Base de dados : MEDLINE
Pesquisa : D12.776.543.750.705.408.100.900 [Categoria DeCS]
Referências encontradas : 776 [refinar]
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[PMID]:29079415
[Au] Autor:Boguslawska J; Rodzik K; Poplawski P; Kedzierska H; Rybicka B; Sokól E; Tanski Z; Piekielko-Witkowska A
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Centre of Postgraduate Medical Education, ul. Marymoncka 99/103, 01-813 Warsaw, Poland.
[Ti] Título:TGF-ß1 targets a microRNA network that regulates cellular adhesion and migration in renal cancer.
[So] Source:Cancer Lett;412:155-169, 2018 Jan 01.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:In our previous study we found altered expression of 19 adhesion-related genes in renal tumors. In this study we hypothesized that disturbed expression of adhesion-related genes could be caused by microRNAs: short, non-coding RNAs that regulate gene expression. Here, we found that expression of 24 microRNAs predicted to target adhesion-related genes was disturbed in renal tumors and correlated with expression of their predicted targets. miR-25-3p, miR-30a-5p, miR-328 and miR-363-3p directly targeted adhesion-related genes, including COL5A1, COL11A1, ITGA5, MMP16 and THBS2. miR-363-3p and miR-328 inhibited proliferation of renal cancer cells, while miR-25-3p inhibited adhesion, promoted proliferation and migration of renal cancer cells. TGF-ß1 influenced the expression of miR-25-3p, miR-30a-5p, and miR-328. The analyzed microRNAs, their target genes and TGF-ß1 formed a network of strong correlations in tissue samples from renal cancer patients. The expression signature of microRNAs linked with TGF-ß1 levels correlated with poor survival of renal cancer patients. The results of our study suggest that TGF-ß1 coordinates the expression of microRNA network that regulates cellular adhesion in cancer.
[Mh] Termos MeSH primário: Regulação Neoplásica da Expressão Gênica
Neoplasias Renais/patologia
MicroRNAs/fisiologia
Fator de Crescimento Transformador beta1/fisiologia
[Mh] Termos MeSH secundário: Adesão Celular
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Colágeno Tipo V/genética
Biologia Computacional
Matriz Extracelular/fisiologia
Redes Reguladoras de Genes
Seres Humanos
Integrina alfaV/genética
Neoplasias Renais/genética
Neoplasias Renais/mortalidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (COL5A1 protein, human); 0 (Collagen Type V); 0 (Integrin alphaV); 0 (MicroRNAs); 0 (Transforming Growth Factor beta1)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171205
[Lr] Data última revisão:
171205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171029
[St] Status:MEDLINE


  2 / 776 MEDLINE  
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[PMID]:28739685
[Au] Autor:Wu YJ; Pagel MA; Muldoon LL; Fu R; Neuwelt EA
[Ad] Endereço:Department of Neurology, Oregon Health & Sciences University, Portland, OR, U.S.A.
[Ti] Título:High αv Integrin Level of Cancer Cells Is Associated with Development of Brain Metastasis in Athymic Rats.
