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Pesquisa : D12.644.276.954 [Categoria DeCS]
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[PMID]:27048518
[Au] Autor:Caronia-Brown G; Anderegg A; Awatramani R
[Ad] Endereço:Department of Neurology and Center for Genetic Medicine, Northwestern University Feinberg School of Medicine, 7-113 Lurie Bldg., 303 E. Superior Street, Chicago, IL, 60611, USA. giuliana.caronia-brown@northwestern.edu.
[Ti] Título:Expression and functional analysis of the Wnt/beta-catenin induced mir-135a-2 locus in embryonic forebrain development.
[So] Source:Neural Dev;11:9, 2016 Apr 05.
[Is] ISSN:1749-8104
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Brain size and patterning are dependent on dosage-sensitive morphogen signaling pathways - yet how these pathways are calibrated remains enigmatic. Recent studies point to a new role for microRNAs in tempering the spatio-temporal range of morphogen functions during development. Here, we investigated the role of miR-135a, derived from the mir-135a-2 locus, in embryonic forebrain development. METHOD: 1. We characterized the expression of miR-135a, and its host gene Rmst, by in situ hybridization (ish). 2. We conditionally ablated, or activated, beta-catenin in the dorsal forebrain to determine if this pathway was necessary and/or sufficient for Rmst/miR-135a expression. 3. We performed bioinformatics analysis to unveil the most predicted pathways targeted by miR-135a. 4. We performed gain and loss of function experiments on mir-135a-2 and analyzed by ish the expression of key markers of cortical hem, choroid plexus, neocortex and hippocampus. RESULTS: 1. miR-135a, embedded in the host long non-coding transcript Rmst, is robustly expressed, and functional, in the medial wall of the embryonic dorsal forebrain, a Wnt and TGFß/BMP-rich domain. 2. Canonical Wnt/beta-catenin signaling is critical for the expression of Rmst and miR-135a, and the cortical hem determinant Lmx1a. 3. Bioinformatics analyses reveal that the Wnt and TGFß/BMP cascades are among the top predicted pathways targeted by miR-135a. 4. Analysis of mir-135a-2 null embryos showed that dorsal forebrain development appeared normal. In contrast, modest mir-135a-2 overexpression, in the early dorsal forebrain, resulted in a phenotype resembling that of mutants with Wnt and TGFß/BMP deficits - a smaller cortical hem and hippocampus primordium associated with a shorter neocortex as well as a less convoluted choroid plexus. Interestingly, late overexpression of mir-135a-2 revealed no change. CONCLUSIONS: All together, our data suggests the existence of a Wnt/miR-135a auto-regulatory loop, which could serve to limit the extent, the duration and/or intensity of the Wnt and, possibly, the TGFß/BMP pathways.
[Mh] Termos MeSH primário: MicroRNAs/metabolismo
Prosencéfalo/embriologia
Prosencéfalo/metabolismo
Via de Sinalização Wnt
[Mh] Termos MeSH secundário: Animais
Proteínas com Homeodomínio LIM/metabolismo
Camundongos
Proteínas da Superfamília de TGF-beta/metabolismo
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (LIM-Homeodomain Proteins); 0 (Lmx1a protein, mouse); 0 (MicroRNAs); 0 (Mirn135 microRNA, mouse); 0 (TGF-beta Superfamily Proteins); 0 (Transcription Factors)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160407
[St] Status:MEDLINE
[do] DOI:10.1186/s13064-016-0065-y


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[PMID]:26683658
[Au] Autor:Myers JS; von Lersner AK; Robbins CJ; Sang QX
[Ad] Endereço:Department of Chemistry and Biochemistry, Florida State University, Tallahassee, Florida, United States of America.
[Ti] Título:Differentially Expressed Genes and Signature Pathways of Human Prostate Cancer.
