Base de dados : MEDLINE
Pesquisa : G04.144 [Categoria DeCS]
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[PMID]:29385191
[Au] Autor:Chuerduangphui J; Ekalaksananan T; Chaiyarit P; Patarapadungkit N; Chotiyano A; Kongyingyoes B; Promthet S; Pientong C
[Ad] Endereço:Department of Microbiology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
[Ti] Título:Effects of arecoline on proliferation of oral squamous cell carcinoma cells by dysregulating c-Myc and miR-22, directly targeting oncostatin M.
[So] Source:PLoS One;13(1):e0192009, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Arecoline, the major alkaloid of areca nut, is known to induce oral carcinogenesis, however, its mechanism is still needed to elucidate. This study investigated the effects of arecoline on cell viability and cell-cycle progression of oral squamous cell carcinoma (OSCC) cells as well as a relevant cellular gene expression. The results showed that a low concentration of arecoline (0.025 µg/ml) increased OSCC cell viability, proportion of cells in G2/M phase and cell proliferation. Simultaneously, it induced IL-6, STAT3 and c-Myc expression. Interestingly, c-myc promoter activity was also induced by arecoline. MiR-22 expression in arecoline-treated OSCC cells was suppressed and comparable to an upregulated c-Myc expression. In arecoline-treated OSCC cells, oncostatin M (OSM) expression was significantly upregulated and inversely correlated with miR-22 expression. Likewise, OSM expression and its post-transcriptional activity were significantly decreased in miR-22-transfected OSCC and 293FT cells. This result demonstrated that miR-22 directly targeted OSM. Interestingly, miR-22 played an important role as a tumor suppresser on suppressing cell proliferation, migration and cell-cycle progression of OSCC cells. This result suggested the effect of arecoline to promote cell proliferation and cell-cycle progression of OSCC cells might be involved in induction of c-Myc expression and reduction of miR-22 resulting in OSM upregulation.
[Mh] Termos MeSH primário: Arecolina/farmacologia
Carcinoma de Células Escamosas/patologia
Proliferação Celular/efeitos dos fármacos
MicroRNAs/metabolismo
Neoplasias Bucais/patologia
Proteínas Proto-Oncogênicas c-myc/metabolismo
[Mh] Termos MeSH secundário: Carcinoma de Células Escamosas/metabolismo
Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Seres Humanos
Interleucina-6/biossíntese
MicroRNAs/genética
Neoplasias Bucais/metabolismo
Regiões Promotoras Genéticas
Proteínas Proto-Oncogênicas c-myc/genética
Fator de Transcrição STAT3/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-6); 0 (MIRN22 microRNA, human); 0 (MicroRNAs); 0 (Proto-Oncogene Proteins c-myc); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 4ALN5933BH (Arecoline)
[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
[do] DOI:10.1371/journal.pone.0192009


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[PMID]:29381751
[Au] Autor:Chea C; Miyauchi M; Inubushi T; Febriyanti Ayuningtyas N; Subarnbhesaj A; Nguyen PT; Shrestha M; Haing S; Ohta K; Takata T
[Ad] Endereço:Department of Oral & Maxillofacial Pathobiology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
[Ti] Título:Molecular mechanism of inhibitory effects of bovine lactoferrin on the growth of oral squamous cell carcinoma.
[So] Source:PLoS One;13(1):e0191683, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Lactoferrin (LF), a member of the transferrin family, recently has been demonstrated to have anticancer effects on various cancers including oral squamous cell carcinoma (OSCC). However, little is known about the underlying mechanisms of its effects on OSCC. Therefore, we aimed to investigate the mechanism of the suppressive effects of bovine LF (bLF) on the growth of OSCC cells. METHODS: In the current study, HSC2, HSC3, HSC4 and normal human oral keratinocytes (RT7) cell lines were tested with bLF 1, 10, and 100 µg/ml. The effects and detail mechanisms of bLF on proliferation and apoptosis of cells were investigated using flow cytometry and western blotting. RESULTS: We found that bLF (1, 10, and 100 µg/ml) induced activation of p53, a tumor suppressor gene, is associated with the induction of cell cycle arrest in G1/S phase and apoptosis in OSCC. Moreover, bLF downregulated the phosphorylation of Akt and activated suppressor of cytokine signaling 3 (SOCS3), thereby attenuating multiple signaling pathways including mTOR/S6K and JAK/STAT3. Interestingly, we revealed that bLF exerted its effect selectively against HSC3 but not on RT7 via different effects on the phosphorylation status of NF-κB and Akt. CONCLUSION: This is the first report showing that bLF selectively suppresses proliferation through mTOR/S6K and JAK/STAT3 pathways and induction of apoptosis in OSCC. This study provides important new findings, which might be useful in the prevention and treatment of OSCC.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/patologia
Lactoferrina/farmacologia
Neoplasias Bucais/patologia
[Mh] Termos MeSH secundário: Animais
Bovinos
Ciclo Celular/efeitos dos fármacos
Linhagem Celular Transformada
Proliferação Celular/efeitos dos fármacos
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 3.4.21.- (Lactoferrin)
[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:180131
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191683


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[PMID]:28462910
[Au] Autor:Mihailescu IN; Bociaga D; Popescu-Pelin G; Stan GE; Duta L; Socol G; Chifiriuc MC; Bleotu C; Lazar V; Husanu MA; Zgura I; Miculescu F; Negut I; Hapenciuc C
[Ad] Endereço:National Institute for Lasers, Plasma and Radiation Physics, 077125 Magurele, Romania.