[So] Source:Anticancer Res;37(8):4029-4040, 2017 08.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Brain metastases commonly occur in patients with malignant skin, lung and breast cancers resulting in high morbidity and poor prognosis. Integrins containing an αv subunit are cell adhesion proteins that contribute to cancer cell migration and cancer progression. We hypothesized that high expression of αv integrin cell adhesion protein promoted metastatic phenotypes in cancer cells. MATERIALS AND METHODS: Cancer cells from different origins were used and studied regarding their metastatic ability and intetumumab, anti-αv integrin mAb, sensitivity using in vitro cell migration assay and in vivo brain metastases animal models. RESULTS: The number of brain metastases and the rate of occurrence were positively correlated with cancer cell αv integrin levels. High αv integrin-expressing cancer cells showed significantly faster cell migration rate in vitro than low αv integrin-expressing cells. Intetumumab significantly inhibited cancer cell migration in vitro regardless of αv integrin expression level. Overexpression of αv integrin in cancer cells with low αv integrin level accelerated cell migration in vitro and increased the occurrence of brain metastases in vivo. CONCLUSION: αv integrin promotes brain metastases in cancer cells and may mediate early steps in the metastatic cascade, such as adhesion to brain vasculature. Targeting αv integrin with intetumumab could provide clinical benefit in treating cancer patients who develop metastases.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/genética
Adesão Celular/genética
Integrina alfaV/genética
Neoplasias/genética
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/administração & dosagem
Encéfalo/metabolismo
Encéfalo/patologia
Neoplasias Encefálicas/tratamento farmacológico
Neoplasias Encefálicas/patologia
Neoplasias Encefálicas/secundário
Modelos Animais de Doenças
Regulação Neoplásica da Expressão Gênica/genética
Seres Humanos
Integrina alfaV/biossíntese
Metástase Neoplásica
Neoplasias/tratamento farmacológico
Neoplasias/patologia
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Integrin alphaV); GQE1BJE2NI (intetumumab)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE


  3 / 776 MEDLINE  
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[PMID]:28604746
[Au] Autor:Zhang K; Myllymäki SM; Gao P; Devarajan R; Kytölä V; Nykter M; Wei GH; Manninen A
[Ad] Endereço:Biocenter Oulu, Centre of Excellence in Cell-Extracellular Matrix Research, Faculty of Biochemistry and Molecular Medicine, University of Oulu, Oulu, Finland.
[Ti] Título:Oncogenic K-Ras upregulates ITGA6 expression via FOSL1 to induce anoikis resistance and synergizes with αV-Class integrins to promote EMT.
[So] Source:Oncogene;36(41):5681-5694, 2017 Oct 12.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In many cancer types, integrin-mediated signaling regulates proliferation, survival and invasion of tumorigenic cells. However, it is still unclear how integrins crosstalk with oncogenes to regulate tumorigenesis and metastasis. Here we show that oncogenic K-Ras upregulates α6-integrin expression in Madin-Darby canine kidney (MDCK) cells via activation of the mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK)/Fos-related antigen 1-signaling cascade. Activated α6-integrins promoted metastatic capacity and anoikis resistance, and led to perturbed growth of MDCK cysts. Transcriptomic analysis of K-Ras -transformed MDCK cells also revealed robust downregulation of αV-class integrins. Re-expression of αV-integrin in K-Ras -transformed MDCK cells synergistically upregulated the expression of Zinc finger E-box-binding homeobox 1 and Twist-related protein 1 and triggered epithelial-mesenchymal transition leading to induced cell motility and invasion. These results delineate the signaling cascades connecting oncogenic K-Ras with α6- and αV-integrin functions to modulate cancer cell survival and tumorigenesis, and reveal new possible strategies to target highly oncogenic K-Ras mutants.
[Mh] Termos MeSH primário: Transição Epitelial-Mesenquimal/genética
Integrina alfaV/genética
Neoplasias/genética
Proteínas Proto-Oncogênicas c-fos/genética
[Mh] Termos MeSH secundário: Animais
Anoikis/genética
Proliferação Celular/genética
Cães
Seres Humanos
Integrina alfa6/genética
Células Madin Darby de Rim Canino
Neoplasias/patologia
Proteínas Proto-Oncogênicas p21(ras)/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ITGA6 protein, human); 0 (Integrin alpha6); 0 (Integrin alphaV); 0 (KRAS protein, human); 0 (Proto-Oncogene Proteins c-fos); 0 (fos-related antigen 1); EC 3.6.5.2 (Proto-Oncogene Proteins p21(ras))
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2017.177


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[PMID]:28376277
[Au] Autor:Pan F; Xiang H; Yan J; Hong L; Zhang L; Liu Y; Feng X; Cai C
[Ti] Título:Dendritic Cells from Rheumatoid Arthritis Patient Peripheral Blood Induce Th17 Cell Differentiation via miR-363/Integrin αv/TGF-ß Axis.
