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[PMID]:28457750
[Au] Autor:Li L; Dong J; Yan L; Yong J; Liu X; Hu Y; Fan X; Wu X; Guo H; Wang X; Zhu X; Li R; Yan J; Wei Y; Zhao Y; Wang W; Ren Y; Yuan P; Yan Z; Hu B; Guo F; Wen L; Tang F; Qiao J
[Ad] Endereço:Beijing Advanced Innovation Center for Genomics (ICG), College of Life Sciences, Department of Obstetrics and Gynecology, Third Hospital, Peking University, Beijing 100871, China; Biomedical Institute for Pioneering Investigation via Convergence and Center for Reproductive Medicine, Ministry of Educ
[Ti] Título:Single-Cell RNA-Seq Analysis Maps Development of Human Germline Cells and Gonadal Niche Interactions.
[So] Source:Cell Stem Cell;20(6):858-873.e4, 2017 Jun 01.
[Is] ISSN:1875-9777
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human fetal germ cells (FGCs) are precursors to sperm and eggs and are crucial for maintenance of the species. However, the developmental trajectories and heterogeneity of human FGCs remain largely unknown. Here we performed single-cell RNA-seq analysis of over 2,000 FGCs and their gonadal niche cells in female and male human embryos spanning several developmental stages. We found that female FGCs undergo four distinct sequential phases characterized by mitosis, retinoic acid signaling, meiotic prophase, and oogenesis. Male FGCs develop through stages of migration, mitosis, and cell-cycle arrest. Individual embryos of both sexes simultaneously contain several subpopulations, highlighting the asynchronous and heterogeneous nature of FGC development. Moreover, we observed reciprocal signaling interactions between FGCs and their gonadal niche cells, including activation of the bone morphogenic protein (BMP) and Notch signaling pathways. Our work provides key insights into the crucial features of human FGCs during their highly ordered mitotic, meiotic, and gametogenetic processes in vivo.
[Mh] Termos MeSH primário: Divisão Celular/fisiologia
Células Germinativas Embrionárias/metabolismo
Feto/metabolismo
Gônadas/enzimologia
Transdução de Sinais/fisiologia
Nicho de Células-Tronco/fisiologia
[Mh] Termos MeSH secundário: Proteínas Morfogenéticas Ósseas/metabolismo
Células Germinativas Embrionárias/citologia
Feminino
Feto/citologia
Gônadas/citologia
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Masculino
Receptores Notch/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bone Morphogenetic Proteins); 0 (Receptors, Notch)
[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


  2 / 11374 MEDLINE  
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[PMID]:27773809
[Au] Autor:Jung B; Staudacher JJ; Beauchamp D
[Ad] Endereço:University of Illinois at Chicago, Chicago, Illinois. Electronic address: bjung@uic.edu.
[Ti] Título:Transforming Growth Factor ß Superfamily Signaling in Development of Colorectal Cancer.
[So] Source:Gastroenterology;152(1):36-52, 2017 Jan.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Transforming growth factor (TGF)-ß cytokines signal via a complex network of pathways to regulate proliferation, differentiation, adhesion, migration, and other functions in many cell types. A high percentage of colorectal tumors contain mutations that disrupt TGF-ß family member signaling. We review how TGF-ß family member signaling is altered during development of colorectal cancer, models of study, interaction of pathways, and potential therapeutic strategies.
[Mh] Termos MeSH primário: Neoplasias Colorretais/genética
Neoplasias Colorretais/metabolismo
Receptores de Fatores de Crescimento Transformadores beta/genética
Transdução de Sinais
Proteínas Smad/genética
Fator de Crescimento Transformador beta/genética
Fator de Crescimento Transformador beta/metabolismo
[Mh] Termos MeSH secundário: Ativinas/metabolismo
Animais
Proteínas Morfogenéticas Ósseas/metabolismo
Neoplasias Colorretais/imunologia
Mutação em Linhagem Germinativa
Homeostase
Seres Humanos
Camundongos
Camundongos Knockout
Receptores de Fatores de Crescimento Transformadores beta/imunologia
Proteínas Smad/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Bone Morphogenetic Proteins); 0 (Receptors, Transforming Growth Factor beta); 0 (Smad Proteins); 0 (Transforming Growth Factor beta); 104625-48-1 (Activins)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  3 / 11374 MEDLINE  
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[PMID]:29390526
[Au] Autor:Piesanen JVI; Nikkari ST; Kunnas TA
[Ad] Endereço:Department of Medical Biochemistry, Faculty of Medicine and Life Sciences, University of Tampere.