[So] Source:PLoS One;10(12):e0145322, 2015.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Genomic technologies including microarrays and next-generation sequencing have enabled the generation of molecular signatures of prostate cancer. Lists of differentially expressed genes between malignant and non-malignant states are thought to be fertile sources of putative prostate cancer biomarkers. However such lists of differentially expressed genes can be highly variable for multiple reasons. As such, looking at differential expression in the context of gene sets and pathways has been more robust. Using next-generation genome sequencing data from The Cancer Genome Atlas, differential gene expression between age- and stage- matched human prostate tumors and non-malignant samples was assessed and used to craft a pathway signature of prostate cancer. Up- and down-regulated genes were assigned to pathways composed of curated groups of related genes from multiple databases. The significance of these pathways was then evaluated according to the number of differentially expressed genes found in the pathway and their position within the pathway using Gene Set Enrichment Analysis and Signaling Pathway Impact Analysis. The "transforming growth factor-beta signaling" and "Ran regulation of mitotic spindle formation" pathways were strongly associated with prostate cancer. Several other significant pathways confirm reported findings from microarray data that suggest actin cytoskeleton regulation, cell cycle, mitogen-activated protein kinase signaling, and calcium signaling are also altered in prostate cancer. Thus we have demonstrated feasibility of pathway analysis and identified an underexplored area (Ran) for investigation in prostate cancer pathogenesis.
[Mh] Termos MeSH primário: Neoplasias da Próstata/metabolismo
[Mh] Termos MeSH secundário: Idoso
Perfilação da Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Ontologia Genética
Seres Humanos
Masculino
Meia-Idade
Neoplasias da Próstata/genética
Transdução de Sinais
Proteínas da Superfamília de TGF-beta/genética
Proteínas da Superfamília de TGF-beta/metabolismo
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (TGF-beta Superfamily Proteins)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151220
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0145322


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[PMID]:26268413
[Au] Autor:Xu Q; Cai C; Hu X; Liu Y; Guo Y; Hu P; Chen Z; Peng S; Zhang D; Jiang S; Wu Z; Chan J; Chen L
[Ad] Endereço:Key Laboratory of Sustainable Exploitation of Oceanic Fisheries Resources, Ministry of Education, College of Marine Sciences, Shanghai Ocean University, Shanghai, 201306, China.
[Ti] Título:Evolutionary suppression of erythropoiesis via the modulation of TGF-ß signalling in an Antarctic icefish.
[So] Source:Mol Ecol;24(18):4664-78, 2015 Sep.
[Is] ISSN:1365-294X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The Antarctic icefish, a family (Channichthyidae) of teleosts within the perciform suborder Notothenioidei, are the only known vertebrates without oxygen-transporting haemoglobins and that are largely devoid of circulating erythrocytes. To elucidate the evo-devo mechanisms underpinning the suppressed erythropoiesis in the icefish, we conducted comparative studies on the transcriptomes and microRNAomes of the primary haematopoietic tissues between an icefish (Chionodraco hamatus) and two red-blooded notothenioids (Trematomus bernacchii and Gymnodraco acuticeps). We identified substantial remodelling of the haematopoietic programs in the icefish through which erythropoiesis is selectively suppressed. Experimental verification showed that erythropoietic suppression in the icefish may be attributable to the upregulation of TGF-ß signalling, which coincides with reductions in multiple transcription factors essential for erythropoiesis and the upregulation of hundreds of microRNAs, the majority (> 80%) of which potentially target erythropoiesis regulating factors. Of the six microRNAs selected for verification, three miRNAs (miR-152, miR-1388 and miR-16b) demonstrated suppressive functions on GATA1 and ALAS2, which are two factors important for erythroid differentiation, resulting in reduced numbers of erythroids in microinjected zebra fish embryos. Codon substitution analyses of the genes of the TGF-ß superfamily revealed signs of positive selection in TGF-ß1 and endoglin in the lineages leading to Antarctic notothenioids. Both genes are previously known to function in erythropoietic suppression. These findings implied a general trend of erythropoietic suppression in the cold-adapted notothenioid lineages through evolutionary modulation of the multi-functional TGF-ß signalling pathway. This trend is more pronounced in the haemoglobin-less icefish, which may pre-emptively hinder the otherwise defective erythroids from production.
