
[Mh] Termos MeSH primário: Conexina 43/metabolismo
Proteínas de Choque Térmico HSP90/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Benzoquinonas/farmacologia
Catalase/farmacologia
Hipóxia Celular
Linhagem Celular
Conexina 43/antagonistas & inibidores
Conexina 43/genética
Proteínas de Choque Térmico HSP90/antagonistas & inibidores
Proteínas de Choque Térmico HSP90/genética
Lactamas Macrocíclicas/farmacologia
Microscopia de Fluorescência
Mitocôndrias/metabolismo
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Ratos
Ratos Sprague-Dawley
Espécies Reativas de Oxigênio/química
Espécies Reativas de Oxigênio/metabolismo
Sarcolema/metabolismo
Superóxido Dismutase/farmacologia
Proteína X Associada a bcl-2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzoquinones); 0 (Connexin 43); 0 (HSP90 Heat-Shock Proteins); 0 (Lactams, Macrocyclic); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (RNA, Small Interfering); 0 (Reactive Oxygen Species); 0 (bcl-2-Associated X Protein); EC 1.11.1.6 (Catalase); EC 1.15.1.1 (Superoxide Dismutase); Z3K3VJ16KU (geldanamycin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1159/000485399


  7 / 4793 MEDLINE  
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[PMID]:29176328
[Au] Autor:Xie Y; Liu S; Hu S; Wei Y
[Ti] Título:Cardiomyopathy-Associated Gene 1-Sensitive PKC-Dependent Connexin 43 Expression and Phosphorylation in Left Ventricular Noncompaction Cardiomyopathy.
[So] Source:Cell Physiol Biochem;44(2):828-842, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Cardiomyopathy-associated gene 1 (CMYA1) plays an important role in embryonic cardiac development, postnatal cardiac remodeling and myocardial injury repair. Abnormal CMYA1 expression may be involved in cardiac dysplasia and primary cardiomyopathy. Our study aims to establish the relationship between CMYA1 and Left ventricular noncompaction cardiomyopathy (LVNC) pathogenesis. METHODS: We explored the effects of CMYA1 on connexins (Cx), which contribute to gap junction intercellular communication (GJIC), and the underlying signaling pathway in human normal tissues, LVNC myocardial tissues and HL1 cells by means of western blotting, RT-qPCR, immunohistochemistry, immunofluorescence, co-immunoprecipitation and scrape loading-dye transfer. RESULTS: CMYA1 expression was inversely associated with Cx43 and Cx40 expression, as determined by gap junction PCR array analysis. An increased expression and disordered distribution of CMYA1 at the intercalated discs in LVNC myocardial tissue was also observed. CMYA1 and Cx43 are co-expressed and interact in myocardial cells. CMYA1 expression was positively correlated with p-Cx43 (S368) via the Protein kinase C (PKC) signaling pathway in myocardial tissue and HL1 cells. The diffusion distance of Lucifer Yellow in the HL1 cells in which CMYA1 was over-expressed or knocked down was significantly less or more than that of the control group, respectively. CONCLUSION: Abnormal CMYA1 expression affects the expression and phosphorylation of Cx43 through the PKC signaling pathway, which is involved in the regulation of GJIC. CMYA1 participates in the molecular mechanism of LVNC pathogenesis.
[Mh] Termos MeSH primário: Conexina 43/metabolismo
Proteínas de Ligação a DNA/metabolismo
Proteínas Nucleares/metabolismo
Proteína Quinase C/metabolismo
[Mh] Termos MeSH secundário: Cardiomiopatias/metabolismo
Cardiomiopatias/patologia
Comunicação Celular
Linhagem Celular
Conexina 43/genética
Conexinas/genética
Conexinas/metabolismo
Proteínas de Ligação a DNA/antagonistas & inibidores
Proteínas de Ligação a DNA/genética
Junções Comunicantes/metabolismo
Ventrículos do Coração/fisiopatologia
Seres Humanos
Imuno-Histoquímica
Imunoprecipitação
Microscopia de Fluorescência
Miocárdio/metabolismo
Miocárdio/patologia
Proteínas Nucleares/antagonistas & inibidores
Proteínas Nucleares/genética
Fosforilação
Ligação Proteica
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexin 43); 0 (Connexins); 0 (DNA-Binding Proteins); 0 (Nuclear Proteins); 0 (RNA, Small Interfering); 0 (XIRP1 protein, human); 0 (connexin 40); EC 2.7.11.13 (Protein Kinase C)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1159/000485348