[So] Source:Scand J Immunol;85(6):441-449, 2017 Jun.
[Is] ISSN:1365-3083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Dendritic cells (DCs) are critical regulators of immune responses. This study was to observe the effect of DCs from peripheral blood on the differentiation of Th17 in patients with rheumatoid arthritis (RA). Peripheral blood samples were collected from 30 patients with RA and 20 healthy controls, respectively. Flow cytometry results showed that in contrast to Treg cells, the proportion of Th17 cells in T cells and the Th17/Treg ratio were both increased in patients with RA. The RT-PCR results showed that Foxp3、ROR γt and miR-363 expression in PBMC of patients with RA were reduced, but the ITGAV expression was increased, which was negatively related to miR-363 expression. IL-17, TGF-ß and IL-6 levels detected by ELISA were increased in peripheral blood serum of patients with RA. Moreover, we noted that the CD11C αν /CD11C DCs ratio was obvious increased in patients with RA and has positive correlation to the Th17/Treg ratio. In cocultured system, Th17 cell differentiation was significantly inhibited in the presence of ITGF-ß suggesting that Th17 cell differentiation was controlled by active TGF-ß (aTGF-ß). After DCs transfecting with miR-363 mimics and cocultured with T cells, Th17 cell number, IL-17 level and ROR-γt expression were significantly reduced in the presence of latent TGF-ß (ITGF-ß). In addition, the integrin αv protein expression was both reduced in the presence of aTGF-ß or ITGF-ß. These data demonstrated that DCs induced Th17 cell differentiation through miR-363/Integrin αv/TGF-ß pathway in patients with RA.
[Mh] Termos MeSH primário: Artrite Reumatoide/imunologia
Diferenciação Celular/imunologia
Células Dendríticas/imunologia
Integrina alfaV/imunologia
MicroRNAs/imunologia
Células Th17/imunologia
Fator de Crescimento Transformador beta/imunologia
[Mh] Termos MeSH secundário: Adulto
Artrite Reumatoide/sangue
Western Blotting
Antígeno CD11c/imunologia
Antígeno CD11c/metabolismo
Células Cultivadas
Técnicas de Cocultura
Células Dendríticas/metabolismo
Ensaio de Imunoadsorção Enzimática
Feminino
Fatores de Transcrição Forkhead/genética
Fatores de Transcrição Forkhead/imunologia
Fatores de Transcrição Forkhead/metabolismo
Expressão Gênica/imunologia
Seres Humanos
Integrina alfaV/metabolismo
Interleucina-17/sangue
Interleucina-17/imunologia
Interleucina-17/metabolismo
Interleucina-6/sangue
Interleucina-6/imunologia
Interleucina-6/metabolismo
Masculino
MicroRNAs/genética
MicroRNAs/metabolismo
Meia-Idade
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Transdução de Sinais/genética
Transdução de Sinais/imunologia
Linfócitos T/imunologia
Linfócitos T/metabolismo
Linfócitos T Reguladores/imunologia
Linfócitos T Reguladores/metabolismo
Fator de Crescimento Transformador beta/sangue
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD11c Antigen); 0 (FOXP3 protein, human); 0 (Forkhead Transcription Factors); 0 (Integrin alphaV); 0 (Interleukin-17); 0 (Interleukin-6); 0 (MIRN363 microRNA, human); 0 (MicroRNAs); 0 (Transforming Growth Factor beta)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170405
[St] Status:MEDLINE
[do] DOI:10.1111/sji.12550


  5 / 776 MEDLINE  
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[PMID]:28250242
[Au] Autor:Frank JW; Seo H; Burghardt RC; Bayless KJ; Johnson GA
[Ad] Endereço:Department of Veterinary Integrative BiosciencesCollege of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, Texas, USA.
