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Pesquisa : D12.644.276 [Categoria DeCS]
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  1 / 23225 MEDLINE  
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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


  2 / 23225 MEDLINE  
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[PMID]:28463680
[Au] Autor:Griger J; Schneider R; Lahmann I; Schöwel V; Keller C; Spuler S; Nazare M; Birchmeier C
[Ad] Endereço:Developmental Biology/Signal Transduction Group, Max Delbrück Center for Molecular Medicine (MDC) in the Helmholtz Society, Berlin, Germany.
[Ti] Título:Loss of Ptpn11 (Shp2) drives satellite cells into quiescence.
[So] Source:Elife;6, 2017 05 02.
[Is] ISSN:2050-084X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The equilibrium between proliferation and quiescence of myogenic progenitor and stem cells is tightly regulated to ensure appropriate skeletal muscle growth and repair. The non-receptor tyrosine phosphatase Ptpn11 (Shp2) is an important transducer of growth factor and cytokine signals. Here we combined complex genetic analyses, biochemical studies and pharmacological interference to demonstrate a central role of Ptpn11 in postnatal myogenesis of mice. Loss of Ptpn11 drove muscle stem cells out of the proliferative and into a resting state during muscle growth. This Ptpn11 function was observed in postnatal but not fetal myogenic stem cells. Furthermore, muscle repair was severely perturbed when Ptpn11 was ablated in stem cells due to a deficit in stem cell proliferation and survival. Our data demonstrate a molecular difference in the control of cell cycle withdrawal in fetal and postnatal myogenic stem cells, and assign to Ptpn11 signaling a key function in satellite cell activity.
[Mh] Termos MeSH primário: Proteína Tirosina Fosfatase não Receptora Tipo 11/metabolismo
Células Satélites de Músculo Esquelético/citologia
Células Satélites de Músculo Esquelético/metabolismo
[Mh] Termos MeSH secundário: Animais
Citocinas/metabolismo
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Camundongos Endogâmicos C57BL
Proteína Tirosina Fosfatase não Receptora Tipo 11/genética
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); 0 (Intercellular Signaling Peptides and Proteins); EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 11); EC 3.1.3.48 (Ptpn11 protein, mouse)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


  3 / 23225 MEDLINE  
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[PMID]:28460641
[Au] Autor:Bernardi M; Agostini F; Chieregato K; Amati E; Durante C; Rassu M; Ruggeri M; Sella S; Lombardi E; Mazzucato M; Astori G
[Ad] Endereço:Advanced Cellular Therapy Laboratory, Hematology Unit, Vicenza Hospital, Vicenza, Italy.
[Ti] Título:The production method affects the efficacy of platelet derivatives to expand mesenchymal stromal cells in vitro.
[So] Source:J Transl Med;15(1):90, 2017 May 01.
[Is] ISSN:1479-5876
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The use of fetal bovine serum (FBS) as a media supplement for the ex vivo expansion of bone-marrow derived mesenchymal stromal cells (BM-MSC) has been discouraged by regulatory agencies, due to the risk of transmitting zoonoses and to elicit immune reactions in the host once transplanted. Platelet derivatives are valid FBS substitutes due to their content of growth factors that can be released disrupting the platelets by physical methods or physiological stimuli. We compared platelet derivatives produced by freezing/thawing (platelet lysates, PL) or after CaCl activation (platelet releasate surnatant rich in growth factors, PR-SRGF) for their content in growth factors and their ability to support the ex vivo expansion of BM-MSC. METHODS: The cytokine content in the two platelet derivatives was evaluated. BM-MSC were expanded in complete medium containing 10, 7.5 and 5% PL or PR-SRGF and the cell phenotype, clonogenic capacity, immunomodulation properties and tri-lineage differentiation potential of the expanded cells in both media were investigated. RESULTS: The concentration of PDGF-AB, PDGF-AA, PDGF-BB in PR-SRGF resulted to be respectively 5.7×, 1.7× and 2.3× higher compared to PL. PR-SRGF promoted a higher BM-MSC proliferation rate compared to PL not altering BM-MSC phenotype. Colony forming efficiency of BM-MSC expanded in PR-SRGF showed a frequency of colonies significantly higher than cells expanded in PL. BM-MSC expanded in PL or PR-SRGF maintained their immunomodulatory properties against activated lymphocytes even if BM-MSC expanded in FBS performed significantly better. CONCLUSIONS: The method used to release platelet factors significantly affects the enrichment in growth factors and overall product performance. The standardization of the production process of platelet derivatives and the definition of their release criteria requires further investigation.