  8 / 4793 MEDLINE  
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[PMID]:29277772
[Au] Autor:Ishibashi K; Ishii K; Sugiyama G; Sumida T; Sugiura T; Kamata YU; Seki K; Fujinaga T; Kumamaru W; Kobayashi Y; Hiyake N; Nakano H; Yamada T; Mori Y
[Ad] Endereço:Section of Oral & Maxillofacial Surgery, Division of Maxillofacial Diagnostic and Surgical Sciences, Faculty of Dental Science, Kyushu University, Fukuoka, Japan.
[Ti] Título:Deregulation of Nicotinamide N-Methyltransferase and Gap Junction Protein Alpha-1 Causes Metastasis in Adenoid Cystic Carcinoma.
[So] Source:Anticancer Res;38(1):187-197, 2018 01.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Adenoid cystic carcinoma (AdCC) is a malignant tumor that occurs in the salivary glands and frequently metastasizes. The aim of this study was to identify factors mediating AdCC metastasis. MATERIALS AND METHODS: We established three AdCC cell lines by orthotropic transplantation and in vivo selection: parental, highly metastatic (ACCS-M-GFP), and lymph node metastatic (ACCS-LN-GFP) cells. RESULTS: We examined the three cell lines. DNA microarray indicated significantly altered processes in ACCS-LN-GFP cells: particularly, the expression of nicotinamide N-methyltransferase (NNMT) was enhanced the most. NNMT is associated with tumorigenesis and is a potential tumor biomarker. Concomitantly, we found-significant down-regulation of gap junction protein alpha-1. We suggest that ACCS-LN-GFP cells acquire cancer stem cell features involving the up-regulation of NNMT and the loss of gap junction protein alpha-1, leading to epithelial-mesenchymal transition and consequent AdCC metastasis. CONCLUSION: NNMT is a potential biomarker of AdCC.
[Mh] Termos MeSH primário: Carcinoma Adenoide Cístico/patologia
Conexina 43/metabolismo
Nicotinamida N-Metiltransferase/metabolismo
Neoplasias das Glândulas Salivares/patologia
[Mh] Termos MeSH secundário: Animais
Carcinoma Adenoide Cístico/metabolismo
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Feminino
Seres Humanos
Camundongos Nus
Neoplasias das Glândulas Salivares/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexin 43); 0 (GJA1 protein, mouse); EC 2.1.1.1 (Nicotinamide N-Methyltransferase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