[Ti] Título:Optimized silicon reinforcement of carbon coatings by pulsed laser technique for superior functional biomedical surfaces fabrication.
[So] Source:Biofabrication;9(2):025029, 2017 Jun 01.
[Is] ISSN:1758-5090
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We report on the fabrication of silicon-reinforced carbon (C:Si) structures by combinatorial pulsed laser deposition to search for the best design for a new generation of multi-functional coated implants. The synthesized films were characterized from the morphological, structural, compositional, mechanical and microbiological points of view. Scanning electron microscopy revealed the presence, on top of the deposited layers, of spheroid particulates with sizes in the micron range. No micro-cracks or delaminations were observed. Energy dispersive x-ray spectroscopy and grazing incidence x-ray diffraction pointed to the existence of a C to Si compositional gradient from one end of the film to the other. Raman investigation revealed a relatively high sp hybridization of up to 80% at 40-48 mm apart from the edge with higher C content. Si addition was demonstrated to significantly increase C:Si film bonding to the substrate, with values above the ISO threshold for coatings to be used in high-loading biomedical applications. Surface energy studies pointed to an increase in the hydrophilic character of the deposited structures along with Si content up to 52 mN m . In certain cases, the Si-reinforced C coatings elicited an antimicrobial biofilm action. The presence of Si was proven to be benign to HEp-2 cells of human origin, without interfering with their cellular cycle. On this basis, reliable C:Si structures with good adherence to the substrate and high efficiency against microbial biofilms can be developed for implant coatings and other advanced medical devices.
[Mh] Termos MeSH primário: Tecnologia Biomédica/métodos
Carbono/química
Materiais Revestidos Biocompatíveis/química
Lasers
Silício/química
[Mh] Termos MeSH secundário: Ciclo Celular
Forma Celular
Seres Humanos
Teste de Materiais
Testes de Sensibilidade Microbiana
Microscopia Eletrônica de Varredura
Espectrometria por Raios X
Análise Espectral Raman
Propriedades de Superfície
Água/química
Difração de Raios X
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Coated Materials, Biocompatible); 059QF0KO0R (Water); 7440-44-0 (Carbon); Z4152N8IUI (Silicon)
[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:170503
[St] Status:MEDLINE
[do] DOI:10.1088/1758-5090/aa7076


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[PMID]:28457165
[Au] Autor:de Simone A; Hubbard R; de la Torre NV; Velappan Y; Wilson M; Considine MJ; Soppe WJJ; Foyer CH
[Ad] Endereço:1 Centre for Plant Sciences, Faculty of Biological Sciences, University of Leeds , Leeds, United Kingdom .
[Ti] Título:Redox Changes During the Cell Cycle in the Embryonic Root Meristem of Arabidopsis thaliana.
[So] Source:Antioxid Redox Signal;27(18):1505-1519, 2017 Dec 20.