[Ti] Título:Genetic variation in bone morphogenetic proteins family members (BMPs 2 and 4) and hypertension risk in middle-aged men: The TAMRISK study.
[So] Source:Medicine (Baltimore);96(51):e9362, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bone morphogenetic proteins (BMPs) are important regulators of iron metabolism affecting hepcidin expression. We have previously shown that 2 genetic polymorphisms in different genes (histocompatibility complex class I-like transmembrane protein, hemojuvelin) involved in the regulation of hepcidin expression pathways are associated with hypertension. In this study, we analyzed genetic variation sites in BMP2 (rs235756, rs235768) and BMP4 (rs4901474) to get more evidence linking iron metabolism to hypertension risk in the Finnish population.The study included 321 hypertensive cases and 463 controls from the Tampere Adult Population Cardiovascular Risk study cohort. Genotyping of polymorphisms was done by polymerase chain reaction using DNAs extracted from buccal swabs.We found that men carrying the GG genotype of BMP2 rs235756 (A>G) polymorphic site had a 4.09-fold risk (confidence interval [CI] 1.61-10.39, P = .003) for hypertension at the age of 50 years compared with A-allele carriers. The risk was significant in the age groups of 45 and 40 years as well. In addition, the 15-year follow-up period of the same individuals showed that carriers of the GG-genotype had also significantly higher readings of both systolic (P < .001) and diastolic (P = .01) blood pressure during the follow-up time. No significant association between BMP2 rs235768 (A>T) and hypertension was found. BMP4 polymorphic site rs4901474 (T>C) also had an effect on hypertension. CC genotype carriers had a 1.48-fold risk (CI 1.03-2.13, P = .033) for hypertension at the age of 50 years when compared with T-allele carriers.In conclusion, BMP2 polymorphic site rs235756 was associated with hypertension in Finnish men. An effect of BMP4 polymorphic site on hypertension was also found.
[Mh] Termos MeSH primário: Proteína Morfogenética Óssea 2/genética
Proteína Morfogenética Óssea 4/genética
Doenças Cardiovasculares/genética
Predisposição Genética para Doença/epidemiologia
Variação Genética
Hipertensão/genética
[Mh] Termos MeSH secundário: Fatores Etários
Análise de Variância
Proteínas Morfogenéticas Ósseas/genética
Doenças Cardiovasculares/epidemiologia
Estudos de Casos e Controles
Finlândia/epidemiologia
Genótipo
Seres Humanos
Hipertensão/epidemiologia
Hipertensão/fisiopatologia
Incidência
Estudos Longitudinais
Masculino
Meia-Idade
Estudos Prospectivos
Medição de Risco
Índice de Gravidade de Doença
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BMP2 protein, human); 0 (BMP4 protein, human); 0 (Bone Morphogenetic Protein 2); 0 (Bone Morphogenetic Protein 4); 0 (Bone Morphogenetic Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009362


  4 / 11374 MEDLINE  
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[PMID]:28465413
[Au] Autor:Wu FJ; Lin TY; Sung LY; Chang WF; Wu PC; Luo CW
[Ad] Endereço:Department of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei 112, Taiwan.
[Ti] Título:BMP8A sustains spermatogenesis by activating both SMAD1/5/8 and SMAD2/3 in spermatogonia.
[So] Source:Sci Signal;10(477), 2017 May 02.
