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[PMID]:29381717
[Au] Autor:Tobolowsky FA; Wada N; Martinez-Maza O; Magpantay L; Koletar SL; Palella FJ; Brown TT; Lake JE
[Ad] Endereço:Department of Internal Medicine, Division of Infectious Diseases, University of Colorado, Denver, Colorado, United States of America.
[Ti] Título:Brief report: Circulating markers of fibrosis are associated with immune reconstitution status in HIV-infected men.
[So] Source:PLoS One;13(1):e0191606, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Lymphoid tissue fibrosis may contribute to incomplete immune reconstitution on antiretroviral therapy (ART) via local CD4+ T lymphocyte (CD4) depletion. Hyaluronic acid (HA) increases with fibrotic burden. CXCL4 concentrations increase in response to pro-fibrotic stimuli, but lower CXCL4 concentrations in HIV-infected individuals may reflect successful immune evasion by HIV. We investigated relationships between circulating HA and CXCL4 concentrations and immune reconstitution on ART in HIV-infected Multicenter AIDS Cohort Study participants. METHODS: HIV-infected men on ART for >1 year with cryopreserved plasma samples and suppressed post-ART HIV-1 RNA were included. Men with post-ART CD4 <200 cells/mm3 were defined as immunologic non-responders (n = 25). Age-/race-matched men with post-ART CD4 >500 cells/mm3 served as controls (n = 49). HA and CXCL4 concentrations were measured via ELISA. RESULTS: Median pre-ART CD4 was 297 cells/mm3 for non-responders vs 386 cells/mm3 for controls. Median post-ART CD4 was 141 cells/mm3 for non-responders and 815 cells/mm3 for controls. HIV infection duration was 23 years, with median time on ART 13 years for non-responders vs 11 years for controls. Pre-ART HA and CXCL4 concentrations did not vary by eventual immune reconstitution status. Post-ART HA concentrations tended to be higher (85 vs 36 ng/mL, p = 0.07) and CXCL4 concentrations were lower (563 vs 1459 ng/mL, p = 0.01) among non-responders. Among men with paired pre-/post-ART samples, non-responders had greater HA increases and CXCL4 decreases than controls (HA: 50 vs 12 ng/mL, p = 0.04; CXCL4: -1258 vs -405 ng/mL, p = 0.01). CONCLUSIONS: Higher circulating concentrations of HA and lower concentrations of CXCL4 are associated with failure of immune reconstitution on ART.
[Mh] Termos MeSH primário: Biomarcadores/sangue
Infecções por HIV/imunologia
[Mh] Termos MeSH secundário: Fármacos Anti-HIV/uso terapêutico
Contagem de Linfócito CD4
Fibrose
Infecções por HIV/sangue
Infecções por HIV/tratamento farmacológico
Seres Humanos
Ácido Hialurônico/metabolismo
Tecido Linfoide/patologia
Masculino
Meia-Idade
Fator Plaquetário 4/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-HIV Agents); 0 (Biomarkers); 37270-94-3 (Platelet Factor 4); 9004-61-9 (Hyaluronic Acid)
[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:180131
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191606


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[PMID]:29320561
[Au] Autor:Zhao W; Wang X; Sun KH; Zhou L
[Ad] Endereço:Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America.
[Ti] Título:α-smooth muscle actin is not a marker of fibrogenic cell activity in skeletal muscle fibrosis.
[So] Source:PLoS One;13(1):e0191031, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:α-Smooth muscle actin (α-SMA) is used as a marker for a subset of activated fibrogenic cells, myofibroblasts, which are regarded as important effector cells of tissue fibrogenesis. We address whether α-SMA-expressing myofibroblasts are detectable in fibrotic muscles of mdx5cv mice, a mouse model for Duchenne muscular dystrophy (DMD), and whether the α-SMA expression correlates with the fibrogenic function of intramuscular fibrogenic cells. α-SMA immunostaining signal was not detected in collagen I (GFP)-expressing cells in fibrotic muscles of ColI-GFP/mdx5cv mice, but it was readily detected in smooth muscle cells lining intramuscular blood vessel walls. α-SMA expression was detected by quantitative RT-PCR and Western blot in fibrogenic cells sorted from diaphragm and quadriceps muscles of the ColI-GFP/mdx5cv mice. Consistent with the more severe fibrosis in the ColI-GFP/mdx5cv diaphragm, the fibrogenic cells in the diaphragm exerted a stronger fibrogenic function than the fibrogenic cells in the quadriceps as gauged by their extracellular matrix gene expression. However, both gene and protein expression of α-SMA was lower in the diaphragm fibrogenic cells than in the quadriceps fibrogenic cells in the ColI-GFP/mdx5cv mice. We conclude that myofibroblasts are present in fibrotic skeletal muscles, but their expression of α-SMA is not detectable by immunostaining. The level of α-SMA expression by intramuscular fibrogenic cells does not correlate positively with the level of collagen gene expression or the severity of skeletal muscle fibrosis in the mdx5cv mice. α-SMA is not a functional marker of fibrogenic cells in skeletal muscle fibrosis associated with muscular dystrophy.
[Mh] Termos MeSH primário: Actinas/metabolismo
Biomarcadores/metabolismo
Músculo Esquelético/metabolismo
[Mh] Termos MeSH secundário: Animais
Western Blotting
Fibrose
Camundongos
Camundongos Endogâmicos C57BL
Músculo Esquelético/patologia
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Actins); 0 (Biomarkers); 0 (alpha-smooth muscle actin, mouse)
[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:180111
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191031