[Is] ISSN:1557-7716
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIMS: The aim of this study was to characterize redox changes in the nuclei and cytosol occurring during the mitotic cell cycle in the embryonic roots of germinating Arabidopsis seedlings, and to determine how redox cycling was modified in mutants with a decreased capacity for ascorbate synthesis. RESULTS: Using an in vivo reduction-oxidation (redox) reporter (roGFP2), we show that transient oxidation of the cytosol and the nuclei occurred at G1 in the synchronized dividing cells of the Arabidopsis root apical meristem, with reduction at G2 and mitosis. This redox cycle was absent from low ascorbate mutants in which nuclei were significantly more oxidized than controls. The cell cycle-dependent increase in nuclear size was impaired in the ascorbate-deficient mutants, which had fewer cells per unit area in the root proliferation zone. The transcript profile of the dry seeds and size of the imbibed seeds was strongly influenced by low ascorbate but germination, dormancy release and seed aging characteristics were unaffected. INNOVATION: These data demonstrate the presence of a redox cycle within the plant cell cycle and that the redox state of the nuclei is an important factor in cell cycle progression. CONCLUSIONS: Controlled oxidation is a key feature of the early stages of the plant cell cycle. However, sustained mild oxidation restricts nuclear functions and impairs progression through the cell cycle leading to fewer cells in the root apical meristem. Antioxid. Redox Signal. 27, 1505-1519.
[Mh] Termos MeSH primário: Arabidopsis/crescimento & desenvolvimento
Meristema/embriologia
Oxirredução
Proteínas de Plantas/genética
[Mh] Termos MeSH secundário: Arabidopsis/embriologia
Arabidopsis/genética
Ciclo Celular
Núcleo Celular/genética
Núcleo Celular/metabolismo
Citosol/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Regulação da Expressão Gênica de Plantas
Germinação
Meristema/genética
Raízes de Plantas/embriologia
Raízes de Plantas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Plant 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:170502
[St] Status:MEDLINE
[do] DOI:10.1089/ars.2016.6959


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[PMID]:29441973
[Au] Autor:Gong F; Niu J; Pei X
[Ti] Título:Clinical effects of dressing on patients with I-II phase pressure sores.
[So] Source:Pharmazie;71(11):665-669, 2016 Nov 02.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Angelica dahurica is a well-known traditional Chinese Medicine (TCM), while little information is available about its effects on pressure sores. We aimed to investigate the clinical effect of Angelica dahurica on patients with I-II phase pressure sores, as well as the underlying mechanism. METHODS: Patients (n = 98) with phase I and phase II pressure sores were enrolled and randomly assigned to control and treated groups. In addition to holistic nursing, patients in the control group received compound clotrimazole cream, while patients in the treated group received continuous 4 weeks of external application of Angelica dahurica dressing. Therapeutic effect was recorded, along with the levels of interleukin-8 (IL-8), epidermal growth factor (EGF), transforming growth factor (TGF)-ß, and vascular endothelial growth factor (VEGF). Besides, HaCaT cells were cultured with different concentrations of Angelica dahurica, and then cell viability, clone formation numbers, cell cycle, and levels of cyclin D1 and cyclin-dependent kinase (CDK) 2 were determined. RESULTS: The total effective rate in the treated group was significantly higher than in the control group. Levels of IL-8, EGF, TGF-ß, and VEGF were statistically increased by Angelica dahurica. In addition, the cell viability and clone formation numbers were significantly upregulated by Angelica dahurica in a dose-dependent manner. Also, the percentage of cells in G0/G1 phase, and levels of cyclin D1 and CDK2 were significantly elevated. CONCLUSION: Our results suggest that Angelica dahurica may provide an effective clinical treatment for I-II phase pressure sores.
[Mh] Termos MeSH primário: Angelica/química
Lesão por Pressão/tratamento farmacológico
[Mh] Termos MeSH secundário: Administração Tópica
Idoso
Bandagens
Ciclo Celular/efeitos dos fármacos
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Citocinas/biossíntese
Relação Dose-Resposta a Droga
Feminino
Seres Humanos
Peptídeos e Proteínas de Sinalização Intercelular/biossíntese
Masculino
Meia-Idade
Pomadas
Fitoterapia
Lesão por Pressão/metabolismo
Lesão por Pressão/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Cytokines); 0 (Intercellular Signaling Peptides and Proteins); 0 (Ointments)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6704


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[PMID]:29442036
[Au] Autor:Pivodová V; Zahler S; Karas D; Valentová K; Ulrichova J
[Ti] Título: study of 2,3-dehydrosilybin and its galloyl esters as potential inhibitors of angiogenesis.