[Mh] Termos MeSH primário: Evolução Biológica
Eritropoese
Perciformes/genética
Transdução de Sinais
Fator de Crescimento Transformador beta/genética
[Mh] Termos MeSH secundário: Animais
Regiões Antárticas
MicroRNAs/genética
Filogenia
Seleção Genética
Análise de Sequência de RNA
Proteínas da Superfamília de TGF-beta/genética
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (MicroRNAs); 0 (TGF-beta Superfamily Proteins); 0 (Transforming Growth Factor beta)
[Em] Mês de entrada:1512
[Cu] Atualização por classe:150916
[Lr] Data última revisão:
150916
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150814
[St] Status:MEDLINE
[do] DOI:10.1111/mec.13344


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[PMID]:26246170
[Au] Autor:Rosenberg AS; Puig M; Nagaraju K; Hoffman EP; Villalta SA; Rao VA; Wakefield LM; Woodcock J
[Ad] Endereço:Center for Drug Evaluation and Research, U.S. Food and Drug Administration, Building 71/2238, Silver Spring, MD 20993, USA. amy.rosenberg@fda.hhs.gov.
[Ti] Título:Immune-mediated pathology in Duchenne muscular dystrophy.
[So] Source:Sci Transl Med;7(299):299rv4, 2015 Aug 05.
[Is] ISSN:1946-6242
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Immunological and inflammatory processes downstream of dystrophin deficiency as well as metabolic abnormalities, defective autophagy, and loss of regenerative capacity all contribute to muscle pathology in Duchenne muscular dystrophy (DMD). These downstream cascades offer potential avenues for pharmacological intervention. Modulating the inflammatory response and inducing immunological tolerance to de novo dystrophin expression will be critical to the success of dystrophin-replacement therapies. This Review focuses on the role of the inflammatory response in DMD pathogenesis and opportunities for clinical intervention.
[Mh] Termos MeSH primário: Imunidade Inata
Distrofia Muscular de Duchenne
[Mh] Termos MeSH secundário: Citocinas/metabolismo
Distrofina/metabolismo
Fibrose
Seres Humanos
Inflamação
Distrofia Muscular de Duchenne/etiologia
Distrofia Muscular de Duchenne/imunologia
Distrofia Muscular de Duchenne/metabolismo
Distrofia Muscular de Duchenne/patologia
Transdução de Sinais
Proteínas da Superfamília de TGF-beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cytokines); 0 (Dystrophin); 0 (TGF-beta Superfamily Proteins)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:161025
[Lr] Data última revisão:
161025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150807
[St] Status:MEDLINE
[do] DOI:10.1126/scitranslmed.aaa7322


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[PMID]:25931269
[Au] Autor:Wang G; Li X; Tian W; Wang Y; Wu D; Sun Z; Zhao E
[Ad] Endereço:Department of Obstetrics and Gynecology, Tianjin Central Hospital of Obstetrics and Gynecology, Tianjin, 300100, China.
[Ti] Título:Promoter DNA methylation is associated with KLF11 expression in epithelial ovarian cancer.
[So] Source:Genes Chromosomes Cancer;54(7):453-62, 2015 Jul.
[Is] ISSN:1098-2264
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:As a transforming growth factor-ß (TGF-ß)-inducible gene, the expression of Krüppel-like transcription factor 11 (KLF11) is altered in several types of cancer. In the current study, through using human 9K CpG island array, KLF11 was identified as one of hypermethylated genes in RAS-transformed ovarian T29H cells. Methylation of the KLF11 promoter was also observed in ovarian cancer tissue samples accompanied by significantly reduced KLF11 gene expression. Interestingly, the expression of SMAD2, SMAD3, and SMAD7 genes was reduced in the tumour, whilst no change was found in TGF-ß expression. Our data suggest a relationship between promoter DNA methylation and KLF11 gene expression in ovarian cancer tumorigenesis.