  9 / 4793 MEDLINE  
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[PMID]:29255213
[Au] Autor:Donahue HJ; Qu RW; Genetos DC
[Ad] Endereço:Department of Biomedical Engineering, Virginia Commonwealth University, 601 West Main Street, Richmond, Virginia 23284, USA.
[Ti] Título:Joint diseases: from connexins to gap junctions.
[So] Source:Nat Rev Rheumatol;14(1):42-51, 2017 Dec 19.
[Is] ISSN:1759-4804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Connexons form the basis of hemichannels and gap junctions. They are composed of six tetraspan proteins called connexins. Connexons can function as individual hemichannels, releasing cytosolic factors (such as ATP) into the pericellular environment. Alternatively, two hemichannel connexons from neighbouring cells can come together to form gap junctions, membrane-spanning channels that facilitate cell-cell communication by enabling signalling molecules of approximately 1 kDa to pass from one cell to an adjacent cell. Connexins are expressed in joint tissues including bone, cartilage, skeletal muscle and the synovium. Indicative of their importance as gap junction components, connexins are also known as gap junction proteins, but individual connexin proteins are gaining recognition for their channel-independent roles, which include scaffolding and signalling functions. Considerable evidence indicates that connexons contribute to the function of bone and muscle, but less is known about the function of connexons in other joint tissues. However, the implication that connexins and gap junctional channels might be involved in joint disease, including age-related bone loss, osteoarthritis and rheumatoid arthritis, emphasizes the need for further research into these areas and highlights the therapeutic potential of connexins.
[Mh] Termos MeSH primário: Conexina 43/metabolismo
Conexinas/metabolismo
Junções Comunicantes/metabolismo
Artropatias/metabolismo
[Mh] Termos MeSH secundário: Animais
Artrite Reumatoide/metabolismo
Osso e Ossos/metabolismo
Cartilagem/metabolismo
Comunicação Celular/fisiologia
Diferenciação Celular/fisiologia
Conexinas/fisiologia
Conexinas/uso terapêutico
Junções Comunicantes/fisiologia
Seres Humanos
Ativação do Canal Iônico/fisiologia
Canais Iônicos/fisiologia
Camundongos
Camundongos Knockout
Sistema Musculoesquelético/metabolismo
Sistema Musculoesquelético/patologia
Osteoartrite/metabolismo
Osteoporose/metabolismo
Membrana Sinovial/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Connexin 43); 0 (Connexins); 0 (Ion Channels)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171227
[Lr] Data última revisão:
171227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE
[do] DOI:10.1038/nrrheum.2017.204


  10 / 4793 MEDLINE  
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[PMID]:28369869
[Au] Autor:Talbot J; Brion R; Lamora A; Mullard M; Morice S; Heymann D; Verrecchia F
[Ad] Endereço:INSERM, UMR 957, Nantes, France.
[Ti] Título:Connexin43 intercellular communication drives the early differentiation of human bone marrow stromal cells into osteoblasts.
[So] Source:J Cell Physiol;233(2):946-957, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although it has been demonstrated that human bone marrow stromal cells (hBMSCs) express the ubiquitous connexin43 (Cx43) and form functional gap junctions, their role in the early differentiation of hBMSCs into osteoblasts remains poorly documented. Using in vitro assays, we show that Cx43 expression and gap junctional intercellular communication (GJIC) are increased during the differentiation of hBMSCs into osteoblasts, both at the protein and mRNA levels. Two independent procedures to reduce GJIC, a pharmacological approach with GJIC inhibitors (18α-glycyrrhetinic acid and Gap27 peptide) and a molecular approach using small interfering RNA against Cx43, demonstrated that the presence of Cx43 and functional junctional channels are essential to the ability of hBMSCs to differentiate into osteoblasts in vitro. In addition, a reduced GJIC decreases the expression of Runx2, the major transcription factor implicated in the control of osteoblast commitment and early differentiation of hBMSCs into osteoblasts, suggesting that GJIC mediated by Cx43 is implicated in this process. Together our results demonstrate that GJIC mediated by the Cx43 channels plays a central role throughout the differentiation of hBMSC into osteoblasts, from the early stages to the process of mineralization.
[Mh] Termos MeSH primário: Células da Medula Óssea/metabolismo
Comunicação Celular
Diferenciação Celular
Conexina 43/metabolismo
Junções Comunicantes/metabolismo
Osteoblastos/metabolismo
Osteogênese
Células Estromais/metabolismo
[Mh] Termos MeSH secundário: Células da Medula Óssea/efeitos dos fármacos
Comunicação Celular/efeitos dos fármacos
Diferenciação Celular/efeitos dos fármacos
Células Cultivadas
Conexina 43/genética
Conexinas/farmacologia
Junções Comunicantes/efeitos dos fármacos
Ácido Glicirretínico/análogos & derivados
Ácido Glicirretínico/farmacologia
Seres Humanos
Osteoblastos/efeitos dos fármacos
Osteogênese/efeitos dos fármacos
Interferência de RNA
Transdução de Sinais
Células Estromais/efeitos dos fármacos
Fatores de Tempo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexin 43); 0 (Connexins); 0 (GJA1 protein, human); 0 (gap 27 peptide); 1449-05-4 (18alpha-glycyrrhetinic acid); P540XA09DR (Glycyrrhetinic Acid)
[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:170404
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25938



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