[Is] ISSN:1937-9145
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mutation in either of the genes encoding bone morphogenetic protein (BMP) 8A or 8B ( or ) causes postnatal depletion of spermatogonia in mice. We found that , but not , was expressed predominantly in the neonatal mouse spermatogonia. Although most BMPs induce activation of SMADs 1, 5, and 8 (SMAD1/5/8), but not SMADs 2 and 3 (SMAD2/3), we found that BMP8A induced signaling through both sets of transcription factors. In undifferentiated mouse spermatogonia, BMP8A activated SMAD1/5/8 through receptor complexes formed by ALK3 and either ACVR2A or BMPR2 and activated SMAD2/3 through receptor complexes formed by ALK5 and ACVR2A, ACVR2B, or TGFBR2. Signaling through SMAD2/3 promoted the proliferation of germ cells, whereas that through SMAD1/5/8 directed the subsequent differentiation of spermatogonia. BMP8A promoted spermatogenesis in cultured mouse testis explants, and the resulting spermatids were functionally competent for fertilization. These results suggest that the dual role of BMP8A in promoting proliferation and differentiation of spermatogonia may be exploited clinically to treat male infertility.
[Mh] Termos MeSH primário: Proteínas Morfogenéticas Ósseas/metabolismo
Diferenciação Celular
Proteínas Smad Reguladas por Receptor/metabolismo
Espermatogênese/fisiologia
Espermatogônias/citologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos ICR
Transdução de Sinais
Espermatogônias/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BMP8A protein, human); 0 (Bmp8a protein, mouse); 0 (Bone Morphogenetic Proteins); 0 (Smad Proteins, Receptor-Regulated)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:28455454
[Au] Autor:Onodera K; Sugiura H; Yamada M; Koarai A; Fujino N; Yanagisawa S; Tanaka R; Numakura T; Togo S; Sato K; Kyogoku Y; Hashimoto Y; Okazaki T; Tamada T; Kobayashi S; Yanai M; Miura M; Hoshikawa Y; Okada Y; Suzuki S; Ichinose M
[Ad] Endereço:Department of Respiratory Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
[Ti] Título:Decrease in an anti-ageing factor, growth differentiation factor 11, in chronic obstructive pulmonary disease.
[So] Source:Thorax;72(10):893-904, 2017 10.
[Is] ISSN:1468-3296
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Cellular senescence is observed in the lungs of patients with COPD and may contribute to the disease pathogenesis. Growth differentiation factor 11 (GDF11) belongs to the transforming growth factor ß superfamily and was recently reported to be a circulating protein that may have rejuvenating effects in mice. We aimed to investigate the amounts of GDF11 in the plasma and the lungs of patients with COPD and elucidate the possible roles of GDF11 in cellular senescence. METHODS: The plasma levels of GDF11 were investigated in two separate cohorts by western blotting. The localisation and expression of GDF11 in the lungs were investigated by immunohistochemistry and quantitative reverse transcription PCR, respectively. The effects of GDF11 on both cigarette smoke extract (CSE)-induced cellular senescence in vitro and on elastase-induced cellular senescence in vivo were investigated. RESULTS: The levels of plasma GDF11 in the COPD group were decreased compared with the control groups in the two independent cohorts. The levels of plasma GDF11 were significantly positively correlated with pulmonary function data. The mRNA expression of GDF11 in mesenchymal cells from the COPD group was decreased. Chronic exposure to CSE decreased the production of GDF11. Treatment with GDF11 significantly inhibited CSE-induced cellular senescence and upregulation of inflammatory mediators, partly through Smad2/3 signalling in vitro. Daily GDF11 treatment attenuated cellular senescence and airspace enlargement in an elastase-induced mouse model of emphysema. CONCLUSIONS: The decrease in GDF11 may be involved in the cellular senescence observed in COPD.
[Mh] Termos MeSH primário: Proteínas Morfogenéticas Ósseas/metabolismo
Senescência Celular
Fatores de Diferenciação de Crescimento/metabolismo
Doença Pulmonar Obstrutiva Crônica/metabolismo
[Mh] Termos MeSH secundário: Idoso
Animais
Western Blotting
Proteínas Morfogenéticas Ósseas/farmacologia
Modelos Animais de Doenças
Feminino
Fatores de Diferenciação de Crescimento/farmacologia
Seres Humanos
Imuno-Histoquímica
Masculino
Camundongos
Plasma
RNA Mensageiro/metabolismo
Testes de Função Respiratória
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fumaça/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bone Morphogenetic Proteins); 0 (Gdf11 protein, mouse); 0 (Growth Differentiation Factors); 0 (RNA, Messenger); 0 (Smoke)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.1136/thoraxjnl-2016-209352


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[PMID]:28462460
[Au] Autor:Gelberman RH; Linderman SW; Jayaram R; Dikina AD; Sakiyama-Elbert S; Alsberg E; Thomopoulos S; Shen H
[Ad] Endereço:Department of Orthopaedic Surgery, Washington University, 660 South Euclid, Campus Box 8233, St Louis, MO, 63110, USA.