[Mh] Termos MeSH primário: Proteínas de Ciclo Celular/metabolismo
Metilação de DNA
Neoplasias Epiteliais e Glandulares/metabolismo
Neoplasias Ovarianas/metabolismo
Regiões Promotoras Genéticas
Proteínas Repressoras/metabolismo
[Mh] Termos MeSH secundário: Idoso
Proteínas de Ciclo Celular/genética
Linhagem Celular Tumoral
China
Ilhas de CpG
Feminino
Estudos de Associação Genética
Seres Humanos
Meia-Idade
Neoplasias Epiteliais e Glandulares/genética
Neoplasias Ovarianas/genética
Proteínas Repressoras/genética
Proteínas Smad/metabolismo
Proteínas da Superfamília de TGF-beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (KLF11 protein, human); 0 (Repressor Proteins); 0 (Smad Proteins); 0 (TGF-beta Superfamily Proteins)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:150520
[Lr] Data última revisão:
150520
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150502
[St] Status:MEDLINE
[do] DOI:10.1002/gcc.22257


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[PMID]:25681638
[Au] Autor:Hofmann M; Halper B; Oesen S; Franzke B; Stuparits P; Tschan H; Bachl N; Strasser EM; Quittan M; Ploder M; Wagner KH; Wessner B
[Ad] Endereço:Centre for Sport Science and University Sports, University of Vienna, Auf der Schmelz 6, 1150 Vienna, Austria; Research Platform Active Ageing, University of Vienna, Althanstraße 14, 1090 Vienna, Austria.
[Ti] Título:Serum concentrations of insulin-like growth factor-1, members of the TGF-beta superfamily and follistatin do not reflect different stages of dynapenia and sarcopenia in elderly women.
[So] Source:Exp Gerontol;64:35-45, 2015 Apr.
[Is] ISSN:1873-6815
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:There is a high need for blood-based biomarkers detecting age-related changes in muscular performance at an early stage. Therefore, we investigated whether serum levels of growth and differentiation factor-15 (GDF-15), activin A, myostatin, follistatin, and insulin-like growth factor-1 (IGF-1) would reflect age- and physical performance-related differences between young (22-28 years) and elderly (65-92 years) females. Isokinetic peak torque of knee extension (PTE) was measured in young females to obtain reference values for the discrimination of different stages of age-associated muscle weakness. Additionally, elderly women were screened for sarcopenia using the algorithm of the European Working Group on Sarcopenia in Older People (low muscle mass in addition to low PTE and/or low walking speed). IGF-1 levels were higher and GDF-15 levels were lower in young females in comparison to the elderly (p < 0.01), whereas members of the activin A/myostatin/follistatin axis showed similar levels across age groups. In older women, IGF-1 correlated negatively with age (ρ = -0.359, p < 0.01) and positively with muscle mass (ρ = 0.365, p < 0.01). In contrast, GDF-15 correlated positively with age (ρ = 0.388, p < 0.001) and negatively with muscle mass (ρ = -0.320, p < 0.01). However, none of the serum markers differed between women classified as non-, mildly and severely dynapenic/sarcopenic. Multiple linear regression analyses revealed that a combination of all blood-based biomarkers obtained in addition to age and fat mass moderately predicted muscle mass (+2.9%). Neither a single nor a combined set of tested biomarkers reflected the presence of dynapenia or sarcopenia in elderly women. However, due to the associations of IGF-1 and GDF-15 with correlates of muscle mass and function, these parameters remain promising candidates in a potential set of blood-based biomarkers to diagnose sarcopenia and/or dynapenia.
[Mh] Termos MeSH primário: Folistatina/sangue
Fator de Crescimento Insulin-Like I/análise
Atrofia Muscular/diagnóstico
Sarcopenia/diagnóstico
Proteínas da Superfamília de TGF-beta/sangue
[Mh] Termos MeSH secundário: Ativinas/sangue
Adulto
Fatores Etários
Idoso
Idoso de 80 Anos ou mais
Áustria
Biomarcadores/sangue
Composição Corporal
Comorbidade
Feminino
Fator 15 de Diferenciação de Crescimento/sangue
Seres Humanos
Atrofia Muscular/sangue
Miostatina/sangue
Exame Físico
Análise de Regressão
Sarcopenia/sangue
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Follistatin); 0 (GDF15 protein, human); 0 (Growth Differentiation Factor 15); 0 (MSTN protein, human); 0 (Myostatin); 0 (TGF-beta Superfamily Proteins); 0 (activin A); 104625-48-1 (Activins); 67763-96-6 (Insulin-Like Growth Factor I)
[Em] Mês de entrada:1511
[Cu] Atualização por classe:150312
[Lr] Data última revisão:
150312
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150215
[St] Status:MEDLINE


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[PMID]:25345602
[Au] Autor:Ehanire T; Ren L; Bond J; Medina M; Li G; Bashirov L; Chen L; Kokosis G; Ibrahim M; Selim A; Blobe GC; Levinson H
[Ad] Endereço:Duke University School of Medicine, Duke University Medical Center (DUMC), Durham, NC, USA.
