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  1 / 15601 MEDLINE  
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[PMID]:29408309
[Au] Autor:Mohamed DI; Nabih ES; El-Waseef DAA; El-Kharashi OA; Abd El Samad AA
[Ad] Endereço:Department of Pharmacology, Faculty of Medicine, Ain Shams University, Cairo, Egypt.
[Ti] Título:The protective effect of pentoxifylline versus silymarin on the pancreas through increasing adenosine by CD39 in a rat model of liver cirrhosis: Pharmacological, biochemical and histological study.
[So] Source:Gene;651:9-22, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Impaired glucose homoeostasis due to insulin resistance and decrease sensitivity of pancreatic ß-cells is a feature of liver disease and results into hepatogenous diabetes. Decrease expression of CD39 was linked to inflammation and occurrence of diabetes. Therefore, we performed this study to explore the protective effect of pentoxifylline (PTX) and silymarin administration on the ß-cells of the pancreas in a rat model of thioacetamide induced liver cirrhosis. Biochemical, histological and immunohistochemistry studies of the liver and pancreas were performed and provided an evidence on the protective effect of PTX to pancreatic ß-cells compared to silymarin. Also, silymarin induced a significant improvement of liver cirrhosis compared to PTX. In conclusion, the potential protective effect of PTX against ß-cells deterioration could be attributed to increasing pancreatic CD39 expression and the subsequent increase of adenosine.
[Mh] Termos MeSH primário: Adenosina/metabolismo
Antígenos CD/metabolismo
Apirase/metabolismo
Cirrose Hepática Experimental/tratamento farmacológico
Pâncreas/efeitos dos fármacos
Pentoxifilina/uso terapêutico
Substâncias Protetoras/uso terapêutico
Silimarina/uso terapêutico
[Mh] Termos MeSH secundário: Amilases/sangue
Animais
Modelos Animais de Doenças
Células Secretoras de Insulina/efeitos dos fármacos
Fígado/patologia
Cirrose Hepática Experimental/metabolismo
Cirrose Hepática Experimental/patologia
Testes de Função Hepática
Masculino
Pâncreas/patologia
Ratos
Ratos Wistar
Fator de Crescimento Transformador beta1/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Protective Agents); 0 (Silymarin); 0 (Transforming Growth Factor beta1); EC 3.2.1.- (Amylases); EC 3.6.1.5 (Apyrase); EC 3.6.1.5 (CD39 antigen); K72T3FS567 (Adenosine); SD6QCT3TSU (Pentoxifylline)
[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:180207
[St] Status:MEDLINE


  2 / 15601 MEDLINE  
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[PMID]:29337059
[Au] Autor:Lin L; Li M; Lin L; Xu X; Jiang G; Wu L
[Ad] Endereço:Department of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai 200433, China; Tongji University School of Medicine, Shanghai 200092, China.
[Ti] Título:FPPS mediates TGF-ß1-induced non-small cell lung cancer cell invasion and the EMT process via the RhoA/Rock1 pathway.
