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[PMID]:29484749
[Au] Autor:Khosravi AD; Meghdadi H; Ghadiri AA; Alami A; Sina AH; Mirsaeidi M
[Ad] Endereço:Infectious and Tropical Diseases Research Center, Health Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
[Ti] Título:rpoB gene mutations among Mycobacterium tuberculosis isolates from extrapulmonary sites.
[So] Source:APMIS;126(3):241-247, 2018 Mar.
[Is] ISSN:1600-0463
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to analyze mutations occurring in the rpoB gene of Mycobacterium tuberculosis (MTB) isolates from clinical samples of extrapulmonary tuberculosis (EPTB). Seventy formalin-fixed, paraffin-embedded samples and fresh tissue samples from confirmed EPTB cases were analyzed. Nested PCR based on the rpoB gene was performed on the extracted DNAs, combined with cloning and subsequent sequencing. Sixty-seven (95.7%) samples were positive for nester PCR. Sequence analysis of the 81 bp region of the rpoB gene demonstrated mutations in 41 (61.2%) of 67 sequenced samples. Several point mutations including deletion mutations at codons 510, 512, 513 and 515, with 45% and 51% of the mutations in codons 512 and 513 respectively were seen, along with 26% replacement mutations at codons 509, 513, 514, 518, 520, 524 and 531. The most common alteration was Gln → His, at codon 513, presented in 30 (75.6%) isolates. This study demonstrated sequence alterations in codon 513 of the 81 bp region of the rpoB gene as the most common mutation occurred in 75.6% of molecularly confirmed rifampin-resistant strains. In addition, simultaneous mutation at codons 512 and 513 was demonstrated in 34.3% of the isolates.
[Mh] Termos MeSH primário: Antibióticos Antituberculose/farmacologia
Proteínas de Bactérias/genética
RNA Polimerases Dirigidas por DNA/genética
Farmacorresistência Bacteriana/genética
Mycobacterium tuberculosis/genética
Rifampina/farmacologia
Tuberculose/microbiologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Células Cultivadas
Feminino
Seres Humanos
Masculino
Testes de Sensibilidade Microbiana
Meia-Idade
Mycobacterium tuberculosis/efeitos dos fármacos
Mycobacterium tuberculosis/isolamento & purificação
Mutação Puntual/genética
Deleção de Sequência/genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibiotics, Antitubercular); 0 (Bacterial Proteins); 0 (rpoB protein, Mycobacterium tuberculosis); EC 2.7.7.6 (DNA-Directed RNA Polymerases); VJT6J7R4TR (Rifampin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180228
[St] Status:MEDLINE
[do] DOI:10.1111/apm.12804


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[PMID]:29447173
[Au] Autor:Diao YF; Lin T; Li X; Oqani RK; Lee JE; Kim SY; Jin DI
[Ad] Endereço:Institute of Special Animal & Plant Sciences, Chinese Academy of Agricultural Sciences, Changchun, China.
[Ti] Título:Dynamic changes of SETD2, a histone H3K36 methyltransferase, in porcine oocytes, IVF and SCNT embryos.
[So] Source:PLoS One;13(2):e0191816, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:SETD2 (SET domain containing protein 2) acts as a histone H3 lysine 36 (H3K36)-specific methyltransferase and may play important roles in active gene transcription in human cells. However, its expression and role in porcine oocytes and preimplantation embryos are not well understood. Here, we used immunofluorescence and laser scanning confocal microscopy to examine SETD2 expression in porcine fetal fibroblasts, oocytes, and preimplantation embryos derived from in vitro fertilization (IVF), parthenogenetic activation (PA), and somatic cell nuclear transfer (SCNT). In porcine fetal fibroblasts, SETD2 expression was detected in interphase cells, but not in M (mitotic)-phase cells. The SETD2 signal was observed in non-surrounded nucleolus (NSN)-stage oocytes, but not in surrounded nucleolus (SN)-, metaphase I (MI)-, or metaphase II (MII)-stage oocytes. The SETD2 signal was detectable in sperm, and undetectable immediately after fertilization, detectable at the 2-cell stage, and peaked at the 4-cell stage of IVF embryos in which porcine embryonic genome is activated. Similar to the pattern found in IVF embryos, the SETD2 signal was absent from PA embryos at the 1-cell stage, but it was detected at the 2-cell stage and thereafter maintained to the blastocyst stage. Interestingly, unlike the IVF and PA embryos, the SETD2 signal was detected throughout the development of SCNT embryos, including at the 1-cell stage. These data suggest that SETD2 may be functional for embryonic gene transcription in porcine preimplantation embryos. It is further speculated that the aberrant expression of SETD2 at the 1-cell stage of porcine SCNT embryos may be a factor in the low efficiency of cloning in pig.