[Ti] Título:ITGAV (alpha v integrins) bind SPP1 (osteopontin) to support trophoblast cell adhesion.
[So] Source:Reproduction;153(5):695-706, 2017 May.
[Is] ISSN:1741-7899
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Attachment of the conceptus trophoblast (Tr) to the uterine luminal epithelium (LE) is critical for successful implantation. This study determined whether alpha v (av) integrins (ITGAV) directly mediate porcine trophoblast cell adhesion to secreted phosphoprotein 1 (SPP1, also known as osteopontin (OPN)) and examined the temporal/spatial expression of ITGAV, beta 3 (b3, ITGB3) and beta 6 (b6, ITGB6) integrin subunits, and SPP1, at the uterine-placental interface of pigs. Knockdown of in porcine Tr (pTr2) cells by siRNA reduced pTr2 attachment to SPP1. hybridization confirmed the presence of , and mRNAs in uterine LE and conceptus Tr between Days 9 and 60 of gestation, with no change in the magnitude of expression over the course of pregnancy. Exogenous E2 or P4 did not affect , and mRNA expression in the uteri of ovariectomized gilts. Immunofluorescence identified ITGAV, ITGB3 and SPP1 proteins in large aggregates at the uterine LE-placental Tr/chorion interface on Day 25, but aggregates were no longer observed by Day 50 of gestation. These results are the first to directly demonstrate that pTr2 cells engage ITGAV-containing integrin receptors to adhere to SPP1 and suggest that mechanical forces generated by tethering elongating conceptuses to uterine LE leads to assembly of focal adhesions containing ITGAV and SPP1; however, as placentation progresses, subsequent folding/interdigitation at the uterine-placental interface disperses mechanical forces resulting in the loss of focal adhesions.
[Mh] Termos MeSH primário: Adesão Celular/fisiologia
Integrina alfaV/metabolismo
Osteopontina/metabolismo
Trofoblastos/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Feminino
Imunofluorescência
Hibridização In Situ
Gravidez
Suínos
Trofoblastos/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Integrin alphaV); 106441-73-0 (Osteopontin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170303
[St] Status:MEDLINE
[do] DOI:10.1530/REP-17-0043


  6 / 776 MEDLINE  
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[PMID]:28192121
[Au] Autor:Shih CH; Chiang TB; Wang WJ
[Ad] Endereço:Chang Gung University of Science and Technology, Guishan Dist., Taoyuan City, Taiwan.
[Ti] Título:Convulxin, a C-type lectin-like protein, inhibits HCASMCs functions via WAD-motif/integrin-αv interaction and NF-κB-independent gene suppression of GRO and IL-8.
[So] Source:Exp Cell Res;352(2):234-244, 2017 Mar 15.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Convulxin (CVX), a C-type lectin-like protein (CLPs), is a potent platelet aggregation inducer. To evaluate its potential applications in angiogenic diseases, the multimeric CVX were further explored on its mode of actions toward human coronary artery smooth muscle cells (HCASMCs). The N-terminus of ß-chain of CVX (CVX-ß) contains a putative disintegrin-like domain with a conserved motif upon the sequence comparison with other CLPs. Importantly, native CVX had no cytotoxic activity as examined by electrophoretic pattern. A Trp-Ala-Asp (WAD)-containing octapeptide, MTWADAEK, was thereafter synthesized and analyzed in functional assays. In the case of specific integrin antagonists as positive controls, the anti-angiogenic effects of CVX on HCASMCs were investigated by series of functional analyses. CVX showed to exhibit multiple inhibitory activities toward HCASMCs proliferation, adhesion and invasion with a dose- and integrin αvß3-dependent fashion. However, the WAD-octapeptide exerting a minor potency could also work as an active peptidomimetic. In addition, flow cytometric analysis demonstrated both the intact CVX and synthetic peptide can specifically interact with integrin-αv on HCASMCs and CVX was shown to have a down-regulatory effect on the gene expression of CXC-chemokines, such as growth-related oncogene and interleukin-8. According to nuclear factor-κB (NF-κB) p65 translocation assay and Western blotting analysis, the NF-κB activation was not involved in the signaling events of CVX-induced gene expression. In conclusion, CVX may act as a disintegrin-like protein via the interactions of WAD-motif in CVX-ß with integrin-αv on HCASMCs and it also is a gene suppressor with the ability to diminish the expression of two CXC-chemokines in a NF-κB-independent manner. Indeed, more extensive investigations are needed and might create a new avenue for the development of a novel angiostatic agent.