[Ti] Título:Combined Administration of ASCs and BMP-12 Promotes an M2 Macrophage Phenotype and Enhances Tendon Healing.
[So] Source:Clin Orthop Relat Res;475(9):2318-2331, 2017 Sep.
[Is] ISSN:1528-1132
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Outcomes after intrasynovial tendon repair are highly variable. An intense inflammatory cascade followed by a delayed healing response can cause adhesion formation and repair-site failure that severely impair the function of repaired digits. No effective remedies exist to fully address these issues. Cell- and growth factor-based therapies have been shown to modulate inflammation and improve cell proliferation and matrix synthesis and therefore are promising treatment approaches for intrasynovial tendon repair. QUESTIONS/PURPOSES: (1) Can autologous adipose-derived mesenchymal stromal cells (ASCs) and recombinant bone morphogenetic protein-12 (rBMP-12) be effectively delivered to an intrasynovial flexor tendon repair without adverse effects? (2) Do autologous ASCs modulate the inflammatory response after intrasynovial tendon injury and repair? (3) Does the combined application of autologous ASCs and rBMP-12 modulate the proliferative and remodeling responses after intrasynovial tendon injury and repair? METHODS: Sixteen 1- to 2-year-old female canines were used in this study. Autologous ASC sheets, with and without rBMP-12, were applied to the surface of sutured flexor tendons. Fourteen days after repair, the effects of treatment were determined using quantitative PCR (six per group) for the expression of genes related to macrophage phenotype or inflammation (IL-4, CD163, VEGF, NOS2, IL-1B, and IFNG), cell proliferation (CCND1), and tendon formation (SCX, TNMD, COL1A1 and COL3A1). Proteomics analysis (four per group) was performed to examine changes in tendon protein abundances. CD146 immunostaining and hematoxylin and eosin staining (four per group) were used to detect tendon stem or progenitor cells and to semiquantitatively evaluate cellularity at the tendon repair; analyses were done blinded to group. RESULTS: Gross inspection and cell tracing showed that autologous ASCs and rBMP-12 were delivered to the flexor tendon repair site without the deleterious effects of adhesion and repair-site gap formation. Quantitative assessment of gene and protein expression showed effects of treatment: ASC-sheet treatment modulated the postrepair inflammatory response and facilitated healing by increasing regenerative M2 macrophages (M2 marker CD204, twofold of normal, p = 0.030), inflammatory inhibitor (prostaglandin reductase 1 [PTRG1], 1.6-fold of normal, p = 0.026), and proteins involved in tendon formation (periostin [POSTN], 1.9-fold of normal, p = 0.035). Consistently, semiquantitative and qualitative evaluations of repaired tissue showed that ASC-sheet treatment reduced mononuclear cell infiltration (12% less than nontreated tendons, p = 0.021) and introduced CD146+ stem or progenitor cells to the repair site. The combined administration of ASCs and rBMP-12 further stimulated M2 macrophages by increasing IL-4 (116-fold of normal, p = 0.002) and led to the increase of M2 effector matrix metalloproteinase-12 involved in matrix remodeling (twofold of normal, p = 0.016) and reduction of a negative regulator of angiogenesis and cell migration (StAR-related lipid transfer domain protein13 [STARD13]; 84% of normal, p = 0.000), thus facilitating the proliferative stage of tendon repair. CONCLUSIONS: ASCs and BMP-12 accelerated the progression of healing in the proliferative stage of tendon repair. The effects of ASCs and BMP-12 on tendon functional recovery should be evaluated in future studies. CLINICAL RELEVANCE: The cell sheet approach is an effective, biocompatible, and surgeon-friendly approach for cell and growth factor delivery during tendon repair. Combined application of ASCs and BMP-12 may accelerate intrasynovial tendon healing while suppressing the adverse inflammatory response.