[Mh] Termos MeSH primário: Fertilização In Vitro
Histona-Lisina N-Metiltransferase/metabolismo
Técnicas de Transferência Nuclear
Oócitos/enzimologia
[Mh] Termos MeSH secundário: Animais
Blastocisto
Células Cultivadas
Oócitos/citologia
Partenogênese
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 2.1.1.43 (Histone-Lysine N-Methyltransferase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180216
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191816


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[PMID]:29412476
[Au] Autor:Bakela K; Dimakopoulou M; Batsou P; Manidakis N; Athanassakis I
[Ad] Endereço:Laboratory of Immunology, Department of Biology, University of Crete, Heraklion, Crete, Greece.
[Ti] Título:Soluble MHC class II-driven therapy for a systemic lupus erythematosus murine experimental in vitro and in vivo model.
[So] Source:Scand J Immunol;87(3), 2018 Mar.
[Is] ISSN:1365-3083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Taking into consideration the multiparametric nature of systemic lupus erythematosus (SLE), the severity and variability of symptoms and the lack of effective therapeutic approaches, this study took advantage of the recently described role of soluble major histocompatibility complex class II (sMHCII) molecules in maintaining tolerance to the organism and attempted to apply sMHCII proteins as a treatment to murine SLE experimental models in vitro as well as in vivo. After breaking tolerance to DNA in vitro, which was accompanied by development of specific anti-dsDNA antibodies, syngeneic or allogeneic sMHCII molecules, purified from healthy mouse serum, could significantly reduce the specific antibody levels and drive the system towards immunosuppression, as assessed by specific marker analysis on T cells and cytokine production by flow cytometry and ELISA, respectively. The in vivo experimental model consisted of pristane-induced SLE symptoms to BALB/c mice, which developed maximal levels of anti-dsDNA 2 months after pristane inoculation. Syngeneic or allogeneic sMHCII administration could alleviate pristane-induced symptoms, significantly decrease specific anti-dsDNA antibody production and develop immunosuppression to the host, as manifested by increase of CD4 + CTLA-4 +  and CD4 + CD25 +  cell populations in the spleen. Thus, the results presented in this study introduced the ability of sMHCII proteins to suppress specific autoantigen response, opening new areas of research and offering novel therapeutic approaches to SLE with expanding features to other autoimmune diseases.
[Mh] Termos MeSH primário: Anticorpos Antinucleares/imunologia
Autoantígenos/imunologia
Antígenos de Histocompatibilidade Classe II/imunologia
Tolerância Imunológica/imunologia
Imunoterapia/métodos
Lúpus Eritematoso Sistêmico/imunologia
Lúpus Eritematoso Sistêmico/terapia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Antígenos CD4/metabolismo
Antígeno CTLA-4/metabolismo
Células Cultivadas
DNA/imunologia
Modelos Animais de Doenças
Imunossupressão
Subunidade alfa de Receptor de Interleucina-2/metabolismo
Lúpus Eritematoso Sistêmico/induzido quimicamente
Camundongos
Camundongos Endogâmicos BALB C
Baço/citologia
Baço/imunologia
Terpenos/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Antinuclear); 0 (Autoantigens); 0 (CD4 Antigens); 0 (CTLA-4 Antigen); 0 (Histocompatibility Antigens Class II); 0 (Il2ra protein, mouse); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Terpenes); 26HZV48DT1 (pristane); 9007-49-2 (DNA)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180208
[St] Status:MEDLINE
[do] DOI:10.1111/sji.12644


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[PMID]:29408208
[Au] Autor:Yue J; Wan F; Zhang Q; Wen P; Cheng L; Li P; Guo W
[Ad] Endereço:Beijing University of Chinese Medicine, Yinghuadong Road, Chaoyang District, Beijing, China; Department of Joint Surgery, China-Japan Friendship Hospital, Yinghuadong Road, Chaoyang District, Beijing, China. Electronic address: 20150941122@bucm.edu.cn.
