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[PMID]:29320969
[Au] Autor:Hachim MY; Hachim IY; Dai M; Ali S; Lebrun JJ
[Ad] Endereço:1 Cancer Research Program, Department of Medicine, McGill University Health Centre, Montreal, QC, Canada.
[Ti] Título:Differential expression of TGFß isoforms in breast cancer highlights different roles during breast cancer progression.
[So] Source:Tumour Biol;40(1):1010428317748254, 2018 Jan.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:While TGFß plays a critical role in tumor formation and progression, the role and contribution of its three different isoforms remain unclear. In this study, we aimed at elucidating the prognostic value of the TGFß isoforms and assessed their expression levels in breast cancer patients at different stages of the disease. We found higher levels of TGFß1 and TGFß3 in cancer patients compared to normal tissues, with no significant changes in TGFß2 expression. Similarly, TGFß1 and TGFß3, but not TGFß2, showed higher expression levels in advanced lymph node-positive and metastatic tumors, suggesting different roles for the different isoforms in tumor progression and the metastatic process, while in the least aggressive molecular subtype (luminal A), expression of the three TGFß isoforms significantly correlated with expression of both TGFß receptors, such correlation only occurred between TGFß1 and TGFß3 and the TGFß type II receptor (TßRII) in the highly aggressive basal-like subtype. Interestingly, a distinct and somehow opposite pattern was observed in HER-2 tumors, only showing significant association pattern between TGFß2 and the TGFß type I receptor (TßRI). Finally, the three TGFß isoforms showed distinct association patterns with patient outcome depending on the different molecular subtype, highlighting context-dependent, differential prognostic values.
[Mh] Termos MeSH primário: Neoplasias da Mama/genética
Perfilação da Expressão Gênica/métodos
Fator de Crescimento Transformador beta1/genética
Fator de Crescimento Transformador beta2/genética
Fator de Crescimento Transformador beta3/genética
[Mh] Termos MeSH secundário: Neoplasias da Mama/metabolismo
Neoplasias da Mama/patologia
Linhagem Celular Tumoral
Progressão da Doença
Feminino
Seres Humanos
Imuno-Histoquímica
Meia-Idade
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Receptores de Fatores de Crescimento Transformadores beta/genética
Receptores de Fatores de Crescimento Transformadores beta/metabolismo
Esferoides Celulares/metabolismo
Fator de Crescimento Transformador beta1/metabolismo
Fator de Crescimento Transformador beta2/metabolismo
Fator de Crescimento Transformador beta3/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 0 (Receptors, Transforming Growth Factor beta); 0 (Transforming Growth Factor beta1); 0 (Transforming Growth Factor beta2); 0 (Transforming Growth Factor beta3)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317748254


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[PMID]:29244857
[Au] Autor:Zbucka-Kretowska M; Charkiewicz K; Goscik J; Wolczynski S; Laudanski P
[Ad] Endereço:Department of Reproduction and Gynecological Endocrinology, Medical University of Bialystok, Bialystok, Poland.
[Ti] Título:Maternal plasma angiogenic and inflammatory factor profiling in foetal Down syndrome.
[So] Source:PLoS One;12(12):e0189762, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE AND DESIGN: Angiogenic factors are proteins that are related to certain foetal chromosomal abnormalities. The aim of this study was to determine the concentration of 60 angiogenic factors in the plasma of women with offspring possessing trisomy 21/Down syndrome (DS). METHOD: After analysing karyotyping results, we selected 20 patients with foetuses possessing DS, and for the control group, we selected 28 healthy patients with uncomplicated pregnancies who delivered healthy newborns at term (i.e., 15-18 weeks of gestation). To assess the concentration of proteins in the blood plasma, we used a protein macroarray which enabled simultaneous determination of 60 angiogenic factors per sample. RESULTS: We observed a statistically significant increase in the concentration of these five angiogenic and inflammatory factors: TGFb1 (p = 0.039), angiostatin (p = 0.0142), I-309 (p = 0.0476), TGFb3 (p = 0.0395), and VEGF-D (p = 0.0173)-compared to concentrations in patients with healthy foetuses. CONCLUSION: Our findings suggest that angiogenic factors may play role in DS pathogenesis.