[So] Source:Biochem Biophys Res Commun;496(2):536-541, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Farnesyl pyrophosphate synthase (FPPS), a key enzyme in the mevalonate pathway, was recently shown to play a role in cancer progression. However, its role in non-small cell lung cancer (NSCLC) metastasis and the underlying mechanism remain unclear. In this study, FPPS expression was significantly correlated with TNM stage, and metastasis. Inhibition or knockdown of FPPS blocked TGF-ß1-induced cell invasion and epithelial-to-mesenchymal transition (EMT) process. FPPS expression of FPPS was induced by TGF-ß1 and FPPS promoted cell invasion and EMT via the RhoA/Rock1 pathway. In conclusion, FPPS mediates TGF-ß1-induced lung cancer cell invasion and EMT via the RhoA/Rock1 pathway. These findings suggest new treatment strategies to reduce mortality associated with metastasis in patients with NSCLC.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/metabolismo
Transição Epitelial-Mesenquimal
Geraniltranstransferase/metabolismo
Neoplasias Pulmonares/metabolismo
Fator de Crescimento Transformador beta1/metabolismo
Quinases Associadas a rho/metabolismo
Proteína rhoA de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Idoso
Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma Pulmonar de Células não Pequenas/patologia
Linhagem Celular Tumoral
Feminino
Regulação Neoplásica da Expressão Gênica
Geraniltranstransferase/análise
Geraniltranstransferase/genética
Seres Humanos
Pulmão/metabolismo
Pulmão/patologia
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
Masculino
Meia-Idade
Invasividade Neoplásica/genética
Invasividade Neoplásica/patologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Transforming Growth Factor beta1); EC 2.5.1.10 (Geranyltranstransferase); EC 2.7.11.1 (ROCK1 protein, human); EC 2.7.11.1 (rho-Associated Kinases); EC 3.6.5.2 (rhoA GTP-Binding Protein)
[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:180117
[St] Status:MEDLINE


  3 / 15601 MEDLINE  
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[PMID]:28453765
[Au] Autor:Marafini I; Monteleone I; Dinallo V; Di Fusco D; De Simone V; Laudisi F; Fantini MC; Di Sabatino A; Pallone F; Monteleone G
[Ad] Endereço:Department of Systems Medicine, University of Rome 'Tor Vergata', Rome, Italy.
[Ti] Título:CCL20 Is Negatively Regulated by TGF-ß1 in Intestinal Epithelial Cells and Reduced in Crohn's Disease Patients With a Successful Response to Mongersen, a Smad7 Antisense Oligonucleotide.
[So] Source:J Crohns Colitis;11(5):603-609, 2017 May 01.
[Is] ISSN:1876-4479
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Background and Aims: The chemokine CCL20 is over-produced in epithelium of Crohn's disease [CD] patients and contributes to recruiting immune cells to inflamed gut. Tumour necrosis factor-α [TNF-α] is a powerful inducer of CCL20 in intestinal epithelial cells. In CD, high levels of Smad7 block the activity of transforming growth factor-ß1 [TGF-ß1], a negative regulator of TNF signalling. We investigated whether intestinal epithelial cell-derived CCL20 is negatively regulated by TGF-ß1 and whether Smad7 knock-down reduces CCL20 in CD. Methods: CCL20 was evaluated in NCM460, a normal colonic epithelial cell line, stimulated with TGF-ß1 and TNF-α, and in Smad7 over-expressing NCM460 cells. CCL20 and Smad7 expression were assessed in sections of CD intestinal specimens by immunochemistry, and in CD colonic explants treated with mongersen, a Smad7 antisense oligonucleotide. CCL20 was examined in serum samples taken from 95 of 166 active CD patients receiving mongersen or placebo for 2 weeks and participating in a phase II, multicentre, double-blind, placebo-controlled study. Results: CCL20 expression was increased by TNF-α, and this effect was inhibited by TGF-ß1 in NCM460 cells, but not in Smad7 over-expressing NCM460 cells. In CD, epithelium CCL20 and Smad7 co-localised, and treatment of CD explants with mongersen reduced CCL20 production. During follow-up, in responders to mongersen, serum CCL20 levels significantly decreased, whereas patients without response/remission to mongersen and placebo patients did not have change in CCL20. Conclusions: TGF-ß1 reduces intestinal epithelial cell-derived CCL20 production, an effect abrogated by Smad7. CD patients responding to mongersen demonstrated a reduction in serum CCL20.