[So] Source:Pharmazie;71(8):478-483, 2016 08 01.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:2,3-Dehydrosilybin exhibits substantial anticancer and antiangiogenic effects, which can be potentially improved by semi-synthetic modification such as esterification with gallic acid. The aim of this study was to examine the potential antiangiogenic effect of 2,3-dehydrosilybin and its galloyl esters (3-O-galloyl-2,3-dehydrosilybin; 7-O-galloyl-2,3-dehydrosilybin; 20-O-galloyl-2,3-dehydrosilybin and 23-O-galloyl-2,3-dehydrosilybin) and to determine which molecular mechanism could be responsible for their activity. The effect on cell proliferation, tube formation, signal transduction pathways (PI3K/Akt and ERK) and the cell cycle was studied in human microvascular endothelial cells (HMEC). The results showed that all compounds decreased the growth of HMEC, but the strongest effect was observed for 20-O-galloyl-2,3-dehydrosilybin at 5 µmol/l. In addition, at 5 and 10 µmol/l, this was the only compound that significantly inhibited HMEC tube formation. Based on an assessment of Akt and ERK1/2 expression, we suggest that 20-O-galloyl-2,3-dehydrosilybin influences the angiogenic process through the Akt pathway.
[Mh] Termos MeSH primário: Inibidores da Angiogênese/farmacologia
Silimarina/farmacologia
[Mh] Termos MeSH secundário: Inibidores da Angiogênese/síntese química
Ciclo Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Células Endoteliais/efeitos dos fármacos
Ésteres/síntese química
Ésteres/farmacologia
Ácido Gálico/síntese química
Ácido Gálico/farmacologia
Seres Humanos
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Microtúbulos/efeitos dos fármacos
Neovascularização Patológica/tratamento farmacológico
Proteína Oncogênica v-akt/efeitos dos fármacos
Fosfatidilinositol 3-Quinases/efeitos dos fármacos
Silimarina/síntese química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Angiogenesis Inhibitors); 0 (Esters); 0 (Silymarin); 4RKY41TBTF (silybin); 632XD903SP (Gallic Acid); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Oncogene Protein v-akt)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6579


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[PMID]:28903484
[Au] Autor:Yang Y; Gao X; Zhang M; Yan S; Sun C; Xiao F; Huang N; Yang X; Zhao K; Zhou H; Huang S; Xie B; Zhang N
[Ad] Endereço:Department of Neurosurgery, The 1st Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong Province, PR China; Guangdong Provincial Key Laboratory of Pituitary Tumor, Guangzhou, Guangdong Province, PR China; Department of Scientific Research Section, The 1st Affiliated Hospital of Sun Y
[Ti] Título:Novel Role of FBXW7 Circular RNA in Repressing Glioma Tumorigenesis.
[So] Source:J Natl Cancer Inst;110(3), 2018 Mar 01.
[Is] ISSN:1460-2105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Circular RNAs (circRNAs) are RNA transcripts that are widespread in the eukaryotic genome. Recent evidence indicates that circRNAs play important roles in tissue development, gene regulation, and carcinogenesis. However, whether circRNAs encode functional proteins remains elusive, although translation of several circRNAs was recently reported. Methods: CircRNA deep sequencing was performed by using 10 pathologically diagnosed glioblastoma samples and their paired adjacent normal brain tissues. Northern blotting, Sanger sequencing, antibody, and liquid chromatograph Tandem Mass Spectrometer were used to confirm the existence of circ-FBXW7 and its encoded protein in in two cell lines. Lentivirus-transfected stable U251 and U373 cells were used to assess the biological functions of the novel protein invitro and invivo (five mice per group). Clinical implications of circ-FBXW7 were assessed in 38 pathologically diagnosed glioblastoma samples and their paired periphery normal brain tissues by using quantitative polymerase chain reaction (two-sided log-rank test). Results: Circ-FBXW7 is abundantly expressed in the normal human brain (reads per kilobase per million mapped reads [RPKM] = 9.31). The spanning junction open reading frame in circ-FBXW7 driven by internal ribosome entry site encodes a novel 21-kDa protein, which we termed FBXW7-185aa. Upregulation of FBXW7-185aa in cancer cells inhibited proliferation and cell cycle acceleration, while knockdown of FBXW7-185aa promoted malignant phenotypes invitro and invivo. FBXW7-185aa reduced the half-life of c-Myc by antagonizing USP28-induced c-Myc stabilization. Moreover, circ-FBXW7 and FBXW7-185aa levels were reduced in glioblastoma clinical samples compared with their paired tumor-adjacent tissues (P < .001). Circ-FBXW7 expression positively associated with glioblastoma patient overall survival (P = .03). Conclusions: Endogenous circRNA encodes a functional protein in human cells, and circ-FBXW7 and FBXW7-185aa have potential prognostic implications in brain cancer.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/genética