[Mh] Termos MeSH primário: Plaquetas/metabolismo
Técnicas de Cultura de Células/métodos
Células Mesenquimais Estromais/citologia
[Mh] Termos MeSH secundário: Diferenciação Celular
Linhagem da Célula
Proliferação Celular
Ensaio de Unidades Formadoras de Colônias
Seres Humanos
Imunomodulação
Imunofenotipagem
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Intercellular Signaling Peptides and Proteins)
[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:170503
[St] Status:MEDLINE
[do] DOI:10.1186/s12967-017-1185-9


  4 / 23225 MEDLINE  
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[PMID]:27778404
[Au] Autor:Menzel L; Kleber L; Friedrich C; Hummel R; Dangel L; Winter J; Schmitz K; Tegeder I; Schäfer MK
[Ad] Endereço:Department of Anesthesiology, University Medical Center, Johannes Gutenberg-University, Mainz, Germany.
[Ti] Título:Progranulin protects against exaggerated axonal injury and astrogliosis following traumatic brain injury.
[So] Source:Glia;65(2):278-292, 2017 02.
[Is] ISSN:1098-1136
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In response to traumatic brain injury (TBI) microglia/macrophages and astrocytes release inflammatory mediators with dual effects on secondary brain damage progression. The neurotrophic and anti-inflammatory glycoprotein progranulin (PGRN) attenuates neuronal damage and microglia/macrophage activation in brain injury but mechanisms are still elusive. Here, we studied histopathology, neurology and gene expression of inflammatory markers in PGRN-deficient mice (Grn ) 24 h and 5 days after experimental TBI. Grn mice displayed increased perilesional axonal injury even though the overall brain tissue loss and neurological consequences were similar to wild-type mice. Brain inflammation was elevated in Grn mice as reflected by increased transcription of pro-inflammatory cytokines TNFα, IL-1ß, IL-6, and decreased transcription of the anti-inflammatory cytokine IL-10. However, numbers of Iba1 microglia/macrophages and immigrated CD45 leukocytes were similar at perilesional sites while determination of IgG extravasation suggested stronger impairment of blood brain barrier integrity in Grn compared to wild-type mice. Most strikingly, Grn mice displayed exaggerated astrogliosis 5 days after TBI as demonstrated by anti-GFAP immunohistochemistry and immunoblot. GFAP astrocytes at perilesional sites were immunolabelled for iNOS and TNFα suggesting that pro-inflammatory activation of astrocytes was attenuated by PGRN. Accordingly, recombinant PGRN (rPGRN) attenuated LPS- and cytokine-evoked iNOS and TNFα mRNA expression in cultured astrocytes. Moreover, intracerebroventricular administration of rPGRN immediately before trauma reduced brain damage and neurological deficits, and restored normal levels of cytokine transcription, axonal injury and astrogliosis 5 days after TBI in Grn mice. Our results show that endogenous and recombinant PGRN limit axonal injury and astrogliosis and suggest therapeutic potential of PGRN in TBI. GLIA 2017;65:278-292.
[Mh] Termos MeSH primário: Axônios/patologia
Lesões Encefálicas Traumáticas/complicações
Lesões Encefálicas Traumáticas/patologia
Gliose/etiologia
Gliose/prevenção & controle
Peptídeos e Proteínas de Sinalização Intercelular/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Astrócitos/efeitos dos fármacos
Astrócitos/patologia
Axônios/metabolismo
Barreira Hematoencefálica/patologia
Proteínas de Ligação ao Cálcio/metabolismo
Células Cultivadas
Citocinas/genética
Citocinas/metabolismo
Modelos Animais de Doenças
Expressão Gênica/efeitos dos fármacos
Expressão Gênica/genética
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/genética
Gliose/patologia
Peptídeos e Proteínas de Sinalização Intercelular/genética
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Lipopolissacarídeos/farmacologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Proteínas dos Microfilamentos/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Doenças do Sistema Nervoso/etiologia
Doenças do Sistema Nervoso/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aif1 protein, mouse); 0 (Calcium-Binding Proteins); 0 (Cytokines); 0 (Grn protein, mouse); 0 (Intercellular Signaling Peptides and Proteins); 0 (Lipopolysaccharides); 0 (Microfilament Proteins); 0 (Nerve Tissue Proteins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1002/glia.23091


  5 / 23225 MEDLINE  
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[PMID]:28460335
[Au] Autor:Feng Y; Li Q; Wu D; Niu Y; Yang C; Dong L; Wang C
[Ad] Endereço:State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macau SAR, China.