[Mh] Termos MeSH primário: Quimiocina CCL20/metabolismo
Doença de Crohn/tratamento farmacológico
Mucosa Intestinal/metabolismo
Oligonucleotídeos/uso terapêutico
Proteína Smad7/antagonistas & inibidores
Fator de Crescimento Transformador beta1/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular
Quimiocina CCL20/sangue
Doença de Crohn/metabolismo
Método Duplo-Cego
Seres Humanos
Mucosa Intestinal/efeitos dos fármacos
Resultado do Tratamento
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (CCL20 protein, human); 0 (Chemokine CCL20); 0 (GED0301); 0 (Oligonucleotides); 0 (SMAD7 protein, human); 0 (Smad7 Protein); 0 (Transforming Growth Factor beta1)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/ecco-jcc/jjw191


  4 / 15601 MEDLINE  
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[PMID]:29428600
[Au] Autor:Yao ZH; Xie HJ; Yuan YL; Huo YT; Cao J; Lai WY; Cai RJ; Cheng YX
[Ad] Endereço:Department of Respiratory Disease, Academy of Orthopedics of Guangdong Province, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China; Department of Respiratory Disease, Hengyang NO.1 Peoples Hospital, Hengyang, Hunan, China.
[Ti] Título:Contraction-dependent TGF-ß1 activation is required for thrombin-induced remodeling in human airway smooth muscle cells.
[So] Source:Life Sci;197:130-139, 2018 Mar 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Thrombin is a serine proteinase that is not only involved in coagulation cascade, but also mediates a number of biological responses relevant to tissues repair, and induces bronchoconstriction. TGF-ß plays a pivotal role in airway remodeling due to its effects on airway smooth muscle proliferation and extracellular matrix (ECM) deposition. Recently, bronchoconstriction itself is found to constitute a form of strain and is highly relevant to asthmatic airway remodeling. However, the underlying mechanisms remain unknown. Here, we investigated the role of contraction- dependent TGF-ß activation in thrombin-induced remodeling in human airway smooth muscle (HASM) cells. MATERIALS AND METHODS: Primary HASM cells were treated with or without thrombin in the absence or presence of anti-TGF-ß antibody, cytochalasin D and formoterol. CFSE labeling index or CCK-8 assay were performed to test cell proliferation. RT-PCR and Western blotting were used to examined ECM mRNA level and collagen Iα1, α-actin protein expression, respectively. Immunofluorescence was also used to confirm contraction induced by thrombin in HASM cells. KEY FINDING: Thrombin stimulation enhanced HASM cells proliferation and activated TGF-ß signaling. Thrombin induced ECM mRNA and collagen Iα1 protein expression, and these effects are mediated by TGF-ß. Abrogation of TGF-ß activation by contraction inhibitors cytochalasin D and formoterol prevents the thrombin-induced effects. SIGNIFICANCE: These findings suggest that contraction-dependent TGF-ß activation could be a mechanism by which thrombin leads to the development of asthmatic airway remodeling. Blocking physical forces with bronchodilator would be an intriguing way in reducing airway remodeling in asthma.
[Mh] Termos MeSH primário: Remodelação das Vias Aéreas/efeitos dos fármacos
Brônquios/metabolismo
Proliferação Celular/efeitos dos fármacos
Miócitos de Músculo Liso/metabolismo
Transdução de Sinais/efeitos dos fármacos
Trombina/farmacologia
Fator de Crescimento Transformador beta1/metabolismo
[Mh] Termos MeSH secundário: Brônquios/patologia
Células Cultivadas
Seres Humanos
Miócitos de Músculo Liso/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (TGFB1 protein, human); 0 (Transforming Growth Factor beta1); EC 3.4.21.5 (Thrombin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180212
[St] Status:MEDLINE


  5 / 15601 MEDLINE  
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[PMID]:29402324
[Au] Autor:Chi C; Liu XY; Hou F; Yu XZ; Li CY; Cui LJ; Liu RX; Yin CH
[Ad] Endereço:Department of Internal Medicine, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing, 100026, China.
[Ti] Título:Herbal compound 861 prevents hepatic fibrosis by inhibiting the TGF-ß1/Smad/SnoN pathway in bile duct-ligated rats.