[Mh] Termos MeSH primário: Indutores da Angiogênese/sangue
Proteínas Sanguíneas/genética
Síndrome de Down/sangue
Herança Materna/genética
[Mh] Termos MeSH secundário: Angiostatinas/sangue
Quimiocina CCL1/sangue
Aberrações Cromossômicas
Síndrome de Down/genética
Síndrome de Down/patologia
Feminino
Seres Humanos
Recém-Nascido
Cariotipagem
Gravidez
Fator de Crescimento Transformador beta1/sangue
Fator de Crescimento Transformador beta3/sangue
Fator D de Crescimento do Endotélio Vascular/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inducing Agents); 0 (Blood Proteins); 0 (CCL1 protein, human); 0 (Chemokine CCL1); 0 (TGFB1 protein, human); 0 (TGFB3 protein, human); 0 (Transforming Growth Factor beta1); 0 (Transforming Growth Factor beta3); 0 (Vascular Endothelial Growth Factor D); 86090-08-6 (Angiostatins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180102
[Lr] Data última revisão:
180102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189762


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[PMID]:28729364
[Au] Autor:Angelov SN; Hu JH; Wei H; Airhart N; Shi M; Dichek DA
[Ad] Endereço:From the Department of Medicine, University of Washington School of Medicine, Seattle.
[Ti] Título:TGF-ß (Transforming Growth Factor-ß) Signaling Protects the Thoracic and Abdominal Aorta From Angiotensin II-Induced Pathology by Distinct Mechanisms.
[So] Source:Arterioscler Thromb Vasc Biol;37(11):2102-2113, 2017 Nov.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The role of TGF-ß (transforming growth factor-ß) signaling in abdominal aortic aneurysm (AAA) formation is controversial. Others reported that systemic blockade of TGF-ß by neutralizing antibodies accelerated AAA development in angiotensin II-infused mice. This result is consistent with other studies suggesting that TGF-ß signaling prevents AAA. Development of a therapy for AAA that exploits the protective actions of TGF-ß would be facilitated by identification of the mechanisms through which TGF-ß prevents AAA. We hypothesized that TGF-ß signaling prevents AAA by its actions on aortic medial smooth muscle cells. APPROACH AND RESULTS: We compared the prevalence, severity, and histopathology of angiotensin II-induced AAA among control mice (no TGF-ß blockade), mice with antibody-mediated systemic neutralization of TGF-ß, and mice with genetically based smooth muscle-specific loss of TGF-ß signaling. Surprisingly, we found that systemic-but not smooth muscle-specific-TGF-ß blockade significantly increased the prevalence of AAA and tended to increase AAA severity, adventitial thickening, and aortic wall macrophage accumulation. In contrast, abdominal aortas of mice with smooth muscle-specific loss of TGF-ß signaling differed from controls only in having a thinner media. We examined thoracic aortas of the same mice. Here we found that smooth muscle-specific loss of -but not systemic TGF-ß neutralization-significantly accelerated development of aortic pathology, including increased prevalence of intramural hematomas, medial thinning, and adventitial thickening. CONCLUSION: Our results suggest that TGF-ß signaling prevents both abdominal and thoracic aneurysmal disease but does so by distinct mechanisms. Smooth muscle extrinsic signaling protects the abdominal aorta and smooth muscle intrinsic signaling protects the thoracic aorta.