[Ti] Título:Angiotensin II stimulates canonical TGF-ß signaling pathway through angiotensin type 1 receptor to induce granulation tissue contraction.
[So] Source:J Mol Med (Berl);93(3):289-302, 2015 Mar.
[Is] ISSN:1432-1440
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: Hypertrophic scar contraction (HSc) is caused by granulation tissue contraction propagated by myofibroblast and fibroblast migration and contractility. Identifying the stimulants that promote migration and contractility is key to mitigating HSc. Angiotensin II (AngII) promotes migration and contractility of heart, liver, and lung fibroblasts; thus, we investigated the mechanisms of AngII in HSc. Human scar and unwounded dermis were immunostained for AngII receptors angiotensin type 1 receptor (AT1 receptor) and angiotensin type 2 receptor (AT2 receptor) and analyzed for AT1 receptor expression using Western blot. In vitro assays of fibroblast contraction and migration under AngII stimulation were conducted with AT1 receptor, AT2 receptor, p38, Jun N-terminal kinase (JNK), MEK, and activin receptor-like kinase 5 (ALK5) antagonism. Excisional wounds were created on AT1 receptor KO and wild-type (WT) mice treated with AngII ± losartan and ALK5 and JNK inhibitors SB-431542 and SP-600125, respectively. Granulation tissue contraction was quantified, and wounds were analyzed by immunohistochemistry. AT1 receptor expression was increased in scar, but not unwounded tissue. AngII induced fibroblast contraction and migration through AT1 receptor. Cell migration was inhibited by ALK5 and JNK, but not p38 or MEK blockade. In vivo experiments determined that absence of AT1 receptor and chemical AT1 receptor antagonism diminished granulation tissue contraction while AngII stimulated wound contraction. AngII granulation tissue contraction was diminished by ALK5 inhibition, but not JNK. AngII promotes granulation tissue contraction through AT1 receptor and downstream canonical transforming growth factor (TGF)-ß signaling pathway, ALK5. Further understanding the pathogenesis of HSc as an integrated signaling mechanism could improve our approach to establishing effective therapeutic interventions. KEY MESSAGE: AT1 receptor expression is increased in scar tissue compared to unwounded tissue. AngII stimulates expression of proteins that confer cell migration and contraction. AngII stimulates fibroblast migration and contraction through AT1 receptor, ALK5, and JNK. AngII-stimulated in vivo granulation tissue contraction is AT1 receptor and ALK5 dependent.
[Mh] Termos MeSH primário: Angiotensina II/fisiologia
Cicatriz Hipertrófica/metabolismo
Receptor Tipo 1 de Angiotensina/fisiologia
[Mh] Termos MeSH secundário: Células 3T3
Adulto
Animais
Movimento Celular
Colágeno/metabolismo
Epiderme/metabolismo
Epiderme/patologia
Epiderme/fisiopatologia
Feminino
Seres Humanos
Macrófagos/fisiologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Meia-Idade
Proteínas Serina-Treonina Quinases/metabolismo
Receptor Tipo 2 de Angiotensina/metabolismo
Receptores de Fatores de Crescimento Transformadores beta/metabolismo
Transdução de Sinais
Proteínas da Superfamília de TGF-beta/fisiologia
Cicatrização
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Receptor, Angiotensin, Type 1); 0 (Receptor, Angiotensin, Type 2); 0 (Receptors, Transforming Growth Factor beta); 0 (TGF-beta Superfamily Proteins); 11128-99-7 (Angiotensin II); 9007-34-5 (Collagen); EC 2.7.1.11 (TGF-beta type I receptor); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141028
[St] Status:MEDLINE
[do] DOI:10.1007/s00109-014-1211-9


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[PMID]:25868269
[Au] Autor:Yang W; Liu C
[Ti] Título:[Growth factors-mediated effects on the differentiation of human adipose-derived stem cells into chondrocytes].
[So] Source:Sheng Wu Yi Xue Gong Cheng Xue Za Zhi;31(6):1409-13, 2014 Dec.