Proteínas de Ciclo Celular/genética
Transformação Celular Neoplásica/genética
Proteínas F-Box/genética
Glioblastoma/genética
RNA/análise
Ubiquitina-Proteína Ligases/genética
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Neoplasias Encefálicas/química
Ciclo Celular/genética
Proteínas de Ciclo Celular/análise
Linhagem Celular Tumoral
Proliferação Celular/genética
Proteínas F-Box/análise
Proteína 7 com Repetições F-Box-WD
Feminino
Glioblastoma/química
Meia-Vida
Seres Humanos
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Transplante de Neoplasias
Fases de Leitura Aberta
Proteínas Proto-Oncogênicas c-myc/metabolismo
Análise de Sequência de RNA
Taxa de Sobrevida
Ubiquitina Tiolesterase/metabolismo
Ubiquitina-Proteína Ligases/análise
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (F-Box Proteins); 0 (F-Box-WD Repeat-Containing Protein 7); 0 (FBXW7 protein, human); 0 (Proto-Oncogene Proteins c-myc); 0 (RNA, circular); 63231-63-0 (RNA); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 3.1.2.15 (USP28 protein, human); EC 3.4.19.12 (Ubiquitin Thiolesterase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1093/jnci/djx166


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[PMID]:28467935
[Au] Autor:Qiu WL; Zhang YW; Feng Y; Li LC; Yang L; Xu CR
[Ad] Endereço:Ministry of Education Key Laboratory of Cell Proliferation, College of Life Sciences, Peking-Tsinghua Center for Life Sciences, Peking University, Beijing 100871, China; PKU-Tsinghua-NIBS Graduate Program, Peking University, Beijing 100871, China.
[Ti] Título:Deciphering Pancreatic Islet ß Cell and α Cell Maturation Pathways and Characteristic Features at the Single-Cell Level.
[So] Source:Cell Metab;25(5):1194-1205.e4, 2017 May 02.
[Is] ISSN:1932-7420
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pancreatic ß and α cells play essential roles in maintaining glucose homeostasis. However, the mechanisms by which these distinct cell populations are generated, expand, and mature during pancreas development remain unclear. In this study, we addressed this critical question by performing a single-cell transcriptomic analysis of mouse ß and α cells sorted from fetal to adult stages. We discovered that ß and α cells use different regulatory strategies for their maturation and that cell proliferation peaks at different developmental times. However, the quiescent and proliferative cells in both the ß lineage and α lineage are synchronous in their maturation states. The heterogeneity of juvenile ß cells reflects distinct cell-cycling phases, origins, and maturation states, whereas adult ß cells are relatively homogeneous at the transcriptomic level. These analyses provide not only a high-resolution roadmap for islet lineage development but also insights into the mechanisms of cellular heterogeneity, cell number expansion, and maturation of both ß and α cells.
[Mh] Termos MeSH primário: Células Secretoras de Glucagon/citologia
Células Secretoras de Insulina/citologia
[Mh] Termos MeSH secundário: Animais
Ciclo Celular
Diferenciação Celular
Proliferação Celular
Células Cultivadas
Feminino
Células Secretoras de Glucagon/metabolismo
Células Secretoras de Insulina/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Transdução de Sinais
Análise de Célula Única
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:29339718
[Au] Autor:Parfejevs V; Debbache J; Shakhova O; Schaefer SM; Glausch M; Wegner M; Suter U; Riekstina U; Werner S; Sommer L
[Ad] Endereço:Institute of Anatomy, University of Zürich, 8057, Zürich, Switzerland.
[Ti] Título:Injury-activated glial cells promote wound healing of the adult skin in mice.
[So] Source:Nat Commun;9(1):236, 2018 01 16.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cutaneous wound healing is a complex process that aims to re-establish the original structure of the skin and its functions. Among other disorders, peripheral neuropathies are known to severely impair wound healing capabilities of the skin, revealing the importance of skin innervation for proper repair. Here, we report that peripheral glia are crucially involved in this process. Using a mouse model of wound healing, combined with in vivo fate mapping, we show that injury activates peripheral glia by promoting de-differentiation, cell-cycle re-entry and dissemination of the cells into the wound bed. Moreover, injury-activated glia upregulate the expression of many secreted factors previously associated with wound healing and promote myofibroblast differentiation by paracrine modulation of TGF-ß signalling. Accordingly, depletion of these cells impairs epithelial proliferation and wound closure through contraction, while their expansion promotes myofibroblast formation. Thus, injury-activated glia and/or their secretome might have therapeutic potential in human wound healing disorders.