[Ti] Título:Effect of glucocorticoids on miRNA expression spectrum of rat femoral head microcirculation endothelial cells.
[So] Source:Gene;651:126-133, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The study profiled the differential miRNA expression from femoral head bone microvascular endothelial cells (BMECs) between model group and control group to explore the pathogenesis of steroid-induced osteonecrosis of femoral head (ONFH). Twenty 8-week-old Female Sprague-Dawley (SD) rats were randomly divided into control and model groups. Rats in model group received an intraperitoneal injection of 20-µg/kg lipopolysaccharide (LPS) at an interval of 24 h. Then, 24 h later, rats received three doses of 40-mg/kg methylprednisolone by intramuscular injection at intervals of 24 h. In control group, rats received the same volume of normal saline. After 4 weeks, the femoral heads were sectioned to confirm the establishment of the model. To replicate the animal model ex vivo, BMECs were isolated. Different miRNAs were screened using Agilent Gene Spring GX software, and real-time quantitative polymerase chain reaction (qPCR) was used to confirm the results of miRNA microarray analysis. The differentially expressed miRNA were assessed by bioinformatics analysis. Four differentially expressed miRNAs were identified (two upregulated: miR-132-3p, miR-335 and two down regulated: miR-466b-2-3p, let-7c-1-3p). qPCR results were consistent with the gene-chip results. Steroid-induced ONFH may cause miRNA changes in BMSCs. miR-132-3p and miR-335 may be important in steroid-induced ONFH.
[Mh] Termos MeSH primário: Endotélio Vascular/metabolismo
Necrose da Cabeça do Fêmur/metabolismo
Cabeça do Fêmur/metabolismo
Glucocorticoides/farmacologia
Metilprednisolona/farmacologia
MicroRNAs/biossíntese
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Biologia Computacional
Modelos Animais de Doenças
Endotélio Vascular/efeitos dos fármacos
Feminino
Cabeça do Fêmur/irrigação sanguínea
Cabeça do Fêmur/efeitos dos fármacos
Necrose da Cabeça do Fêmur/sangue
Necrose da Cabeça do Fêmur/induzido quimicamente
Necrose da Cabeça do Fêmur/patologia
MicroRNAs/genética
Microcirculação
Ratos
Ratos Sprague-Dawley
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucocorticoids); 0 (MicroRNAs); X4W7ZR7023 (Methylprednisolone)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE


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[PMID]:29391275
[Au] Autor:Yang X; Wang J; Bing G; Bie P; De Y; Lyu Y; Wu Q
[Ad] Endereço:Key Laboratory of Animal Epidemiology and Zoonosis of the Ministry of Agriculture, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China.
[Ti] Título:Ortholog-based screening and identification of genes related to intracellular survival.
[So] Source:Gene;651:134-142, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Bioinformatics and comparative genomics analysis methods were used to predict unknown pathogen genes based on homology with identified or functionally clustered genes. In this study, the genes of common pathogens were analyzed to screen and identify genes associated with intracellular survival through sequence similarity, phylogenetic tree analysis and the λ-Red recombination system test method. The total 38,952 protein-coding genes of common pathogens were divided into 19,775 clusters. As demonstrated through a COG analysis, information storage and processing genes might play an important role intracellular survival. Only 19 clusters were present in facultative intracellular pathogens, and not all were present in extracellular pathogens. Construction of a phylogenetic tree selected 18 of these 19 clusters. Comparisons with the DEG database and previous research revealed that seven other clusters are considered essential gene clusters and that seven other clusters are associated with intracellular survival. Moreover, this study confirmed that clusters screened by orthologs with similar function could be replaced with an approved uvrY gene and its orthologs, and the results revealed that the usg gene is associated with intracellular survival. The study improves the current understanding of intracellular pathogens characteristics and allows further exploration of the intracellular survival-related gene modules in these pathogens.