[Is] ISSN:1001-5515
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:In recent years, there has been a growing emphasis on use of human adipose-derived stem cells (hADSCs) for cartilage tissue engineering owing to their ability to differentiate into chondrocytes, which is mainly induced by growth factors (GFs). In general, GFs for chondrogenic induction come from the transforming growth factor beta (TGF-beta) superfamily. To date, the most commonly used GFs for chondrogenes is TGF-beta1/3. However, the response of hADSCs to GFs may differ significantly from that of human bone marrow stem cells (hBMSCs). It has been reported that bone morphogenetic protein-6 (BMP-6) treatment induced TGF-beta receptor-I expression of hADSCs. It seems that these two cell populations varied strongly in their potency to undergo chondrogenesis in the same medium conditions. Here, we provide a concise review on various GFs used in chondrogenic differentiation of hADSCs in vitro.
[Mh] Termos MeSH primário: Adipócitos/citologia
Diferenciação Celular
Condrócitos/citologia
Condrogênese
Células-Tronco/citologia
[Mh] Termos MeSH secundário: Cartilagem
Seres Humanos
Proteínas da Superfamília de TGF-beta
Engenharia Tecidual
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (TGF-beta Superfamily Proteins)
[Em] Mês de entrada:1507
[Cu] Atualização por classe:150414
[Lr] Data última revisão:
150414
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150415
[St] Status:MEDLINE


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[PMID]:25390002
[Au] Autor:Martín-Fernández B; Valero Muñoz M; de las Heras N; Ballesteros S; Lahera V
[Ti] Título:Relevance of SGK1 in structural, functional and molecular alterations produced by aldosterone in heart.
[So] Source:Horm Mol Biol Clin Investig;18(2):53-61, 2014 May.
[Is] ISSN:1868-1891
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Aldosterone regulates sodium (Na+) and potassium (K+) transports in epithelial cells. Besides, aldosterone participates in cardiac alterations associated with hypertension, heart failure, diabetes, and other pathological alterations. One of the main cardiac alterations induced by aldosterone is cardiac hypertrophy in which different mechanisms are involved such as increased cardiomyocyte, calcium concentration, oxidative stress, and inflammatory and fibrotic mediators stimulation. Many epidemiological studies have demonstrated that left ventricular hypertrophy is associated with significantly increased risk of heart failure and malignant arrhythmias. SGK1 is a member of the serine/threonine kinase gene family that plays an important role in the absorption of Na+ and water through the Na+ channel in the apical membrane of tubular epithelial cells. SGK1 has been related to fibrotic mediator increase such as connective tissue growth factor (CTGF) and transforming growth factor-ß (TGF-ß) as well as inflammatory [tumor necrosis factor-α (TNF-α) and interleukin (IL)-1ß] and oxidative (NADPH oxidase) species. It has been shown that aldosterone induces SGK1 gene expression not only in kidneys but also in the heart. Supporting the central role of SGK1 in cardiac alterations induced by aldosterone, treatment with the mineralocorticoid antagonist spironolactone is able to reduce the gene expression of SGK1 in aldosterone-treated rats. Taken together, data suggest the involvement of SGK1 in a complex intracellular signaling, involving fibrotic, inflammatory, and oxidative pathways, which lead to cardiac hypertrophy and fibrosis induced by aldosterone.
[Mh] Termos MeSH primário: Aldosterona/metabolismo
Proteínas Imediatamente Precoces/metabolismo
Miocárdio/metabolismo
Proteínas Serina-Treonina Quinases/metabolismo
[Mh] Termos MeSH secundário: Animais
Cardiomegalia/metabolismo
Cardiomegalia/patologia
Fator de Crescimento do Tecido Conjuntivo/metabolismo
Endotélio Vascular/metabolismo
Fibrose
Expressão Gênica
Seres Humanos
Inflamação/metabolismo
Inflamação/patologia
Miocárdio/patologia
NADPH Oxidases/metabolismo
Estresse Oxidativo
Transdução de Sinais
Proteínas da Superfamília de TGF-beta/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (CTGF protein, human); 0 (Immediate-Early Proteins); 0 (TGF-beta Superfamily Proteins); 0 (TNF protein, human); 0 (Tumor Necrosis Factor-alpha); 139568-91-5 (Connective Tissue Growth Factor); 4964P6T9RB (Aldosterone); EC 1.6.3.- (NADPH Oxidases); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (serum-glucocorticoid regulated kinase)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141113
[St] Status:MEDLINE


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[PMID]:25153355
[Au] Autor:Klauzinska M; Castro NP; Rangel MC; Spike BT; Gray PC; Bertolette D; Cuttitta F; Salomon D
[Ad] Endereço:Mouse Cancer Genetics Program, Center for Cancer Research, Frederick, MD 21702, USA.