[So] Source:BMC Complement Altern Med;18(1):52, 2018 Feb 05.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: This study was to evaluate the effects of herbal compound 861 (Cpd861) on ski-related novel protein N (SnoN) and transforming growth factor-ß1 (TGF-ß1) /Smad signaling in rats with bile duct ligation (BDL)-induced hepatic fibrosis, and to explore the mechanisms of Cpd861 on hepatic fibrosis. METHODS: Thirty Wistar male rats were randomly divided into three groups: sham operation, BDL, and Cpd861. To induce hepatic fibrosis, BDL and Cpd861 group rats underwent bile duct ligation. Cpd861 at 9 g/kg/d or an equal volume of normal saline was administered intragastrically for 28 days. Liver injury was assessed biochemically and histologically. Protein and mRNA changes for SnoN and TGF-ß1/Smad signaling (TGF-ß1, Smad2, phosphorylated Smad2 [p-Smad2], phosphorylated Smad3 [p-Smad3], fibronectin, and collagen III) were determined by Western blotting and quantitative real-time PCR. RESULTS: BDL rats treated with Cpd861 had significantly alleviated hepatic fibrosis compared to BDL rats not receiving Cpd861 treatment. Moreover, Cpd861 decreased the expression of fibrosis-associated proteins fibronectin and collagen III in liver tissue. Cpd861 administration increased the expression of SnoN protein, did not change SnoN mRNA level, and decreased TGF-ß1, p-Smad2, and p-Smad3 protein expression compared to BDL without Cpd861 treatment. CONCLUSIONS: Cpd861 attenuates hepatic fibrosis by increasing SnoN protein expression and inhibiting the TGF-ß1/Smad signaling pathway.
[Mh] Termos MeSH primário: Medicamentos de Ervas Chinesas/farmacologia
Cirrose Hepática/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Transdução de Sinais/efeitos dos fármacos
Proteínas Smad/metabolismo
Fatores de Transcrição/metabolismo
Fator de Crescimento Transformador beta1/metabolismo
[Mh] Termos MeSH secundário: Animais
Ductos Biliares/lesões
Ductos Biliares/cirurgia
Modelos Animais de Doenças
Imuno-Histoquímica
Fígado/química
Fígado/efeitos dos fármacos
Fígado/metabolismo
Masculino
Proteínas do Tecido Nervoso/análise
Proteínas do Tecido Nervoso/genética
Ratos
Ratos Wistar
Proteínas Smad/análise
Proteínas Smad/genética
Fatores de Transcrição/análise
Fatores de Transcrição/genética
Fator de Crescimento Transformador beta1/análise
Fator de Crescimento Transformador beta1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drugs, Chinese Herbal); 0 (Nerve Tissue Proteins); 0 (Smad Proteins); 0 (SnoN protein, rat); 0 (Transcription Factors); 0 (Transforming Growth Factor beta1); 0 (herbal compound 861)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-018-2119-7


  6 / 15601 MEDLINE  
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[PMID]:29284784
[Au] Autor:Liubich LD; Kovalevska L; Lisyany MI; Semenova VM; Malysheva TA; Stayno LP; Vaslovych VV
[Ad] Endereço:SI "Romodanov Neurosurgery Institute, National Academy of Medical Sciences of Ukraine", Kyiv 04050, Ukraine.
[Ti] Título:TGF-ß1 expression by glioma C6 cells in vitro.
[So] Source:Exp Oncol;39(4):258-263, 2017 Dec.