[Mh] Termos MeSH primário: Proteínas Morfogenéticas Ósseas/uso terapêutico
Macrófagos/metabolismo
Transplante de Células-Tronco Mesenquimais/métodos
Células Mesenquimais Estromais/fisiologia
Traumatismos dos Tendões/genética
Cicatrização/fisiologia
[Mh] Termos MeSH secundário: Animais
Proteínas Morfogenéticas Ósseas/administração & dosagem
Proliferação Celular/genética
Modelos Animais de Doenças
Cães
Feminino
Expressão Gênica
Mediadores da Inflamação/análise
Fenótipo
Proteômica
Reação em Cadeia da Polimerase em Tempo Real
Proteínas Recombinantes/administração & dosagem
Traumatismos dos Tendões/etiologia
Traumatismos dos Tendões/metabolismo
Traumatismos dos Tendões/cirurgia
Transplante Autólogo
Resultado do Tratamento
Cicatrização/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bone Morphogenetic Proteins); 0 (Inflammation Mediators); 0 (Recombinant Proteins); 0 (growth differentiation factor 7)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1007/s11999-017-5369-7


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[PMID]:28471520
[Au] Autor:Bansho Y; Lee J; Nishida E; Nakajima-Koyama M
[Ad] Endereço:Department of Cell and Developmental Biology, Graduate School of Biostudies, Kyoto University, Japan.
[Ti] Título:Identification and characterization of secreted factors that are upregulated during somatic cell reprogramming.
[So] Source:FEBS Lett;591(11):1584-1600, 2017 06.
[Is] ISSN:1873-3468
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The process of cell reprogramming has been characterized considerably since the successful generation of induced pluripotent stem cells. However, the importance of cell-cell communications for cellular reprogramming remains largely unknown. Secreted factors, which are expressed and secreted during reprogramming, may influence the reprogramming efficiency. Here, we have identified Sostdc1, Glb1l2, Fetub, Dpp4, Gdf3, Trh, and Tdgf1 as prominently upregulated secreted factors during reprogramming. Our detailed analysis reveals that these seven factors may be categorized into four groups based on their expression patterns in relation to the reprogramming stages. Remarkably, knockdown of Sostdc1, which is the most prominently upregulated factor and which is expressed earlier than the other six factors, results in reduced reprogramming efficiency, suggesting its involvement in the reprogramming process.
[Mh] Termos MeSH primário: Reprogramação Celular/genética
Regulação da Expressão Gênica
[Mh] Termos MeSH secundário: Animais
Proteínas Morfogenéticas Ósseas/genética
Proteínas Morfogenéticas Ósseas/metabolismo
Células Cultivadas
Dipeptidil Peptidase 4/genética
Dipeptidil Peptidase 4/metabolismo
Fator de Crescimento Epidérmico/genética
Fator de Crescimento Epidérmico/metabolismo
Fetuína-B/genética
Fetuína-B/metabolismo
Fibroblastos/metabolismo
Citometria de Fluxo
Fator 3 de Diferenciação de Crescimento/genética
Fator 3 de Diferenciação de Crescimento/metabolismo
Immunoblotting
Glicoproteínas de Membrana/genética
Glicoproteínas de Membrana/metabolismo
Camundongos
Análise em Microsséries
Proteínas de Neoplasias/genética
Proteínas de Neoplasias/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:LETTER; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bone Morphogenetic Proteins); 0 (Fetub protein, mouse); 0 (Fetuin-B); 0 (Gdf3 protein, mouse); 0 (Growth Differentiation Factor 3); 0 (Membrane Glycoproteins); 0 (Neoplasm Proteins); 0 (Sostdc1 protein, mouse); 0 (Tdgf1 protein, mouse); 62229-50-9 (Epidermal Growth Factor); EC 3.4.14.5 (Dipeptidyl Peptidase 4); EC 3.4.14.5 (Dpp4 protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180130
[Lr] Data última revisão:
180130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1002/1873-3468.12665


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[PMID]:28450417
[Au] Autor:Li H; Li Y; Xiang L; Zhang J; Zhu B; Xiang L; Dong J; Liu M; Xiang G
[Ad] Endereço:Department of Endocrinology, Wuhan General Hospital of Guangzhou Command, Wuhan, Hubei Province, China.
[Ti] Título:GDF11 Attenuates Development of Type 2 Diabetes via Improvement of Islet ß-Cell Function and Survival.