[Mh] Termos MeSH primário: Bactérias/genética
Fenômenos Fisiológicos Bacterianos
Células/microbiologia
Genes Bacterianos
[Mh] Termos MeSH secundário: Animais
Proteínas de Bactérias/genética
Proteínas de Bactérias/fisiologia
Células Cultivadas
Genes Essenciais
Interações Hospedeiro-Patógeno
Camundongos
Família Multigênica
Filogenia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE


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[PMID]:29382572
[Au] Autor:Lv C; Mo C; Liu H; Wu C; Li Z; Li J; Wang Y
[Ad] Endereço:Key Laboratory of Bio-resources and Eco-environment of Ministry of Education, College of Life Sciences, Sichuan University, Chengdu 610065, PR China.
[Ti] Título:Dopamine D2-like receptors (DRD2 and DRD4) in chickens: Tissue distribution, functional analysis, and their involvement in dopamine inhibition of pituitary prolactin expression.
[So] Source:Gene;651:33-43, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Dopamine (DA) D2-like (and D1-like) receptors are suggested to mediate the dopamine actions in the anterior pituitary and/or CNS of birds. However, the information regarding the structure, functionality, and expression of avian D2-like receptors have not been fully characterized. In this study, we cloned two D2-like receptors (cDRD2, cDRD4) from chicken brain using RACE PCR. The cloned cDRD4 is a 378-amino acid receptor, which shows 57% amino acid (a.a.) identity with mouse DRD4. As in mammals, two cDRD2 isoforms, cDRD2L (long isoform, 437 a.a.) and cDRD2S (short isoform, 408 a.a.), which differ in their third intracellular loop, were identified in chickens. Using cell-based luciferase reporter assays or Western blot, we demonstrated that cDRD4, cDRD2L and cDRD2S could be activated by dopamine and quinpirole (a D2-like receptor agonist) dose-dependently, and their activation inhibits cAMP signaling pathway and stimulates MAPK/ERK signaling cascade, indicating that they are functional receptors capable of mediating dopamine actions. Quantitative real-time PCR revealed that cDRD2 and cDRD4 are widely expressed in chicken tissues with abundant expression noted in anterior pituitary, and their expressions are likely controlled by their promoters near exon 1, as demonstrated by dual-luciferase reporter assays in DF-1 cells. In accordance with cDRD2/cDRD4 expression in the pituitary, DA or quinpirole could partially inhibit vasoactive intestinal peptide-induced prolactin expression in cultured chick pituitary cells. Together, our data proves the functionality of DRD2 and DRD4 in birds and aids to uncover the conserved roles of DA/D2-like receptor system in vertebrates, such as its action on the pituitary.
[Mh] Termos MeSH primário: Galinhas/metabolismo
Dopamina/metabolismo
Hipófise/metabolismo
Prolactina/biossíntese
Receptores de Dopamina D2/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Galinhas/genética
Clonagem Molecular
DNA Complementar
Feminino
Regulação da Expressão Gênica
Células HEK293
Seres Humanos
Masculino
Prolactina/antagonistas & inibidores
Regiões Promotoras Genéticas
Receptores de Dopamina D2/genética
Receptores de Dopamina D2/fisiologia
Transdução de Sinais
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (Receptors, Dopamine D2); 9002-62-4 (Prolactin); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE


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[PMID]:29373584
[Au] Autor:Zhao X; Li R; Jin H; Jin H; Wang Y; Zhang W; Wang H; Chen W
[Ad] Endereço:Tianjin Institute of Health and Environmental Medicine, Tianjin, China.
[Ti] Título:Epigallocatechin-3-gallate confers protection against corticosterone-induced neuron injuries via restoring extracellular signal-regulated kinase 1/2 and phosphatidylinositol-3 kinase/protein kinase B signaling pathways.
[So] Source:PLoS One;13(1):e0192083, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Extensive studies suggested epigallocatechin-3-gallate (EGCG) has significant neuroprotection against multiple central neural injuries, but the underlying mechanisms still remain poorly elucidated. Here we provide evidence to support the possible involvement of extracellular signal-regulated kinase 1/2 (ERK1/2) and phosphatidylinositol-3 kinase/ protein kinase B (PI3K/AKT) pathways in EGCG-mediated protection against corticosterone-induced neuron injuries. As an essential stress hormone, corticosterone could induce obvious neurotoxicity in primary hippocampal neurons. Pre-treatment with EGCG ameliorated the corticosterone-induced neuronal injuries; however, it was blocked by pharmacological inhibitors for ERK1/2 (U0126) and PI3K/AKT (LY294002). Furthermore, the results confirmed that EGCG restored the corticosterone-induced decrease of ERK1/2 and PI3K/AKT phosphorylation, and attenuated the corticosterone-induced reduction of peroxisome proliferators-activated receptor-γ coactivator-1α (PGC-1α) expression and ATP production. Taken together, these findings indicated that EGCG has significant neuroprotection against corticosterone-induced neuron injuries partly via restoring the ERK1/2 and PI3K/AKT signaling pathways as well as the PGC-1α-mediated ATP production.