[Is] ISSN:1812-9269
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:The aim of the work was to study the impact of fetal rat brain cell supernatant (FRBCS) on the expression of transforming growth factor ß1 (TGF-ß1) and p53 in C6 cells of rat glioma in vitro. MATERIALS AND METHODS: FRBCS was obtained from suspensions of fetal rat brain cells on the 14 (E14) day of gestation. C6 glioma cells were cultured for 48 h in the presence of FRBCS or FRBCS + anti-TGF-ß1 monoclonal antibody. Immunocytochemical staining for TGF-ß1 and p53 was performed. RESULTS: The proportion of TGF-ß1-immunopositive tumor cells in C6 glioma cultures was statistically significantly higher than in the control cell cultures of normal fetal rat brain. FRBCS reduced the proportion of TGF-ß1-immunopositive tumor cells and increased the proportion of p53-immunopositive cells in C6 glioma cultures. In cells cultured with FRBCS + anti-TGF-ß1 monoclonal antibody, the above effects of FRBCS were abrogated. CONCLUSION: The obtained results suggest that TGF-ß1 seems to be responsible for decrease in TGF-ß1 expression and increase in p53 expression in C6 glioma cells treated with FRBCS.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/metabolismo
Glioma/metabolismo
Fator de Crescimento Transformador beta1/biossíntese
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Transforming Growth Factor beta1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171230
[St] Status:MEDLINE


  7 / 15601 MEDLINE  
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[PMID]:29195901
[Au] Autor:Chen H; Chen Q; Jiang CM; Shi GY; Sui BW; Zhang W; Yang LZ; Li ZY; Liu L; Su YM; Zhao WC; Sun HQ; Li ZZ; Fu Z
[Ad] Endereço:Department of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, China; China International Science and Technology Cooperation base of Child development and Critical Disorders, China; Chongqing Engineeri
[Ti] Título:Triptolide suppresses paraquat induced idiopathic pulmonary fibrosis by inhibiting TGFB1-dependent epithelial mesenchymal transition.
[So] Source:Toxicol Lett;284:1-9, 2018 Mar 01.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Idiopathic pulmonary fibrosis (IPF) and tumor are highly similar to abnormal cell proliferation that damages the body. This malignant cell evolution in a stressful environment closely resembles that of epithelial-mesenchymal transition (EMT). As a popular EMT-inducing factor, TGFß plays an important role in the progression of multiple diseases. However, the drugs that target TGFB1 are limited. In this study, we found that triptolide (TPL), a Chinese medicine extract, exerts an anti-lung fibrosis effect by inhibiting the EMT of lung epithelial cells. In addition, triptolide directly binds to TGFß and subsequently increase E-cadherin expression and decrease vimentin expression. In in vivo studies, TPL improves the survival state and inhibits lung fibrosis in mice. In summary, this study revealed the potential therapeutic effect of paraquat induced TPL in lung fibrosis by regulating TGFß-dependent EMT progression.
[Mh] Termos MeSH primário: Diterpenos/uso terapêutico
Medicamentos de Ervas Chinesas/uso terapêutico
Transição Epitelial-Mesenquimal/efeitos dos fármacos
Fibrose Pulmonar Idiopática/prevenção & controle
Paraquat/toxicidade
Fenantrenos/uso terapêutico
Fator de Crescimento Transformador beta1/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Movimento Celular/efeitos dos fármacos
Modelos Animais de Doenças
Diterpenos/farmacologia
Medicamentos de Ervas Chinesas/farmacologia
Células Epiteliais/efeitos dos fármacos
Células Epiteliais/metabolismo
Células Epiteliais/patologia
Compostos de Epóxi/farmacologia
Compostos de Epóxi/uso terapêutico
Seres Humanos
Fibrose Pulmonar Idiopática/induzido quimicamente
Fibrose Pulmonar Idiopática/metabolismo
Fibrose Pulmonar Idiopática/patologia
Pulmão/efeitos dos fármacos
Pulmão/metabolismo
Pulmão/patologia
Camundongos
Simulação de Acoplamento Molecular
Fenantrenos/farmacologia
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Diterpenes); 0 (Drugs, Chinese Herbal); 0 (Epoxy Compounds); 0 (Phenanthrenes); 0 (Tgfb1 protein, mouse); 0 (Transforming Growth Factor beta1); 19ALD1S53J (triptolide); PLG39H7695 (Paraquat)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171203
[St] Status:MEDLINE


  8 / 15601 MEDLINE  
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[PMID]:28456773
[Au] Autor:Beck B
[Ad] Endereço:Medical Centre of Science and Diagnostic BB-Med, Medical Laboratory, Opole, Poland. brygida.beck@bb-med.pl.