[So] Source:Diabetes;66(7):1914-1927, 2017 07.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Growth differentiation factor 11 (GDF11) has been implicated in the regulation of islet development and a variety of aging conditions, but little is known about the physiological functions of GDF11 in adult pancreatic islets. Here, we showed that systematic replenishment of GDF11 not only preserved insulin secretion but also improved the survival and morphology of ß-cells and improved glucose metabolism in both nongenetic and genetic mouse models of type 2 diabetes (T2D). Conversely, anti-GDF11 monoclonal antibody treatment caused ß-cell failure and lethal T2D. In vitro treatment of isolated murine islets and MIN6 cells with recombinant GDF11 attenuated glucotoxicity-induced ß-cell dysfunction and apoptosis. Mechanistically, the GDF11-mediated protective effects could be attributed to the activation of transforming growth factor-ß/Smad2 and phosphatidylinositol-4,5-bisphosphate 3-kinase-AKT-FoxO1 signaling. These findings suggest that GDF11 repletion may improve ß-cell function and mass and thus may lead to a new therapeutic approach for T2D.
[Mh] Termos MeSH primário: Glicemia/efeitos dos fármacos
Proteínas Morfogenéticas Ósseas/farmacologia
Diabetes Mellitus Experimental/metabolismo
Diabetes Mellitus Tipo 2/metabolismo
Fatores de Diferenciação de Crescimento/farmacologia
Células Secretoras de Insulina/efeitos dos fármacos
Insulina/secreção
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/farmacologia
Apoptose
Glicemia/metabolismo
Western Blotting
Proteínas Morfogenéticas Ósseas/antagonistas & inibidores
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Dieta Hiperlipídica
Modelos Animais de Doenças
Proteína Forkhead Box O1/efeitos dos fármacos
Proteína Forkhead Box O1/metabolismo
Teste de Tolerância a Glucose
Fatores de Diferenciação de Crescimento/antagonistas & inibidores
Células Secretoras de Insulina/secreção
Ilhotas Pancreáticas/efeitos dos fármacos
Ilhotas Pancreáticas/secreção
Camundongos
Fosfotransferases (Aceptor do Grupo Álcool)/efeitos dos fármacos
Fosfotransferases (Aceptor do Grupo Álcool)/metabolismo
Proteínas Proto-Oncogênicas c-akt/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-akt/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Receptores para Leptina/genética
Transdução de Sinais/efeitos dos fármacos
Proteína Smad2/efeitos dos fármacos
Proteína Smad2/metabolismo
Fator de Crescimento Transformador beta/efeitos dos fármacos
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Blood Glucose); 0 (Bone Morphogenetic Proteins); 0 (Forkhead Box Protein O1); 0 (Foxo1 protein, mouse); 0 (Gdf11 protein, mouse); 0 (Growth Differentiation Factors); 0 (Insulin); 0 (Receptors, Leptin); 0 (Smad2 Protein); 0 (Smad2 protein, mouse); 0 (Transforming Growth Factor beta); 0 (leptin receptor, mouse); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor)); EC 2.7.1.- (phosphatidylinositol 4,5-biphosphate kinase); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.2337/db17-0086


  9 / 11374 MEDLINE  
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[PMID]:29240821
[Au] Autor:Kim JH; Kim AR; Choi YH; Jang S; Woo GH; Cha JH; Bak EJ; Yoo YJ
[Ad] Endereço:Department of Oral Biology, Yonsei University College of Dentistry, Seoul, Republic of Korea.
[Ti] Título:Tumor necrosis factor-α antagonist diminishes osteocytic RANKL and sclerostin expression in diabetes rats with periodontitis.