[Ti] Título:A macrophage-activating, injectable hydrogel to sequester endogenous growth factors for in situ angiogenesis.
[So] Source:Biomaterials;134:128-142, 2017 Jul.
[Is] ISSN:1878-5905
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Biomaterials scaffolds designed for many regenerative applications are expected to support neo-vascularisation, which is now being hampered by two limitations - the instability of exogenous growth factors (GFs) that are delivered to promote angiogenesis; and the loss of extracellular matrix components that bind and stabilise GFs. Here, we report the design and evaluation of an injectable hydrogel system aimed at restoring a GF-binding microenvironment to enhance the pro-angiogenic functions of endogenous GFs. This gel comprises two polysaccharides with their unique bioactivities: Konjac glucomannan (KGM) as the building block of the gel scaffold, for its demonstrated capacity to activate macrophages/monocytes to secrete pro-angiogenic/-mitogenic GFs; and heparin (Hep), a representative glycosaminoglycan molecule that binds numerous pro-angiogenic GFs, as functional moieties to sequester the macrophage-produced GFs. Modified with tyramine (TA) groups, the two polysaccharides can be co-polymerised and rapidly form into hydrogel upon enzyme catalysis. The designed KGM-TA/Hep-TA hydrogel successfully preserves the macrophage-activating function and GF-binding affinity of the two components, respectively, and, once subcutaneously implanted, effectively sequestered the locally-produced GFs in situ and promote the formation and maturation of blood vessels in mice. In summary, the designed hydrogel system demonstrates a feasible approach to stimulate the production and harness the function of endogenous GFs for inducing blood vessel formation in vivo, without the addition of any exogenous proteins. This design may provide an innovative, open platform to promote vascularisation for various regenerative purposes.
[Mh] Termos MeSH primário: Materiais Biocompatíveis/química
Materiais Biocompatíveis/farmacologia
Hidrogel de Polietilenoglicol-Dimetacrilato/química
Hidrogel de Polietilenoglicol-Dimetacrilato/farmacologia
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Macrófagos/metabolismo
[Mh] Termos MeSH secundário: Indutores da Angiogênese/química
Indutores da Angiogênese/farmacologia
Animais
Glicosaminoglicanos/metabolismo
Seres Humanos
Integrina beta1/metabolismo
Lectinas Tipo C/metabolismo
Masculino
Mananas/metabolismo
Lectinas de Ligação a Manose/metabolismo
Camundongos
Neovascularização Fisiológica/efeitos dos fármacos
Polissacarídeos/metabolismo
Células RAW 264.7
Receptores de Superfície Celular/metabolismo
Células THP-1
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inducing Agents); 0 (Biocompatible Materials); 0 (Glycosaminoglycans); 0 (Integrin beta1); 0 (Intercellular Signaling Peptides and Proteins); 0 (Lectins, C-Type); 0 (Mannans); 0 (Mannose-Binding Lectins); 0 (Polysaccharides); 0 (Receptors, Cell Surface); 0 (mannose receptor); 25852-47-5 (Hydrogel, Polyethylene Glycol Dimethacrylate); 36W3E5TAMG ((1-6)-alpha-glucomannan)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


  6 / 23225 MEDLINE  
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[PMID]:29337067
[Au] Autor:Yassa ME; Mansour IA; Sewelam NI; Hamza H; Gaafar T
[Ad] Endereço:Department of Clinical and Chemical Pathology, Kasr Al-Ainy School of Medicine, Cairo University, Kasr Al-Ainy St., 11562, Cairo, Egypt. Electronic address: marianne.yassa@kasralainy.edu.eg.
[Ti] Título:The impact of growth factors on human induced pluripotent stem cells differentiation into cardiomyocytes.