[Mh] Termos MeSH primário: Angiotensina II
Aneurisma da Aorta Abdominal/prevenção & controle
Aneurisma da Aorta Torácica/prevenção & controle
Músculo Liso Vascular/metabolismo
Transdução de Sinais
Fator de Crescimento Transformador beta/metabolismo
Remodelação Vascular
[Mh] Termos MeSH secundário: Túnica Adventícia/metabolismo
Túnica Adventícia/patologia
Animais
Anticorpos/farmacologia
Aorta Abdominal/efeitos dos fármacos
Aorta Abdominal/metabolismo
Aorta Abdominal/patologia
Aorta Torácica/efeitos dos fármacos
Aorta Torácica/metabolismo
Aorta Torácica/patologia
Aneurisma da Aorta Abdominal/induzido quimicamente
Aneurisma da Aorta Abdominal/metabolismo
Aneurisma da Aorta Abdominal/patologia
Aneurisma da Aorta Torácica/induzido quimicamente
Aneurisma da Aorta Torácica/metabolismo
Aneurisma da Aorta Torácica/patologia
Dilatação Patológica
Modelos Animais de Doenças
Feminino
Predisposição Genética para Doença
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Músculo Liso Vascular/efeitos dos fármacos
Músculo Liso Vascular/patologia
Fenótipo
Proteínas Serina-Treonina Quinases/deficiência
Proteínas Serina-Treonina Quinases/genética
Receptores de Fatores de Crescimento Transformadores beta/deficiência
Receptores de Fatores de Crescimento Transformadores beta/genética
Índice de Gravidade de Doença
Transdução de Sinais/efeitos dos fármacos
Fator de Crescimento Transformador beta/antagonistas & inibidores
Fator de Crescimento Transformador beta1/antagonistas & inibidores
Fator de Crescimento Transformador beta1/metabolismo
Fator de Crescimento Transformador beta2/antagonistas & inibidores
Fator de Crescimento Transformador beta2/metabolismo
Fator de Crescimento Transformador beta3/antagonistas & inibidores
Fator de Crescimento Transformador beta3/metabolismo
Túnica Média/metabolismo
Túnica Média/patologia
Remodelação Vascular/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Receptors, Transforming Growth Factor beta); 0 (Tgfb1 protein, mouse); 0 (Tgfb2 protein, mouse); 0 (Tgfb3 protein, mouse); 0 (Transforming Growth Factor beta); 0 (Transforming Growth Factor beta1); 0 (Transforming Growth Factor beta2); 0 (Transforming Growth Factor beta3); 11128-99-7 (Angiotensin II); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.30 (transforming growth factor-beta type II receptor)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170722
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309401


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[PMID]:28637902
[Au] Autor:Ndaw VS; Abebayehu D; Spence AJ; Paez PA; Kolawole EM; Taruselli MT; Caslin HL; Chumanevich AP; Paranjape A; Baker B; Barnstein BO; Haque TT; Kiwanuka KN; Oskeritzian CA; Ryan JJ
[Ad] Endereço:Department of Biology, Virginia Commonwealth University, Richmond, VA 23284.
[Ti] Título:TGF-ß1 Suppresses IL-33-Induced Mast Cell Function.
[So] Source:J Immunol;199(3):866-873, 2017 Aug 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TGF-ß1 is involved in many pathological conditions, including autoimmune disorders, cancer, and cardiovascular and allergic diseases. We have previously found that TGF-ß1 can suppress IgE-mediated mast cell activation of human and mouse mast cells. IL-33 is a member of the IL-1 family capable of inducing mast cell responses and enhancing IgE-mediated activation. In this study, we investigated the effects of TGF-ß on IL-33-mediated mast cell activation. Bone marrow-derived mast cells cultured in TGF-ß1, ß2, or ß3 showed reduced IL-33-mediated production of TNF, IL-6, IL-13, and MCP-1 in a concentration-dependent manner. TGF-ß1 inhibited IL-33-mediated Akt and ERK phosphorylation as well as NF-κB- and AP-1-mediated transcription. These effects were functionally important, as TGF-ß1 injection suppressed IL-33-induced systemic cytokines in vivo and inhibited IL-33-mediated cytokine release from human mast cells. TGF-ß1 also suppressed the combined effects of IL-33 and IgE-mediated activation on mouse and human mast cells. The role of IL-33 in the pathogenesis of allergic diseases is incompletely understood. These findings, consistent with our previously reported effects of TGF-ß1 on IgE-mediated activation, demonstrate that TGF-ß1 can provide broad inhibitory signals to activated mast cells.