[So] Source:PLoS One;12(12):e0189702, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Type 1 diabetes with periodontitis shows elevated TNF-α expression. Tumor necrosis factor (TNF)-α stimulates the expression of receptor activator of nuclear factor-κB ligand (RANKL) and sclerostin. The objective of this study was to determine the effect of TNF-α expression of osteocytic RANKL and sclerostin in type 1 diabetes rats with periodontitis using infliximab (IFX), a TNF-α antagonist. Rats were divided into two timepoint groups: day 3 and day 20. Each timepoint group was then divided into four subgroups: 1) control (C, n = 6 for each time point); 2) periodontitis (P, n = 6 for each time point); 3) diabetes with periodontitis (DP, n = 8 for each time point); and 4) diabetes with periodontitis treated with IFX (DP+IFX, n = 8 for each time point). To induce type 1 diabetes, rats were injected with streptozotocin (50 mg/kg dissolved in 0.1 M citrate buffer). Periodontitis was then induced by ligature of the mandibular first molars at day 7 after STZ injection (day 0). IFX was administered once for the 3 day group (on day 0) and twice for the 20 day group (on days 7 and 14). The DP group showed greater alveolar bone loss than the P group on day 20 (P = 0.020). On day 3, higher osteoclast formation and RANKL-positive osteocytes in P group (P = 0.000 and P = 0.011, respectively) and DP group (P = 0.006 and P = 0.017, respectively) than those in C group were observed. However, there was no significant difference in osteoclast formation or RANKL-positive osteocytes between P and DP groups. The DP+IFX group exhibited lower alveolar bone loss (P = 0.041), osteoclast formation (P = 0.019), and RANKL-positive osteocytes (P = 0.009) than that of the DP group. On day 20, DP group showed a lower osteoid area (P = 0.001) and more sclerostin-positive osteocytes (P = 0.000) than P group. On days 3 and 20, the DP+IFX group showed more osteoid area (P = 0.048 and 0.040, respectively) but lower sclerostin-positive osteocytes (both P = 0.000) than DP group. Taken together, these results suggest that TNF-α antagonist can diminish osteocytic RANKL/sclerostin expression and osteoclast formation, eventually recovering osteoid formation. Therefore, TNF-α might mediate alveolar bone loss via inducing expression of osteocytic RANKL and sclerostin in type 1 diabetes rats with periodontitis.
[Mh] Termos MeSH primário: Proteínas Morfogenéticas Ósseas/metabolismo
Diabetes Mellitus Experimental/metabolismo
Infliximab/farmacologia
Osteócitos/efeitos dos fármacos
Periodontite/metabolismo
Ligante RANK/metabolismo
Fator de Necrose Tumoral alfa/antagonistas & inibidores
[Mh] Termos MeSH secundário: Perda do Osso Alveolar
Animais
Diabetes Mellitus Experimental/complicações
Marcadores Genéticos
Imuno-Histoquímica
Masculino
Osteócitos/metabolismo
Periodontite/complicações
Ratos
Ratos Endogâmicos F344
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bone Morphogenetic Proteins); 0 (Genetic Markers); 0 (RANK Ligand); 0 (Sost protein, rat); 0 (Tumor Necrosis Factor-alpha); B72HH48FLU (Infliximab)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171229
[Lr] Data última revisão:
171229
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189702


  10 / 11374 MEDLINE  
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[PMID]:27771382
[Au] Autor:Sebastian A; Loots GG
[Ad] Endereço:Biology and Biotechnology Division, Lawrence Livermore National Laboratory, 7000 East Avenue, L-452, Livermore, CA 94550, USA; School of Natural Sciences, University of California, Merced, CA 95343, USA.
[Ti] Título:Transcriptional control of Sost in bone.
[So] Source:Bone;96:76-84, 2017 03.
[Is] ISSN:1873-2763
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sclerostin is an osteocyte derived negative regulator of bone formation. A highly specific expression pattern and the exclusive bone phenotype have made Sclerostin an attractive target for therapeutic intervention in treating metabolic bone diseases such as osteoporosis and in facilitating fracture repair. Understanding the molecular mechanisms that regulate Sclerostin transcription is of great interest as it may unveil new avenues for therapeutic approaches. Such studies may also elucidate how various signaling pathways intersect to modulate bone metabolism. Here we review the current understanding of the upstream molecular mechanisms that regulate Sost/SOST transcription, in bone.
[Mh] Termos MeSH primário: Proteínas Morfogenéticas Ósseas/genética
Osso e Ossos/metabolismo
Regulação da Expressão Gênica
Transcrição Genética
[Mh] Termos MeSH secundário: Animais
Proteínas Morfogenéticas Ósseas/metabolismo
Seres Humanos
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Bone Morphogenetic Proteins)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171223
[Lr] Data última revisão:
171223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161106
[St] Status:MEDLINE



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