[Ti] Título:Transforming growth factor-ß1 and tumor necrosis factor-α concentration in serum during disturbed lymph flow from a liver in rats.
[So] Source:J Physiol Pharmacol;68(1):91-98, 2017 Feb.
[Is] ISSN:1899-1505
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:In the last decades an increasing attention has been devoted to the role of lymphatic system in pathomechanism. The disturbed lymph flow from a liver contributes to liver fibrogenesis and probably to hepatocirrhosis. Cytokines play a major role in the development of hepatic fibrosis, the wound-healing response of the liver to chronic injury. Cytokines in hepatic fibrogenesis may be pro- or antifibrogenic. Transforming growth factor-ß1 (TGF-ß1) is pro-fibrogenic cytokine and plays a key role in liver fibrogenesis. Interferon-γ (INF-γ) is anti-fibrogenic by downregulating hepatic stellate cell activation. We described the negative correlation between tumor necrosis factor-α (TNF-α) and IFN-γ concentration in serum during disturbed lymph flow from a liver of rats. TNF-α plays a antifibrogenic role in liver fibrogenesis too. Male Albino Wistar rats weighing 250 - 300 grams were selected for the experiment. The animals were kept in stable condition and were fed a standard diet with no fluid restriction. The rats were divided into 3 groups: group B - mechanical insufficiency was obtained by ligation of hepatic trunc, group K - underwent sham operation, group 0 - rats not subjected to any surgery. The animals were sacrificed for experiment in 1, 3, 7, 14, 21, 28, 35, 56 and 103 day after operation. During experiment TGF-ß1 and TNF-α concentration in serum were assayed. We observed a positive correlation between TGF-ß1 and TNF-α concentration in serum. During disturbed lymph flow from the liver TNF-α plays probably a antifibrogenic role in liver fibrogenesis.
[Mh] Termos MeSH primário: Cirrose Hepática/sangue
Fígado/metabolismo
Fator de Crescimento Transformador beta1/sangue
Fator de Necrose Tumoral alfa/sangue
[Mh] Termos MeSH secundário: Animais
Cirrose Hepática/metabolismo
Linfa/metabolismo
Masculino
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Transforming Growth Factor beta1); 0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


  9 / 15601 MEDLINE  
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[PMID]:28467929
[Au] Autor:Calvier L; Chouvarine P; Legchenko E; Hoffmann N; Geldner J; Borchert P; Jonigk D; Mozes MM; Hansmann G
[Ad] Endereço:Department of Pediatric Cardiology and Critical Care, Hannover Medical School, Hannover 30625, Germany.
[Ti] Título:PPARγ Links BMP2 and TGFß1 Pathways in Vascular Smooth Muscle Cells, Regulating Cell Proliferation and Glucose Metabolism.
[So] Source:Cell Metab;25(5):1118-1134.e7, 2017 May 02.
[Is] ISSN:1932-7420
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BMP2 and TGFß1 are functional antagonists of pathological remodeling in the arteries, heart, and lung; however, the mechanisms in VSMCs, and their disturbance in pulmonary arterial hypertension (PAH), are unclear. We found a pro-proliferative TGFß1-Stat3-FoxO1 axis in VSMCs, and PPARγ as inhibitory regulator of TGFß1-Stat3-FoxO1 and TGFß1-Smad3/4, by physically interacting with Stat3 and Smad3. TGFß1 induces fibrosis-related genes and miR-130a/301b, suppressing PPARγ. Conversely, PPARγ inhibits TGFß1-induced mitochondrial activation and VSMC proliferation, and regulates two glucose metabolism-related enzymes, platelet isoform of phosphofructokinase (PFKP, a PPARγ target, via miR-331-5p) and protein phosphatase 1 regulatory subunit 3G (PPP1R3G, a Smad3 target). PPARγ knockdown/deletion in VSMCs activates TGFß1 signaling. The PPARγ agonist pioglitazone reverses PAH and inhibits the TGFß1-Stat3-FoxO1 axis in TGFß1-overexpressing mice. We identified PPARγ as a missing link between BMP2 and TGFß1 pathways in VSMCs. PPARγ activation can be beneficial in TGFß1-associated diseases, such as PAH, parenchymal lung diseases, and Marfan's syndrome.