[Mh] Termos MeSH primário: Interleucina-33/imunologia
Mastócitos/imunologia
Fator de Crescimento Transformador beta1/fisiologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Citocinas/antagonistas & inibidores
Citocinas/biossíntese
Citocinas/imunologia
Seres Humanos
Imunoglobulina E/imunologia
Interleucina-6/biossíntese
Interleucina-6/imunologia
Ativação Linfocitária/efeitos dos fármacos
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Mastócitos/efeitos dos fármacos
Mastócitos/metabolismo
Camundongos
NF-kappa B/genética
Fosforilação/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-akt/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-akt/metabolismo
Receptores de IgE/imunologia
Fator de Transcrição AP-1/genética
Fator de Crescimento Transformador beta1/farmacologia
Fator de Crescimento Transformador beta3/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (IL33 protein, human); 0 (Interleukin-33); 0 (Interleukin-6); 0 (NF-kappa B); 0 (Receptors, IgE); 0 (Transcription Factor AP-1); 0 (Transforming Growth Factor beta1); 0 (Transforming Growth Factor beta3); 37341-29-0 (Immunoglobulin E); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601983


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[PMID]:28613059
[Au] Autor:Wang T; Muhetaer H; Li J
[Ad] Endereço:Department of Stomatology, People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi 830001, China.
[Ti] Título:[Experimental study of transforming growth factor-ß3 combined with dental pulp stem cells in promoting the implant's osseointegration].
[So] Source:Zhonghua Kou Qiang Yi Xue Za Zhi;52(6):367-373, 2017 Jun 09.
[Is] ISSN:1002-0098
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the effect of transforming growth factor-ß3 (TGF-ß3) and dental pulp stem cells (DPSC) in promoting the implant's osteointegration. Thirty-three New Zealand white rabbits were randomly divided into phosphate buffer saline (PBS) group, DPSC group and TGF-ß3 + DPSC group (12 rabbits/group). Two teeth from the rabbits's mandibular incisors or molars were pulled out randomly, then implant were placed in the tooth extraction site immediately. In PBS group, the implant area was filled with Bio-Oss powder 0.30 g mixed by PBS 20 µl only; while the implant area was filled with Bio-oss powder 0.30 g and 1×10(8)/L DPSC 20 µl in DPSC group; in the the TGF-ß3+DPSC group the implant area was filled with Bio-Oss powder 0.30 g mixed with 1×10(8)/L DPSC 20 µl and 80 µg/L TGF-ß3 20 µl. Eighteen New Zealand rabbits were executed in the 4 weeks and 8 weeks respectively. The treated alveolar bone tissue and implant were collected for plastic section. Alizarin red staining (ARS), immunohistochemical detection (IHC) of bone sialoprotein (BSP), osteocalcin (OC) and type â…  collagen (COL-â… ) were performed after 4 weeks and 8 weeks. Combined bone lamelta width (CBLW) and implant bone contact rate (IBCR), trabecular width (TW) and trabecular area percentage (TA) were observed by histomorphometric measurement. ARS staining: 4 weeks after the operation, the TGF-ß3+ DPSC group showed more red calcified nodules than the other two groups; 8 weeks after operation, the red calcified nodule was further increased. 4 weeks after the operation, the expression of BSP, OC and COL-â…  was (0.35± 0.04), (0.36 ± 0.03) and (0.39 ± 0.01) respectively in TGF-ß3+ DPSC group, (0.27 ± 0.02), (0.24 ± 0.01) and (0.28±0.03) respectively in DPSC group, and (0.13±0.03), (0.15±0.02) and (0.16±0.02) respectively in PBS group. Eight weeks after operation, the expression of BSP, OC and COL-â…  was (0.51±0.02), (0.49±0.03) and (0.53±0.02) respectively in TGF-ß3+DPSC group, (0.35±0.02), (0.37±0.01) and (0.38±0.01) respectively in DPSC group, and (0.21±0.03), (0.19±0.01) and (0.22±0.02) respectively in PBS group. After 4 weeks and 8 weeks, the expression of BSP, OC and COL-â…  in TGF-ß3+DPSC group were significantly higher than the other groups ( 0.05), there was no significant difference between DPSC group and PBS group ( 0.05). Eight weeks after operation, the CBLW, IBCR, TW and TA around implant in TGF-ß3+ DPSC group were significantly higher than that in the other groups ( 0.05), there was no significant difference between DPSC group and PBS group ( 0.05). The DPSC has the potential osteogenic differentiation ability; TGF-ß3 can accelerate the osteogenic differentiation of DPSC to some extent; TGF-ß3 combined with DPSC can effectively promote the implant's osseointegration.