[Mh] Termos MeSH primário: Proliferação Celular
Quimiocina CXCL1/metabolismo
Integrina alfaV/metabolismo
Interleucina-8/metabolismo
Lectinas Tipo C/metabolismo
Miócitos de Músculo Liso/metabolismo
[Mh] Termos MeSH secundário: Sítios de Ligação
Adesão Celular
Linhagem Celular
Quimiocina CXCL1/genética
Vasos Coronários/citologia
Venenos de Crotalídeos/química
Venenos de Crotalídeos/metabolismo
Venenos de Crotalídeos/farmacologia
Seres Humanos
Lectinas Tipo C/química
Músculo Liso Vascular/citologia
Músculo Liso Vascular/metabolismo
NF-kappa B/metabolismo
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL1 protein, human); 0 (Chemokine CXCL1); 0 (Crotalid Venoms); 0 (Integrin alphaV); 0 (Interleukin-8); 0 (Lectins, C-Type); 0 (NF-kappa B); 37206-04-5 (convulxin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170526
[Lr] Data última revisão:
170526
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170214
[St] Status:MEDLINE


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[PMID]:27593923
[Au] Autor:Wang J; Zhang B; Wu H; Cai J; Sui X; Wang Y; Li H; Qiu Y; Wang T; Chen Z; Zhu Q; Xia H; Song W; Xiang AP
[Ad] Endereço:Program of Stem Cells and Regenerative Medicine, Affiliated Guangzhou Women and Children's Hospital, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China.
[Ti] Título:CD51 correlates with the TGF-beta pathway and is a functional marker for colorectal cancer stem cells.
[So] Source:Oncogene;36(10):1351-1363, 2017 Mar.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Colorectal cancer (CRC) is one of the top three most prevalent and deadly cancers. A cancer stem cell (CSC) sub-population that is characterized by the abilities of tumor initiation, self-renewal, metastasis and resistance to chemotherapy can suggest new therapeutic targets. However, no such sub-population has been conclusively identified for CRC, and we lack any marker to identify cells with all of the above characteristics. Here, we report that CD51 CRC cells displayed greater sphere-forming and tumorigenic capacities, increased migratory and invasive potentials, and enhanced chemoresistance compared with CD51 CRC cells. CD51 knockdown reduced the side population, sphere formation, cell motility and inhibited tumor incidence and metastasis in an in vivo tumor model. Furthermore, CD51 could bind transforming growth factor beta (TGF-ß) receptors, and that it upregulated TGF-ß/Smad signaling. These results indicate that CD51 is a novel functional marker for colorectal CSCs which may provide an therapeutic target for the efficient elimination of colorectal CSCs.
[Mh] Termos MeSH primário: Neoplasias Colorretais/metabolismo
Integrina alfaV/metabolismo
Células-Tronco Neoplásicas/metabolismo
Transdução de Sinais
Fator de Crescimento Transformador beta/metabolismo
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacologia
Biomarcadores
Linhagem Celular Tumoral
Transformação Celular Neoplásica/genética
Transformação Celular Neoplásica/metabolismo
Neoplasias Colorretais/genética
Modelos Animais de Doenças
Resistência a Medicamentos Antineoplásicos/genética
Expressão Gênica
Xenoenxertos
Seres Humanos
Imuno-Histoquímica
Integrina alfaV/genética
Camundongos
Células-Tronco Neoplásicas/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
Proteínas Smad/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Biomarkers); 0 (Integrin alphaV); 0 (Smad Proteins); 0 (Transforming Growth Factor beta)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160906
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2016.299


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[PMID]:27367918
[Au] Autor:Maredziak M; Tomaszewski K; Polinceusz P; Lewandowski D; Marycz K
[Ad] Endereço:a Faculty of Veterinary Medicine , University of Environmental and Life Sciences , Wroclaw , Poland.