[Ti] Título:The multifaceted role of the embryonic gene Cripto-1 in cancer, stem cells and epithelial-mesenchymal transition.
[So] Source:Semin Cancer Biol;29:51-8, 2014 Dec.
[Is] ISSN:1096-3650
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cripto-1 (CR-1)/Teratocarcinoma-derived growth factor1 (TDGF-1) is a cell surface glycosylphosphatidylinositol (GPI)-linked glycoprotein that can function either in cis (autocrine) or in trans (paracrine). The cell membrane cis form is found in lipid rafts and endosomes while the trans acting form lacking the GPI anchor is soluble. As a member of the epidermal growth factor (EGF)/Cripto-1-FRL-1-Cryptic (CFC) family, CR-1 functions as an obligatory co-receptor for the transforming growth factor-ß (TGF-ß) family members, Nodal and growth and differentiation factors 1 and 3 (GDF1/3) by activating Alk4/Alk7 signaling pathways that involve Smads 2, 3 and 4. In addition, CR-1 can activate non-Smad-dependent signaling elements such as PI3K, Akt and MAPK. Both of these pathways depend upon the 78kDa glucose regulated protein (GRP78). Finally, CR-1 can facilitate signaling through the canonical Wnt/ß-catenin and Notch/Cbf-1 pathways by functioning as a chaperone protein for LRP5/6 and Notch, respectively. CR-1 is essential for early embryonic development and maintains embryonic stem cell pluripotentiality. CR-1 performs an essential role in the etiology and progression of several types of human tumors where it is expressed in a population of cancer stem cells (CSCs) and facilitates epithelial-mesenchymal transition (EMT). In this context, CR-1 can significantly enhance tumor cell migration, invasion and angiogenesis. Collectively, these facts suggest that CR-1 may be an attractive target in the diagnosis, prognosis and therapy of several types of human cancer.
[Mh] Termos MeSH primário: Transição Epitelial-Mesenquimal/genética
Proteínas Ligadas por GPI/genética
Peptídeos e Proteínas de Sinalização Intercelular/genética
Invasividade Neoplásica/genética
Proteínas de Neoplasias/genética
Neoplasias/genética
Neovascularização Patológica/genética
[Mh] Termos MeSH secundário: Receptores de Ativinas Tipo I/metabolismo
Membrana Celular/metabolismo
Proteínas de Choque Térmico/metabolismo
Seres Humanos
Proteínas de Membrana/genética
Neoplasias/patologia
Células-Tronco Neoplásicas/citologia
Fosfatidilinositol 3-Quinases/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Receptores Notch/metabolismo
Proteína Smad2/metabolismo
Proteína Smad3/metabolismo
Proteína Smad4/metabolismo
Proteínas da Superfamília de TGF-beta/metabolismo
Fator de Crescimento Transformador beta/metabolismo
Proteínas Wnt/metabolismo
Via de Sinalização Wnt/genética
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (GPI-Linked Proteins); 0 (Heat-Shock Proteins); 0 (Intercellular Signaling Peptides and Proteins); 0 (Membrane Proteins); 0 (Neoplasm Proteins); 0 (Receptors, Notch); 0 (SMAD2 protein, human); 0 (Smad2 Protein); 0 (Smad3 Protein); 0 (Smad4 Protein); 0 (TDGF1 protein, human); 0 (TGF-beta Superfamily Proteins); 0 (Transforming Growth Factor beta); 0 (Wnt Proteins); 0 (beta Catenin); 0 (molecular chaperone GRP78); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.30 (ACVR1B protein, human); EC 2.7.11.30 (ACVR1C protein, human); EC 2.7.11.30 (Activin Receptors, Type I)
[Em] Mês de entrada:1507
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140826
[St] Status:MEDLINE



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