[Mh] Termos MeSH primário: Substitutos Ósseos/administração & dosagem
Implantes Dentários
Polpa Dentária/citologia
Minerais/administração & dosagem
Osseointegração
Transplante de Células-Tronco
Fator de Crescimento Transformador beta3/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Colágeno Tipo I/análise
Sialoproteína de Ligação à Integrina/análise
Osteocalcina/análise
Osteogênese
Coelhos
Distribuição Aleatória
Células-Tronco
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bio-Oss); 0 (Bone Substitutes); 0 (Collagen Type I); 0 (Dental Implants); 0 (Integrin-Binding Sialoprotein); 0 (Minerals); 0 (Transforming Growth Factor beta3); 104982-03-8 (Osteocalcin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:170615
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1002-0098.2017.06.009


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[PMID]:28604778
[Au] Autor:Richardson R; Mitchell K; Hammond NL; Mollo MR; Kouwenhoven EN; Wyatt ND; Donaldson IJ; Zeef L; Burgis T; Blance R; van Heeringen SJ; Stunnenberg HG; Zhou H; Missero C; Romano RA; Sinha S; Dixon MJ; Dixon J
[Ad] Endereço:Faculty of Biology, Medicine & Health, Manchester Academic Health Sciences Centre, Michael Smith Building, University of Manchester, Manchester, United Kingdom.
[Ti] Título:p63 exerts spatio-temporal control of palatal epithelial cell fate to prevent cleft palate.
[So] Source:PLoS Genet;13(6):e1006828, 2017 Jun.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cleft palate is a common congenital disorder that affects up to 1 in 2500 live births and results in considerable morbidity to affected individuals and their families. The aetiology of cleft palate is complex with both genetic and environmental factors implicated. Mutations in the transcription factor p63 are one of the major individual causes of cleft palate; however, the gene regulatory networks in which p63 functions remain only partially characterized. Our findings demonstrate that p63 functions as an essential regulatory molecule in the spatio-temporal control of palatal epithelial cell fate to ensure appropriate fusion of the palatal shelves. Initially, p63 induces periderm formation and controls its subsequent maintenance to prevent premature adhesion between adhesion-competent, intra-oral epithelia. Subsequently, TGFß3-induced down-regulation of p63 in the medial edge epithelia of the palatal shelves is a pre-requisite for palatal fusion by facilitating periderm migration from, and reducing the proliferative potential of, the midline epithelial seam thereby preventing cleft palate.
[Mh] Termos MeSH primário: Fissura Palatina/genética
Redes Reguladoras de Genes/genética
Fosfoproteínas/genética
Transativadores/genética
Fator de Crescimento Transformador beta3/genética
[Mh] Termos MeSH secundário: Animais
Movimento Celular/genética
Proliferação Celular/genética
Fissura Palatina/fisiopatologia
Modelos Animais de Doenças
Células Epiteliais/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Seres Humanos
Camundongos
Mutação
Fosfoproteínas/biossíntese
Transdução de Sinais/genética
Transativadores/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Phosphoproteins); 0 (Tgfb3 protein, mouse); 0 (Trans-Activators); 0 (Transforming Growth Factor beta3); 0 (Trp63 protein, mouse)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1006828


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[PMID]:28599847
[Au] Autor:Sriram S; Tran JA; Guo X; Hutcheon AEK; Kazlauskas A; Zieske JD
[Ad] Endereço:The Schepens Eye Research Institute/Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Electronic address: Sriniwas_Sriram@meei.harvard.edu.
[Ti] Título:Development of wound healing models to study TGFß3's effect on SMA.
[So] Source:Exp Eye Res;161:52-60, 2017 Aug.