[Ti] Título:Static magnetic field enhances the viability and proliferation rate of adipose tissue-derived mesenchymal stem cells potentially through activation of the phosphoinositide 3-kinase/Akt (PI3K/Akt) pathway.
[So] Source:Electromagn Biol Med;36(1):45-54, 2017.
[Is] ISSN:1536-8386
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The aim of this work was to investigate the effects of 0.5T static magnetic field (sMF) on the viability and proliferation rate of human adipose-derived mesenchymal stromal stem cells (hASCs) via activation of the phosphoinositide 3-kinase/Akt (PI3K/Akt) signaling pathway. In a 7-d culture we examined cell growth kinetic and population doubling time (PDT). We also examined cell morphology and the cellular senescence markers level. Exposure to sMF enhanced the viability of these cells. However, the effect was blocked by treating the cells with LY294002, a P13K inhibitor. We compared this effect by Western Blot analysis of Akt protein expression. We also examined whether the cell response on sMF stimulation is dependent on integrin engagement and we measured integrin gene expression. Our results suggest that stimulation using sMF is a viable method to improve hASC viability. sMF is involved in mechanisms associated with controlling cell proliferative potential signaling events.
[Mh] Termos MeSH primário: Tecido Adiposo/citologia
Campos Magnéticos
Células Mesenquimais Estromais/classificação
Fosfatidilinositol 3-Quinases/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Cromonas/farmacologia
Ativação Enzimática/efeitos dos fármacos
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Integrina alfaV/genética
Integrina beta3/genética
Células Mesenquimais Estromais/citologia
Células Mesenquimais Estromais/efeitos dos fármacos
Células Mesenquimais Estromais/metabolismo
Morfolinas/farmacologia
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chromones); 0 (Integrin alphaV); 0 (Integrin beta3); 0 (Morpholines); 0 (RNA, Messenger); 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170210
[Lr] Data última revisão:
170210
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160702
[St] Status:MEDLINE


  9 / 776 MEDLINE  
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[PMID]:27693080
[Au] Autor:Takahashi M; Sakota E; Nakamura Y
[Ad] Endereço:The institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo 108-8639, Japan.
[Ti] Título:The efficient cell-SELEX strategy, Icell-SELEX, using isogenic cell lines for selection and counter-selection to generate RNA aptamers to cell surface proteins.
[So] Source:Biochimie;131:77-84, 2016 Dec.
[Is] ISSN:1638-6183
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Aptamers are short single-stranded nucleic acid molecules that are selected in vitro from a large random sequence library based on their high and specific affinity to a target molecule by a process known as SELEX. Cell-SELEX that employs whole living cells overexpressing the defined cell surface proteins (for selection) and appropriate mock cells (for counter-selection) has been widely used as a valid and feasible method for generating aptamers against specific cell surface proteins. However, the endogenous expression of target proteins in mock cells or the heterogeneity of surface proteins between selection and counter-selection cells often impeded the isolation of proper aptamers against target proteins. To solve this problem, we developed "Isogenic cell-SELEX" (Icell SELEX in short) method, in which isogenic cell lines were manipulated for counter-selection by microRNA-mediated silencing and for selection by overexpression of target proteins. As a model experiment, we targeted integrin alpha V (ITGAV), which is a major transmembrane receptor expressed in almost all the cells, and established ITGAV-overexpressed and -downregulated HEK293 cells for selection and counter-selection, respectively. By taking advantage of a hundred-fold difference in the expression level of ITGAV between these two isogenic cell lines, we easily isolated several anti-ITGAV aptamers, whose binding to the cell-surface ITGAV was confirmed by flow cytometry with the dissociation constant of 300-400 nM range. We assume that Icell-SELEX could be applicable to a wide range of cell-surface proteins including various transmembrane proteins of biological and pharmacological significance.