[Mh] Termos MeSH primário: Catequina/análogos & derivados
Corticosterona/efeitos adversos
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Fosfatidilinositol 3-Quinases/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-akt/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/biossíntese
Animais
Catequina/farmacologia
Células Cultivadas
Hipocampo/citologia
Hipocampo/efeitos dos fármacos
Fármacos Neuroprotetores/farmacologia
Fosforilação
Ratos
Ratos Wistar
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Neuroprotective Agents); 8L70Q75FXE (Adenosine Triphosphate); 8R1V1STN48 (Catechin); BQM438CTEL (epigallocatechin gallate); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); W980KJ009P (Corticosterone)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180127
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0192083


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[PMID]:29373585
[Au] Autor:Espitia O; Chatelais M; Steenman M; Charrier C; Maurel B; Georges S; Houlgatte R; Verrecchia F; Ory B; Lamoureux F; Heymann D; Gouëffic Y; Quillard T
[Ad] Endereço:INSERM, UMR 1238, Nantes, France; Université de Nantes, Nantes Atlantique Universités, Laboratoire « Sarcome osseux et remodelage des tissus osseux calcifiés ¼, Faculté de Médecine, Nantes, France.
[Ti] Título:Implication of molecular vascular smooth muscle cell heterogeneity among arterial beds in arterial calcification.
[So] Source:PLoS One;13(1):e0191976, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Vascular calcification is a strong and independent predictive factor for cardiovascular complications and mortality. Our previous work identified important discrepancies in plaque composition and calcification types between carotid and femoral arteries. The objective of this study is to further characterize and understand the heterogeneity in vascular calcification among vascular beds, and to identify molecular mechanisms underlying this process. We established ECLAGEN biocollection that encompasses human atherosclerotic lesions and healthy arteries from different locations (abdominal, thoracic aorta, carotid, femoral, and infrapopliteal arteries) for histological, cell isolation, and transcriptomic analysis. Our results show that lesion composition differs between these locations. Femoral arteries are the most calcified arteries overall. They develop denser calcifications (sheet-like, nodule), and are highly susceptible to osteoid metaplasia. These discrepancies may derive from intrinsic differences between SMCs originating from these locations, as microarray analysis showed specific transcriptomic profiles between primary SMCs isolated from each arterial bed. These molecular differences translated into functional disparities. SMC from femoral arteries showed the highest propensity to mineralize due to an increase in basal TGFß signaling. Our results suggest that biological heterogeneity of resident vascular cells between arterial beds, reflected by our transcriptomic analysis, is critical in understanding plaque biology and calcification, and may have strong implications in vascular therapeutic approaches.
[Mh] Termos MeSH primário: Artérias/patologia
Calcinose/patologia
Músculo Liso Vascular/patologia
[Mh] Termos MeSH secundário: Diferenciação Celular
Células Cultivadas
Seres Humanos
Placa Aterosclerótica/patologia
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180127
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191976


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[PMID]:29364969
[Au] Autor:Rahali S; Li Y; Anand-Srivastava MB
[Ad] Endereço:Department of Pharmacology and Physiology, Faculty of Medicine, University of Montreal, Quebec, Canada.
[Ti] Título:Contribution of oxidative stress and growth factor receptor transactivation in natriuretic peptide receptor C-mediated attenuation of hyperproliferation of vascular smooth muscle cells from SHR.