[So] Source:Life Sci;196:38-47, 2018 Mar 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Human induced pluripotent stem cells (hiPSCs) act as a promising therapeutic alternative for cardiovascular diseases. They yield a large number of functional cardiomyocytes (CMs) from autologous cell sources without ethical or immunological problems. However, significant limitations still remain in terms of line-to-line variability in CM yield and reproducibility. AIM: To efficiently enhance NP0040 hiPSCs differentiation into CMs. MAIN METHODS: Following a standard cardiac differentiation protocol using small molecules targeting the canonical Wnt signaling, growth factors (BMP4 and FGF2) and ascorbic acid were added further in order to increase the cardiac differentiation efficiency. All cultures were conducted in serum-free, feeder-free monolayer system followed by lactate purification. KEY FINDINGS: Using NP0040 hiPSCs, the CM yield resulting from modulation of the Wnt signaling pathway alone was inefficient compared to previous studies while the addition of BMP4, FGF2 and ascorbic acid resulted in enhanced cardiac differentiation outcome. The later resulted in a high yield (up to 92%) of cardiac troponin-T (cTnT) + CMs contracting spontaneously as organized sheets in 15 independent experiments. They were validated structurally and functionally using immunofluorescent staining for sarcomeric α-actinin, cTnT, MLC2v and Connexin 43. Reverse-transcriptase PCR revealed cardiac transcription factors and cardiac-specific genes expression. CMs were electrically connected to one another. Recorded action potential (AP) showed waves of relatively mature ventricular-like phenotype. SIGNIFICANCE: We demonstrated that hiPSC lines respond differently to a standard cardiac differentiation protocol and that a well-orchestrated interplay between Wnt, BMP4, FGF/MEK and Ascorbic acid MEK/ERK1/2 signaling pathways is beneficial in enhancing the differentiation outcome.
[Mh] Termos MeSH primário: Células-Tronco Pluripotentes Induzidas/efeitos dos fármacos
Peptídeos e Proteínas de Sinalização Intercelular/farmacologia
Miócitos Cardíacos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Ácido Ascórbico/farmacologia
Proteína Morfogenética Óssea 4/metabolismo
Diferenciação Celular/efeitos dos fármacos
Espaço Extracelular/efeitos dos fármacos
Expressão Gênica/efeitos dos fármacos
Glucose/deficiência
Seres Humanos
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Contração Miocárdica
Miócitos Cardíacos/metabolismo
Troponina T/metabolismo
Vitaminas/farmacologia
Via de Sinalização Wnt/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bone Morphogenetic Protein 4); 0 (Intercellular Signaling Peptides and Proteins); 0 (Troponin T); 0 (Vitamins); IY9XDZ35W2 (Glucose); PQ6CK8PD0R (Ascorbic Acid)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE


  7 / 23225 MEDLINE  
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[PMID]:28453791
[Au] Autor:Beel S; Moisse M; Damme M; De Muynck L; Robberecht W; Van Den Bosch L; Saftig P; Van Damme P
[Ad] Endereço:Department of Neurosciences, Experimental Neurology and Leuven Institute for Neuroscience and Disease (LIND), KU Leuven - University of Leuven, B-3000 Leuven, Belgium.
[Ti] Título:Progranulin functions as a cathepsin D chaperone to stimulate axonal outgrowth in vivo.
[So] Source:Hum Mol Genet;26(15):2850-2863, 2017 08 01.
[Is] ISSN:1460-2083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Loss of function mutations in progranulin (GRN) cause frontotemporal dementia, but how GRN haploinsufficiency causes neuronal dysfunction remains unclear. We previously showed that GRN is neurotrophic in vitro. Here, we used an in vivo axonal outgrowth system and observed a delayed recovery in GRN-/- mice after facial nerve injury. This deficit was rescued by reintroduction of human GRN and relied on its C-terminus and on neuronal GRN production. Transcriptome analysis of the facial motor nucleus post injury identified cathepsin D (CTSD) as the most upregulated gene. In aged GRN-/- cortices, CTSD was also upregulated, but the relative CTSD activity was reduced and improved upon exogenous GRN addition. Moreover, GRN and its C-terminal granulin domain granulinE (GrnE) both stimulated the proteolytic activity of CTSD in vitro. Pull-down experiments confirmed a direct interaction between GRN and CTSD. This interaction was also observed with GrnE and stabilized the CTSD enzyme at different temperatures. Investigating the importance of this interaction for axonal regeneration in vivo we found that, although individually tolerated, a combined reduction of GRN and CTSD synergistically reduced axonal outgrowth. Our data links the neurotrophic effect of GRN and GrnE with a lysosomal chaperone function on CTSD to maintain its proteolytic capacity.