[Is] ISSN:1096-0007
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The goal of this study was to test the efficacy of transforming growth factor beta 3 (TGFß3) in reducing α-smooth muscle actin (SMA) expression in two models-an ex vivo organ culture and an in vitro 3D cell construct-both of which closely mimic an in vivo environment. For the ex vivo organ culture system, a central 6.0 mm corneal keratectomy was performed on freshly excised rabbit globes The corneas were then excised, segregated into groups treated with 1.0 ng/ml TGFß1 or ß3 (T1 or T3, respectively), and cultured for 2 weeks. The corneas were assessed for levels of haze and analyzed for SMA mRNA levels. For the 3D in vitro model, rabbit corneal fibroblasts (RbCFs) were cultured for 4 weeks on poly-transwell membranes in Eagle's minimum essential media (EMEM) + 10% FBS + 0.5 mM vitamin C ± 0.1 ng/ml T1 or T3. At the end of 4 weeks, the constructs were processed for analysis by indirect-immunofluorescence (IF) and RT-qPCR. The RT-qPCR data showed that SMA mRNA expression in T3 samples for both models was significantly lower (p < 0.05) than T1 treatment (around 3-fold in ex vivo and 2-fold in constructs). T3 also reduced the amount of scarring in ex vivo corneas as compared with the T1 samples. IF data from RbCF constructs confirmed that T3-treated samples had up to 4-fold (p < 0.05) lower levels of SMA protein expression than samples treated with T1. These results show that T3 when compared to T1 decreases the expression of SMA in both ex vivo organ culture and in vitro 3D cell construct models. Understanding the mechanism of T3's action in these systems and how they differ from simple cell culture models, may potentially help in developing T3 as an anti-scarring therapy.
[Mh] Termos MeSH primário: Actinas/genética
Córnea/efeitos dos fármacos
Ceratócitos da Córnea/efeitos dos fármacos
Modelos Animais de Doenças
Fator de Crescimento Transformador beta3/farmacologia
Cicatrização/fisiologia
[Mh] Termos MeSH secundário: Animais
Técnicas de Cultura de Células
Córnea/metabolismo
Ceratócitos da Córnea/metabolismo
Substância Própria/citologia
Técnica Indireta de Fluorescência para Anticorpo
Técnicas de Cultura de Órgãos
Fator de Crescimento Derivado de Plaquetas/metabolismo
RNA Mensageiro/genética
Coelhos
Reação em Cadeia da Polimerase em Tempo Real
Fator de Crescimento Transformador beta1/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Platelet-Derived Growth Factor); 0 (RNA, Messenger); 0 (Transforming Growth Factor beta1); 0 (Transforming Growth Factor beta3)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170902
[Lr] Data última revisão:
170902
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170611
[St] Status:MEDLINE


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[PMID]:28490526
[Au] Autor:Deb DK; Chen Y; Sun J; Wang Y; Li YC
[Ad] Endereço:Department of Medicine, Division of Biological Sciences, The University of Chicago, Chicago, Illinois.
[Ti] Título:ATP-citrate lyase is essential for high glucose-induced histone hyperacetylation and fibrogenic gene upregulation in mesangial cells.
[So] Source:Am J Physiol Renal Physiol;313(2):F423-F429, 2017 Aug 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The goal of this study was to address the role of ATP-citrate lyase (ACL), an enzyme that converts citrate to acetyl-CoA, in high glucose (HG)-induced histone acetylation and profibrotic gene expression. Our recent ChIP-Seq studies have demonstrated that HG induces genome-wide histone hyperacetylation in mesangial cells (MCs). Here, we showed that exposure of MCs to HG markedly increased histone acetylation at the H3K9/14 and H3K18 marks and induced the expression of potent profibrotic factors TGF-ß1, TGF-ß3, and connective tissue growth factor (CTGF). The induction of these profibrotic factors was further enhanced by histone deacetylase inhibitor but suppressed by histone acetyl-transferase inhibitor, confirming the importance of histone acetylation in this regulation. Interestingly, HG not only upregulated ACL expression but also promoted ACL nuclear translocation, evidenced by increased ACL concentration and activity in the nuclear extracts. Consistent with this observation, transfection of MCs with a plasmid-carrying green fluorescent protein (GFP)-ACL fusion protein led to GFP nuclear accumulation when cultured in HG condition. Silencing ACL with siRNAs alleviated HG-induced histone hyperacetylation, as well as upregulation of TGF-ß1, TGF-ß3, CTGF, and extracellular matrix (ECM) proteins fibronectin and collagen type IV, whereas ACL overexpression further enhanced HG induction of histone acetylation, as well as these profibrotic factors and ECM proteins. Collectively, these observations demonstrate that HG promotes ACL expression and translocation into the nucleus, where ACL converts citrate to acetyl-CoA to provide the substrate for histone acetylation, leading to upregulation of fibrogenic genes. Therefore, ACL plays a critical role in epigenetic regulation of diabetic renal fibrosis.