[So] Source:PLoS One;13(1):e0191743, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Earlier studies have shown the implication of growth factor receptor activation in angiotensin II (Ang II)-induced hyperproliferation of aortic VSMC as well as in hyperproliferation of VSMC from spontaneously hypertensive rats (SHR). We previously showed that NPR-C specific agonist C-ANP4-23 attenuates the hyperproliferation of VSMC from SHR through the inhibition of MAP kinase, Giα protein signaling and overexpression of cell cycle proteins. The aim of the present study was to investigate if C-ANP4-23- mediated attenuation of hyperproliferation of VSMC from SHR also involves growth factor receptor activation and upstream signaling molecules. For this study, C-ANP 4-23 (10 nmole/kg body weight) was injected intraperitoneally into 2 week-old prehypertensive SHR and Wistar Kyoto (WKY) rats twice per week for 6 weeks. The blood pressure in SHR was significantly attenuated by C-ANP4-23 treatment. In addition, C-ANP4-23 treatment also attenuated the hyperproliferation of VSMC from SHR as well as the enhanced phosphorylation of EGF-R, PDGF-R, IGF-R and c-Src. Furthermore, the enhanced levels of superoxide anion, NADPH oxidase activity, and enhanced expression of Nox4,Nox1,Nox2 and P47phox in SHR compared to WKY rats was also significantly attenuated by C-ANP4-23 treatment. In addition, N-acetyl cysteine (NAC), a scavenger of O2-, inhibitors of growth factor receptors and of c-Src, all inhibited the overexpression of cell cycle proteins cyclin D1 and cdk4 in VSMC from SHR. These results suggest that in vivo treatment of SHR with C-ANP4-23 inhibits the enhanced oxidative stress, c-Src and EGF-R, PDGF-R, IGF-R activation which through the inhibition of overexpression of cell cycle proteins result in the attenuation of hyperproliferation of VSMC.
[Mh] Termos MeSH primário: Músculo Liso Vascular/patologia
Estresse Oxidativo
Receptores do Fator Natriurético Atrial/fisiologia
Receptores de Fatores de Crescimento/genética
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Masculino
Ratos
Ratos Endogâmicos SHR
Ratos Endogâmicos WKY
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptors, Growth Factor); EC 4.6.1.2 (Receptors, Atrial Natriuretic Factor); EC 4.6.1.2 (atrial natriuretic factor receptor C)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180125
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191743


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[PMID]:29353044
[Au] Autor:Yamamoto H; Kurachi M; Naruse M; Shibasaki K; Ishizaki Y
[Ad] Endereço:Department of Molecular and Cellular Neurobiology, Gunma University Graduate School of Medicine, 3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan.
[Ti] Título:BMP4 signaling in NPCs upregulates Bcl-xL to promote their survival in the presence of FGF-2.
[So] Source:Biochem Biophys Res Commun;496(2):588-593, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We previously reported that BMP4 does not promote proliferation or differentiation of CD44-positive astrocyte precursor cells (APCs) but greatly promotes their survival in the presence of fibroblast growth factor-2 (FGF-2). In this study, we examined if BMP4 acts as a survival factor also for neural stem/progenitor cells (NPCs) isolated from ganglionic eminence of neonatal mouse brain. We found BMP4 promotes survival but not proliferation or differentiation of these cells, just as in the case for CD44-positive APCs. Microarray analysis revealed some candidate molecules in the signaling pathway downstream of BMP4. Among them, we focused on Id1 (inhibitor of DNA-binding 1) and Bcl-xL in this study. Expression of both genes was promoted in the presence of BMP4, and this promotion was reduced by dorsomorphin, an inhibitor of BMP4 signaling. Furthermore, cytochrome c release from mitochondria was significantly reduced in the presence of BMP4, suggesting up-regulation of Bcl-xL activity by BMP4. Id1 siRNA reduced the expression of Bcl-xL, and negated survival promoting effect of BMP4. These data suggest that BMP4 promotes survival of NPCs by enhancing the anti-apoptotic function of Bcl-xL via BMP4-Smad1/5/8-Id1 signaling.
[Mh] Termos MeSH primário: Proteína Morfogenética Óssea 4/metabolismo
Fator 2 de Crescimento de Fibroblastos/metabolismo
Células-Tronco Neurais/metabolismo
Transdução de Sinais
Proteína bcl-X/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose
Diferenciação Celular
Proliferação Celular
Sobrevivência Celular
Células Cultivadas
Camundongos Endogâmicos C57BL
Células-Tronco Neurais/citologia
Regulação para Cima
Proteína bcl-X/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bcl2l1 protein, mouse); 0 (Bone Morphogenetic Protein 4); 0 (bcl-X Protein); 103107-01-3 (Fibroblast Growth Factor 2)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180122
[St] Status:MEDLINE



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