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[PMID]:28453729
[Au] Autor:Chen Z; Xie J; Hao H; Lin H; Wang L; Zhang Y; Chen L; Cao S; Huang X; Liao W; Bin J; Liao Y
[Ad] Endereço:State Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, 1838, Guangzhou Avenue North, Guangzhou 510515, China.
[Ti] Título:Ablation of periostin inhibits post-infarction myocardial regeneration in neonatal mice mediated by the phosphatidylinositol 3 kinase/glycogen synthase kinase 3ß/cyclin D1 signalling pathway.
[So] Source:Cardiovasc Res;113(6):620-632, 2017 May 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aims: To resolve the controversy as to whether periostin plays a role in myocardial regeneration after myocardial infarction (MI), we created a neonatal mouse model of MI to investigate the influence of periostin ablation on myocardial regeneration and clarify the underlying mechanisms. Methods and results: Neonatal periostin-knockout mice and their wildtype littermates were subjected to MI or sham surgery. In the wildtype mice after MI, fibrosis was detectable at 3 days and fibrotic tissue was completely replaced by regenerated myocardium at 21 days. In contrast, in the knockout mice, significant fibrosis in the infarcted area was present at even 3 weeks after MI. Levels of phosphorylated-histone 3 and aurora B in the myocardium, detected by immunofluorescence and western blotting, were significantly lower in knockout than in wildtype mice at 7 days after MI. Similarly, angiogenesis was decreased in the knockout mice after MI. Expression of both the endothelial marker CD-31 and α-smooth muscle actin was markedly lower in the knockout than in wildtype mice at 7 days after MI. The knockout MI group had elevated levels of glycogen synthase kinase (GSK) 3ß and decreased phosphatidylinositol 3-kinase (PI3K), phosphorylated serine/threonine protein kinase B (p-Akt), and cyclin D1, compared with the wildtype MI group. Similar effects were observed in experiments using cultured cardiomyocytes from neonatal wildtype or periostin knockout mice. Administration of SB216763, a GSK3ß inhibitor, to knockout neonatal mice decreased myocardial fibrosis and increased angiogenesis in the infarcted area after MI. Conclusion: Ablation of periostin suppresses post-infarction myocardial regeneration by inhibiting the PI3K/GSK3ß/cyclin D1 signalling pathway, indicating that periostin is essential for myocardial regeneration.
[Mh] Termos MeSH primário: Moléculas de Adesão Celular/deficiência
Ciclina D1/metabolismo
Infarto do Miocárdio/enzimologia
Miocárdio/enzimologia
Fosfatidilinositol 3-Quinase/metabolismo
Regeneração
Proteínas Repressoras/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Moléculas de Adesão Celular/genética
Células Cultivadas
Modelos Animais de Doenças
Fibrose
Camundongos Knockout
Infarto do Miocárdio/genética
Infarto do Miocárdio/patologia
Infarto do Miocárdio/fisiopatologia
Miocárdio/patologia
Neovascularização Fisiológica
Fosforilação
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas c-akt/metabolismo
Regeneração/efeitos dos fármacos
Proteínas Repressoras/antagonistas & inibidores
Transdução de Sinais/efeitos dos fármacos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccnd1 protein, mouse); 0 (Cell Adhesion Molecules); 0 (GSKIP protein, mouse); 0 (Postn protein, mouse); 0 (Protein Kinase Inhibitors); 0 (Repressor Proteins); 136601-57-5 (Cyclin D1); EC 2.7.1.137 (Phosphatidylinositol 3-Kinase); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1802
[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/cvr/cvx001