[Mh] Termos MeSH primário: Catepsina D/metabolismo
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
[Mh] Termos MeSH secundário: Animais
Catepsina D/genética
Nervo Facial/metabolismo
Demência Frontotemporal/genética
Haploinsuficiência
Seres Humanos
Peptídeos e Proteínas de Sinalização Intercelular/genética
Camundongos
Camundongos Transgênicos
Chaperonas Moleculares/genética
Mutação
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (GRN protein, human); 0 (Grn protein, mouse); 0 (Intercellular Signaling Peptides and Proteins); 0 (Molecular Chaperones); 134710-81-9 (granulin precursor protein); EC 3.4.23.5 (Cathepsin D)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180225
[Lr] Data última revisão:
180225
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/hmg/ddx162


  8 / 23225 MEDLINE  
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[PMID]:28449711
[Au] Autor:Blázquez-Prunera A; Díez JM; Gajardo R; Grancha S
[Ad] Endereço:Research and Development, Bioscience Industrial Group, Grifols, Parets del Vallès, Barcelona, Spain.
[Ti] Título:Human mesenchymal stem cells maintain their phenotype, multipotentiality, and genetic stability when cultured using a defined xeno-free human plasma fraction.
[So] Source:Stem Cell Res Ther;8(1):103, 2017 Apr 27.
[Is] ISSN:1757-6512
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Mesenchymal stem cells (MSCs) show promising characteristics for their use in advanced therapy medicinal products. However, there are some unresolved concerns, such as the use of animal components for their expansion. In this study we assessed the suitability of a xeno-free supplement for cell culture (SCC) derived from human plasma, to culture and expand human MSCs (hMSCs) from different origins. Characteristics of viable cultured hMSCs such as genetic stability, phenotype and multipotentiality were qualitatively evaluated. METHODS: hMSCs from adipose tissue (AT), bone marrow (BM) and umbilical cord (UC) and supplier sources (commercial/non-commercial) were used. After hMSCs expansion in a xeno-free medium, classical hMSCs markers were studied by immunocytochemistry, and genetic stability was tested by classic karyotyping. The capacity of hMSCs to differentiate into adipogenic, osteogenic, and chondrogenic cells in differentiation media was assessed using different staining. Different lots of SCC were used to assure consistency between batches. RESULTS: All hMSCs tested maintained their morphology and adherence to plastic during their expansion, and preserved their genetic stability, phenotype and differentiation potential. No differences were observed when using different lots of SCC. Moreover, the proliferation rate, evaluated as population doubling time (PDT) of commercial BM and AT hMSCs, was higher in the xeno-free medium than in the control media provided by the suppliers of the cells (PDT of 4.6 for BM-hMSC and 6.4 for AT-hMSC in xeno-free medium, and 7.0 and 14.7 respectively in the commercial media). UC-hMSCs PDT was similar in all the media tested. When using non-commercial BM-hMSCs, PDT was lower in the xeno-free medium, but reverted to the control level with the addition of growth factors. CONCLUSIONS: SCC-containing medium can be a feasible xeno-free alternative to expand hMSCs for advanced therapies.
[Mh] Termos MeSH primário: Meios de Cultura/farmacologia
Células Mesenquimais Estromais/efeitos dos fármacos
Cultura Primária de Células/métodos
[Mh] Termos MeSH secundário: Diferenciação Celular
Células Cultivadas
Meios de Cultura/química
Instabilidade Genômica
Seres Humanos
Peptídeos e Proteínas de Sinalização Intercelular/farmacologia
Cariótipo
Células Mesenquimais Estromais/citologia
Células Mesenquimais Estromais/metabolismo
Fenótipo
Plasma/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Culture Media); 0 (Intercellular Signaling Peptides and Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1186/s13287-017-0552-z


  9 / 23225 MEDLINE  
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[PMID]:28468864
[Au] Autor:Kalyan A; Carneiro BA; Chandra S; Kaplan J; Chae YK; Matsangou M; Hendrix MJC; Giles F
[Ad] Endereço:Developmental Therapeutics Program, Division of Hematology and Oncology, Northwestern University Feinberg School of Medicine, Olson Pavilion, Chicago, Illinois. aparna.kalyan@northwestern.edu.