[Mh] Termos MeSH primário: ATP Citrato (pro-S)-Liase/metabolismo
Nefropatias Diabéticas/enzimologia
Epigênese Genética/efeitos dos fármacos
Glucose/toxicidade
Histonas/genética
Células Mesangiais/efeitos dos fármacos
Processamento de Proteína Pós-Traducional/efeitos dos fármacos
[Mh] Termos MeSH secundário: ATP Citrato (pro-S)-Liase/genética
Acetilcoenzima A/metabolismo
Acetilação
Transporte Ativo do Núcleo Celular
Animais
Linhagem Celular Transformada
Ácido Cítrico/metabolismo
Colágeno Tipo IV/genética
Colágeno Tipo IV/metabolismo
Fator de Crescimento do Tecido Conjuntivo/genética
Fator de Crescimento do Tecido Conjuntivo/metabolismo
Nefropatias Diabéticas/genética
Nefropatias Diabéticas/patologia
Fibronectinas/genética
Fibronectinas/metabolismo
Fibrose
Células Mesangiais/enzimologia
Células Mesangiais/patologia
Camundongos
Interferência de RNA
Fatores de Tempo
Transfecção
Fator de Crescimento Transformador beta1/genética
Fator de Crescimento Transformador beta1/metabolismo
Fator de Crescimento Transformador beta3/genética
Fator de Crescimento Transformador beta3/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type IV); 0 (Ctgf protein, mouse); 0 (Fibronectins); 0 (Histones); 0 (Tgfb1 protein, mouse); 0 (Tgfb3 protein, mouse); 0 (Transforming Growth Factor beta1); 0 (Transforming Growth Factor beta3); 139568-91-5 (Connective Tissue Growth Factor); 2968PHW8QP (Citric Acid); 72-89-9 (Acetyl Coenzyme A); EC 2.3.3.8 (ATP Citrate (pro-S)-Lyase); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170512
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00029.2017


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[PMID]:28474061
[Au] Autor:Wang GL; Yu YQ; Guo JJ; Qiu LH
[Ad] Endereço:Department of Endodontics, School of Stomatology, China Medical University; Liaoning Key Laboratory of Oral Diseases. Shenyang 110002, Liaoning Province, China. E-mail:451303080@qq.com.
[Ti] Título:[Inhibiting effect of transforming growth factor ß3 on IL-6 expression in MG63 induced by lipopolysaccharide].
[So] Source:Shanghai Kou Qiang Yi Xue;26(1):21-25, 2017 Feb.
[Is] ISSN:1006-7248
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:PURPOSE: To explore the effect of transforming growth factor ß3 (TGF-ß3) on IL-6 expression in inflammatory MG63, and the mechanism by which TGF-ß3 exert its anti-inflammatory effect. METHODS: Cell line MG63 was stimulated by 20 µg/mL lipopolysaccharide of Porphyromonas endodontalis (P.e-LPS) to establish the inflammatory model of osteoblast. TGF-ß3 or TGFß1 varying from 5 to 20 ng/mL was added together with P.e-LPS for 24 h, then the mRNA expression of IL-6 was detected by real-time PCR, the role of TGF-ß3 on IL-6 protein was further verified by ELISA. MG63 was pretreated with 10 ng/mL TGF-ß3 for 30 min in RPMI 1640 medium without fetal bovine serum (FBS), then the cells were cultured for another 20 min with 20 µg/mL P.e-LPS, the phosphorylation level of ERK1/2 was measured by Western blot. Statistical analysis was performed using one-way ANOVA with SPSS13.0 software package. RESULTS: The results of real-time PCR revealed that, when MG63 was treated with 20 µg/mL P.e-LPS alone, the mRNA expression of IL-6 increased significantly(P<0.01). When TGF-ß1 was added with P.e-LPS, it could barely decrease IL-6 prominently at the highest concentration (P<0.05).Whereas, the inhibition effect of TGF-ß3 on IL-6 was dramatic (P<0.01), ELISA results showed that 10-20 ng/mL TGF-ß3 blocked the IL-6 expression at protein level (P<0.05). 20 µg/mL P.e-LPS promoted the phosphorylation level of ERK1/2 in MG63(P<0.01), while with 10 ng/mL TGF-ß3, the effect of P.e-LPS on ERK1/2 was blocked(P<0.05). CONCLUSIONS: TGF-ß3 is more potent than TGF-ß1 in inhibiting MG63, and ERK1/2 is involved in its anti-inflammatory effect.