[Mh] Termos MeSH primário: Proteína Morfogenética Óssea 2/metabolismo
Proliferação Celular
Glucose/metabolismo
Miócitos de Músculo Liso/citologia
PPAR gama/metabolismo
Transdução de Sinais
Fator de Crescimento Transformador beta1/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Feminino
Masculino
Camundongos Endogâmicos C57BL
Músculo Liso Vascular/citologia
Músculo Liso Vascular/metabolismo
Miócitos de Músculo Liso/metabolismo
Artéria Pulmonar/citologia
Artéria Pulmonar/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bone Morphogenetic Protein 2); 0 (PPAR gamma); 0 (Transforming Growth Factor beta1); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:29390467
[Au] Autor:Tian Y; Wang Y; Chen W; Yin Y; Qin M
[Ad] Endereço:Department of Cardiology, the Second Affiliated Hospital of Chongqing Medical University, the Chongqing Cardiac Arrhythmia Service Center, Chongqing.
[Ti] Título:Role of serum TGF-ß1 level in atrial fibrosis and outcome after catheter ablation for paroxysmal atrial fibrillation.
[So] Source:Medicine (Baltimore);96(51):e9210, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study aimed to evaluate the relationship between serum transforming growth factor-ß1 (TGF-ß1) concentration and atrial fibrosis and to determine whether plasma TGF-ß1 concentration is an independent predictor of atrial fibrillation (AF) recurrence after catheter ablation.We included 98 consecutive patients who underwent catheter ablation, including 38 with paroxysmal AF (AF group) and 60 with paroxysmal supraventricular tachycardia (control group). We compared their preablation serum concentration of biomarkers and clinical and echocardiographic findings.Serum TGF-ß1 concentrations, type-III procollagen N-terminal peptides (PIIINP), type-IV procollagen (IV-C), and laminin (LN) were significantly higher in the AF group than in the control group; however, there was no correlation between their concentrations and left atrial diameter (LAD). The area of the low-voltage zone positively correlated with TGF-ß1 and PIIINP concentrations, but not with LAD. Atrial tachyarrhythmia (AF and AFL/AT) recurrence was observed in 15 patients (39.4%) at mean 241.4 ± 68.5 days of follow-up 12 months after ablation. Regression analysis revealed that TGF-ß1 was a major risk factor for AF recurrence (odds ratio, 1.14; 95% confidence interval, 1.11-1.17; P = .02).Serum TGF-ß1 concentration is an independent predictor of AF recurrence in patients with paroxysmal AF and may help identify patients likely to have better outcomes after catheter ablation.
[Mh] Termos MeSH primário: Fibrilação Atrial/sangue
Fibrilação Atrial/cirurgia
Ablação por Cateter/métodos
Átrios do Coração/patologia
Fator de Crescimento Transformador beta1/sangue
[Mh] Termos MeSH secundário: Adulto
Idoso
Análise de Variância
Fibrilação Atrial/diagnóstico por imagem
Biomarcadores/sangue
Estudos de Casos e Controles
Ablação por Cateter/efeitos adversos
Feminino
Fibrose/patologia
Seguimentos
Seres Humanos
Masculino
Meia-Idade
Valor Preditivo dos Testes
Estudos Prospectivos
Recidiva
Valores de Referência
Medição de Risco
Sensibilidade e Especificidade
Resultado do Tratamento
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Transforming Growth Factor beta1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009210



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