[Mh] Termos MeSH primário: Diferenciação Celular/fisiologia
Neuroglia/fisiologia
Pele/fisiopatologia
Cicatrização/fisiologia
[Mh] Termos MeSH secundário: Animais
Ciclo Celular/genética
Ciclo Celular/fisiologia
Diferenciação Celular/genética
Células Cultivadas
Perfilação da Expressão Gênica
Seres Humanos
Camundongos da Linhagem 129
Camundongos Endogâmicos C57BL
Camundongos Endogâmicos DBA
Camundongos Knockout
Camundongos Transgênicos
Miofibroblastos/metabolismo
Miofibroblastos/fisiologia
Neuroglia/citologia
Neuroglia/metabolismo
Fatores de Transcrição SOXE/genética
Fatores de Transcrição SOXE/metabolismo
Transdução de Sinais/genética
Pele/lesões
Pele/inervação
Fator de Crescimento Transformador beta/genética
Fator de Crescimento Transformador beta/metabolismo
Cicatrização/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (SOXE Transcription Factors); 0 (Sox10 protein, mouse); 0 (Transforming Growth Factor beta)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-01488-2


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[PMID]:28464864
[Au] Autor:Shimazu K; Tada Y; Morinaga T; Shingyoji M; Sekine I; Shimada H; Hiroshima K; Namiki T; Tatsumi K; Tagawa M
[Ad] Endereço:Department of Respirology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan.
[Ti] Título:Metformin produces growth inhibitory effects in combination with nutlin-3a on malignant mesothelioma through a cross-talk between mTOR and p53 pathways.
[So] Source:BMC Cancer;17(1):309, 2017 May 02.
[Is] ISSN:1471-2407
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Mesothelioma is resistant to conventional treatments and is often defective in p53 pathways. We then examined anti-tumor effects of metformin, an agent for type 2 diabetes, and combinatory effects of metformin and nutlin-3a, an inhibitor for ubiquitin-mediated p53 degradation, on human mesothelioma. METHODS: We examined the effects with a colorimetric assay and cell cycle analyses, and investigated molecular events in cells treated with metformin and/or nutlin-3a with Western blot analyses. An involvement of p53 was tested with siRNA for p53. RESULTS: Metformin suppressed cell growth of 9 kinds of mesothelioma including immortalized cells of mesothelium origin irrespective of the p53 functional status, whereas susceptibility to nutlin-3a was partly dependent on the p53 genotype. We investigated combinatory effects of metformin and nutlin-3a on, nutlin-3a sensitive MSTO-211H and NCI-H28 cells and insensitive EHMES-10 cells, all of which had the wild-type p53 gene. Knockdown of p53 expression with the siRNA demonstrated that susceptibility of MSTO-211H and NCI-H28 cells to nutlin-3a was p53-dependent, whereas that of EHMES-10 cells was not. Nevertheless, all the cells treated with both agents produced additive or synergistic growth inhibitory effects. Cell cycle analyses also showed that the combination increased sub-G1 fractions greater than metformin or nutlin-3a alone in MSTO-211H and EHMES-10 cells. Western blot analyses showed that metformin inhibited downstream pathways of the mammalian target of rapamycin (mTOR) but did not activate the p53 pathways, whereas nutlin-3a phosphorylated p53 and suppressed mTOR pathways. Cleaved caspase-3 and conversion of LC3A/B were also detected but it was dependent on cells and treatments. The combination of both agents in MSTO-211H cells rather suppressed the p53 pathways that were activated by nutrin-3a treatments, whereas the combination rather augmented the p53 actions in NCI-H28 and EHMES-10 cells. CONCLUSION: These data collectively indicated a possible interactions between mTOR and p53 pathways, and the combinatory effects were attributable to differential mechanisms induced by a cross-talk between the pathways.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Imidazóis/farmacologia
Neoplasias Pulmonares/metabolismo
Mesotelioma/metabolismo
Metformina/farmacologia
Piperazinas/farmacologia
Serina-Treonina Quinases TOR/metabolismo
Proteína Supressora de Tumor p53/metabolismo
[Mh] Termos MeSH secundário: Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Seres Humanos
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Imidazoles); 0 (Piperazines); 0 (Tumor Suppressor Protein p53); 53IA0V845C (nutlin 3); 9100L32L2N (Metformin); EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s12885-017-3300-y



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