[Mh] Termos MeSH primário: Interleucina-6/metabolismo
Lipopolissacarídeos/metabolismo
Fator de Crescimento Transformador beta3/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular
Células Cultivadas
Proteína Quinase 3 Ativada por Mitógeno
Osteoblastos
Fosforilação
Porphyromonas endodontalis
RNA Mensageiro
Fator de Crescimento Transformador beta1
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IL6 protein, human); 0 (Interleukin-6); 0 (Lipopolysaccharides); 0 (RNA, Messenger); 0 (TGFB1 protein, human); 0 (Transforming Growth Factor beta1); 0 (Transforming Growth Factor beta3); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170608
[Lr] Data última revisão:
170608
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:170506
[St] Status:MEDLINE


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[PMID]:28364787
[Au] Autor:Nasroen SL; Tajrin A; Fauziah PN; Maskoen AM; Soemantri ES; Soedjana H; Hilmanto D
[Ad] Endereço:Oral and Maxillofacial Surgery Department, Dentistry Study Program Faculty of Medicine, Universitas Jenderal Achmad Yani Cimahi - Bandung Indonesia.
[Ti] Título:TGFß3 / SfaN1 gene variant and the risk factor of nonsyndromic cleft palate only among Indonesian patients.
[So] Source:Cell Mol Biol (Noisy-le-grand);63(2):88-91, 2017 Feb 28.
[Is] ISSN:1165-158X
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Non-syndromic cleft palate only (NS CPO) is one of the most common congenital malformations that affect between 1 in 1000 - 2500 live births worldwide. The etiopathogenesis of clefts including NS CPO has been widely studied but is still poorly understood. NS CPO is considered to be a genetically complex, multifactorial disease. Based on several studies, mutations of TGFß3 gene emerged as the strong candidate gene associated with NS CPO. The purpose of this study was to analyze the relationship between the TGFß3 / SfaN1 gene variant and the risk of NS CPO in Indonesian patients. This study was case control design using samples from 31 NS CPO subjects and 35 control subjects. DNA was extracted from venous blood and the segment of TGFß3 gene/ SfaN1 were amplified by using polymerase chain reaction (PCR) technique, then digestion products by SfaN1 restriction enzyme which can detect locus of gene variant / polymorphism from restriction fragment length polymorphisms (RFLP) method were evaluated. The results indicated that the gene variant as substitution of base G into A was identified in TGFß3 gene and the frequency of heterozygous mutant GA genotype was 63,6% in NS CPO subjects and 36,4% in control subjects. The frequency of heterozygous mutant GA genotype was associated with increased risk of NS CPO (odds ratio (OR) = 2,260, 95% CI = 0,592 - 8,625). In conclusion, TGFß3 gene / SfaN1 polymorphism can be considered as the risk factor associated with NS CPO in Indonesian patients.
[Mh] Termos MeSH primário: Fissura Palatina/genética
Predisposição Genética para Doença/genética
Polimorfismo de Nucleotídeo Único
Fator de Crescimento Transformador beta3/genética
[Mh] Termos MeSH secundário: Alelos
Sequência de Bases
Sítios de Ligação/genética
Fissura Palatina/patologia
Desoxirribonucleases de Sítio Específico do Tipo II/metabolismo
Frequência do Gene
Genótipo
Seres Humanos
Indonésia
Razão de Chances
Reação em Cadeia da Polimerase
Polimorfismo de Fragmento de Restrição
Fatores de Risco
Fator de Crescimento Transformador beta3/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (TGFB3 protein, human); 0 (Transforming Growth Factor beta3); EC 3.1.21.4 (Deoxyribonucleases, Type II Site-Specific); EC 3.2.21.- (endodeoxyribonuclease SfaNI)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170426
[Lr] Data última revisão:
170426
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170403
[St] Status:MEDLINE
[do] DOI:10.14715/cmb/2017.63.2.13



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