[Ti] Título:Nodal Signaling as a Developmental Therapeutics Target in Oncology.
[So] Source:Mol Cancer Ther;16(5):787-792, 2017 May.
[Is] ISSN:1538-8514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The tumor microenvironment is a vital feature of oncogenesis and tumor progression. There are several parallels between cancer cells and early developmental stem cells, including their plasticity and signaling mechanisms. In early fetal development, Nodal is expressed for endodermal and mesodermal differentiation. This expression has been shown reemerge in the setting of epithelial cancers, such as breast and melanoma. High Nodal expression correlates to an aggressive tumor grade in these malignancies. Nodal signal begins with its interaction with its coreceptor, Cripto-1, leading to activation of Smad2/Smad3 and ultimately downstream transcription and translation. Lefty is the natural inhibitor of Nodal and controls Nodal signaling during fetal development. However, cancer cells lack the presence of Lefty, thus leading to uncontrolled tumor growth. Given this understanding, inhibition of the Nodal pathway offers a new novel therapeutic target in oncology. .
[Mh] Termos MeSH primário: Carcinogênese/genética
Terapia de Alvo Molecular
Neoplasias/genética
Proteína Nodal/genética
[Mh] Termos MeSH secundário: Diferenciação Celular/genética
Proteínas Ligadas por GPI/genética
Seres Humanos
Peptídeos e Proteínas de Sinalização Intercelular/genética
Fatores de Determinação Direita-Esquerda/genética
Proteínas de Neoplasias/genética
Neoplasias/tratamento farmacológico
Transdução de Sinais
Proteína Smad2/genética
Proteína Smad3/genética
Microambiente Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (GPI-Linked Proteins); 0 (Intercellular Signaling Peptides and Proteins); 0 (Left-Right Determination Factors); 0 (NODAL protein, human); 0 (Neoplasm Proteins); 0 (Nodal Protein); 0 (SMAD2 protein, human); 0 (SMAD3 protein, human); 0 (Smad2 Protein); 0 (Smad3 Protein); 0 (TDGF1 protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1158/1535-7163.MCT-16-0215


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[PMID]:28464980
[Au] Autor:Moleirinho S; Hoxha S; Mandati V; Curtale G; Troutman S; Ehmer U; Kissil JL
[Ad] Endereço:Department of Molecular Medicine, The Scripps Research Institute, Jupiter, United States.
[Ti] Título:Regulation of localization and function of the transcriptional co-activator YAP by angiomotin.
[So] Source:Elife;6, 2017 05 03.
[Is] ISSN:2050-084X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The Hippo-YAP pathway is a central regulator of cell contact inhibition, proliferation and death. There are conflicting reports regarding the role of Angiomotin (Amot) in regulating this pathway. While some studies suggest a YAP-inhibitory function other studies indicate Amot is required for YAP activity. Here, we describe an Amot-dependent complex comprised of Amot, YAP and Merlin. The phosphorylation of Amot at Serine 176 shifts localization of this complex to the plasma membrane, where it associates with the tight-junction proteins Pals1/PATJ and E-cadherin. Conversely, hypophosphorylated Amot shifts localization of the complex to the nucleus, where it facilitates the association of YAP and TEAD, induces transcriptional activation of YAP target genes and promotes YAP-dependent cell proliferation. We propose that phosphorylation of Amot is a critical post-translational modification that suppresses YAP's ability to promote cell proliferation and tumorigenesis by altering the subcellular localization of an essential YAP co-factor.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Proteínas de Membrana/metabolismo
Neurofibromina 2/metabolismo
Fosfoproteínas/metabolismo
Multimerização Proteica
Processamento de Proteína Pós-Traducional
[Mh] Termos MeSH secundário: Membrana Celular/química
Núcleo Celular/química
Células HEK293
Células Hep G2
Seres Humanos
Fosforilação
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (AMOT protein, human); 0 (Adaptor Proteins, Signal Transducing); 0 (Intercellular Signaling Peptides and Proteins); 0 (Membrane Proteins); 0 (Neurofibromin 2); 0 (Phosphoproteins); 0 (YAP1 (Yes-associated) protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180211
[Lr] Data última revisão:
180211
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE



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