[Mh] Termos MeSH primário: Aptâmeros de Nucleotídeos/genética
Biblioteca Gênica
Proteínas de Membrana/genética
Técnica de Seleção de Aptâmeros/métodos
[Mh] Termos MeSH secundário: Sequência de Bases
Western Blotting
Citometria de Fluxo
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Células HEK293
Seres Humanos
Imuno-Histoquímica
Integrina alfaV/genética
Integrina alfaV/metabolismo
Proteínas de Membrana/metabolismo
MicroRNAs/genética
Plasmídeos/genética
Interferência de RNA
Reprodutibilidade dos Testes
Ressonância de Plasmônio de Superfície
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aptamers, Nucleotide); 0 (Integrin alphaV); 0 (Membrane Proteins); 0 (MicroRNAs); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170130
[Lr] Data última revisão:
170130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161004
[St] Status:MEDLINE


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[PMID]:27535240
[Au] Autor:Almeida ME; Monteiro KS; Kato EE; Sampaio SC; Braga TT; Câmara NO; Lamers ML; Santos MF
[Ad] Endereço:Department of Cell and Developmental Biology, Biomedical Sciences Institute, University of São Paulo, Av. Prof. Lineu Prestes 1524, Cidade Universitária, São Paulo, SP, CEP 05508-000, Brazil.
[Ti] Título:Hyperglycemia reduces integrin subunits alpha v and alpha 5 on the surface of dermal fibroblasts contributing to deficient migration.
[So] Source:Mol Cell Biochem;421(1-2):19-28, 2016 Oct.
[Is] ISSN:1573-4919
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Deficient wound healing is a common multifactorial complication in diabetic patients, but the cellular and molecular mechanisms involved are poorly defined. In the present study, we analyzed the effects of hyperglycemia on integrins expression in rat dermal fibroblasts and addressed its role in cell adhesion and migration. Diabetes Mellitus was induced in rats by streptozotocin injection and maintained for 30 days. Primary cultures of dermal fibroblasts from control and diabetic rats were maintained under low glucose (5 mM D-glucose) or high glucose (30 mM D-glucose) for 7 days. Cell adhesion and migration were studied by kymography, transwell, and time-lapse assays, and the expressions of integrin subunits αv and α5 were studied by immunocytochemistry and western blotting. Fibroblasts derived from diabetic rats confirmed a reduced migration speed and delayed spreading compared to fibroblasts derived from control rats. The membrane fraction of diabetic-derived fibroblasts showed a decrease of integrin subunits α5 and αv, which was confirmed by immunocytochemistry assays. A reduction in the pericellular fibronectin matrix was also observed. The exposure of diabetic-derived cells to a higher concentration of exogenous fibronectin improved migration velocity and the expression of αv but did not completely restore their migration capacity. In conclusion, the mechanisms involved in the deleterious effects of Diabetes Mellitus on wound healing include the ability of fibroblasts to secrete and to adhere to fibronectin.
[Mh] Termos MeSH primário: Movimento Celular
Derme/metabolismo
Diabetes Mellitus Experimental/metabolismo
Fibroblastos/metabolismo
Hiperglicemia/metabolismo
Integrina alfaV/metabolismo
[Mh] Termos MeSH secundário: Animais
Derme/patologia
Diabetes Mellitus Experimental/patologia
Fibroblastos/patologia
Hiperglicemia/induzido quimicamente
Hiperglicemia/patologia
Masculino
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Integrin alphaV)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160819
[St] Status:MEDLINE
[do] DOI:10.1007/s11010-016-2780-4



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