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[PMID]:28453726
[Au] Autor:Li J; Yousefi K; Ding W; Singh J; Shehadeh LA
[Ad] Endereço:Department of Medicine, Division of Cardiology, University of Miami Leonard M. Miller School of Medicine, Miami, FL 33136, USA.
[Ti] Título:Osteopontin RNA aptamer can prevent and reverse pressure overload-induced heart failure.
[So] Source:Cardiovasc Res;113(6):633-643, 2017 May 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aims: Cardiac myocyte hypertrophy, the main compensatory response to chronic stress in the heart often progresses to a state of decompensation that can lead to heart failure. Osteopontin (OPN) is an effector for extracellular signalling that induces myocyte growth and fibrosis. Although increased OPN activity has been observed in stressed myocytes and fibroblasts, the detailed and long term effects of blocking OPN signalling on the heart remain poorly defined. Targeting cardiac OPN protein by an RNA aptamer may be beneficial for tuning down OPN pathologic signalling. We aimed to demonstrate the therapeutic effects of an OPN RNA aptamer on cardiac dysfunction. Methods and results: In vivo, we show that in a mouse model of pressure overload, treating at the time of surgeries with an OPN aptamer prevented cardiomyocyte hypertrophy and cardiac fibrosis, blocked OPN downstream signalling (PI3K and Akt phosphorylation), reduced expression of extracellular matrix (Lum, Col3a1, Fn1) and hypertrophy (Nppa, Nppb) genes, and prevented cardiac dysfunction. Treating at two months post-surgeries with the OPN aptamer reversed cardiac dysfunction and fibrosis and myocyte hypertrophy. While genetic homozygous deletion of OPN reduced myocardial wall thickness, surprisingly cardiac function and myocardial fibrosis, specifically collagen deposition and myofibroblast infiltration, were worse compared with wild type mice at three months of pressure overload. Conclusion: Taken together, these data demonstrate that tuning down cardiac OPN signalling by an OPN RNA aptamer is a novel and effective approach for preventing cardiac hypertrophy and fibrosis, improving cardiac function, and reversing pressure overload-induced heart failure.
[Mh] Termos MeSH primário: Aorta/fisiopatologia
Aptâmeros de Nucleotídeos/metabolismo
Pressão Arterial
Insuficiência Cardíaca/prevenção & controle
Hipertrofia Ventricular Esquerda/prevenção & controle
Miocárdio/metabolismo
Osteopontina/metabolismo
Disfunção Ventricular Esquerda/prevenção & controle
Função Ventricular Esquerda
Remodelação Ventricular
[Mh] Termos MeSH secundário: Animais
Aorta/cirurgia
Aptâmeros de Nucleotídeos/genética
Colágeno Tipo III/metabolismo
Citocinas/metabolismo
Modelos Animais de Doenças
Fibrose
Regulação da Expressão Gênica
Predisposição Genética para Doença
Insuficiência Cardíaca/genética
Insuficiência Cardíaca/metabolismo
Insuficiência Cardíaca/fisiopatologia
Hipertrofia Ventricular Esquerda/genética
Hipertrofia Ventricular Esquerda/metabolismo
Hipertrofia Ventricular Esquerda/fisiopatologia
Ligadura
Lumicana/metabolismo
Camundongos da Linhagem 129
Camundongos Endogâmicos C57BL
Camundongos Knockout
Miocárdio/patologia
Osteopontina/deficiência
Osteopontina/genética
Fenótipo
Fosfatidilinositol 3-Quinase/metabolismo
Fosforilação
Proteínas Proto-Oncogênicas c-akt/metabolismo
Transdução de Sinais
Fatores de Tempo
Disfunção Ventricular Esquerda/genética
Disfunção Ventricular Esquerda/metabolismo
Disfunção Ventricular Esquerda/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aptamers, Nucleotide); 0 (COL3A1 protein, mouse); 0 (Collagen Type III); 0 (Cytokines); 0 (Lum protein, mouse); 0 (Lumican); 0 (Spp1 protein, mouse); 106441-73-0 (Osteopontin); EC 2.7.1.137 (Phosphatidylinositol 3-Kinase); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1802
[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/cvr/cvx016


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[PMID]:29374928
[Au] Autor:Song CL; Yao M
[Ad] Endereço:Department of Plastic Surgery and Burns, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201900, China.
[Ti] Título:[Advances in the research of relationship between CD26 and hypertrophic scar and keloid].
[So] Source:Zhonghua Shao Shang Za Zhi;34(1):54-56, 2018 Jan 20.
[Is] ISSN:1009-2587
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:In recent years, researchers have found that CD26 (dipeptidyl peptidase 4) is closely related to the formation and development of many fibrotic diseases. Hypertrophic scar, keloid, and other skin fibrosis diseases are major problems nowadays, which may affect the patient's appearance and cause joints deformity and dysfunction due to scar contracture. This article briefly reviews the relationship between CD26 and hypertrophic scar and keloid to provide new insights into the treatment of skin fibrotic diseases.
[Mh] Termos MeSH primário: Cicatriz Hipertrófica/patologia
Dipeptidil Peptidase 4/metabolismo
Queloide/patologia
[Mh] Termos MeSH secundário: Fibrose
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
EC 3.4.14.5 (DPP4 protein, human); EC 3.4.14.5 (Dipeptidyl Peptidase 4)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1009-2587.2018.01.011


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[PMID]:28468787
[Au] Autor:Chandran S; Watkins J; Abdul-Aziz A; Shafat M; Calvert PA; Bowles KM; Flather MD; Rushworth SA; Ryding AD
[Ad] Endereço:Norfolk and Norwich University Hospital, Norwich, United Kingdom.
[Ti] Título:Inflammatory Differences in Plaque Erosion and Rupture in Patients With ST-Segment Elevation Myocardial Infarction.
[So] Source:J Am Heart Assoc;6(5), 2017 May 03.
[Is] ISSN:2047-9980
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Plaque erosion causes 30% of ST-segment elevation myocardial infarctions, but the underlying cause is unknown. Inflammatory infiltrates are less abundant in erosion compared with rupture in autopsy studies. We hypothesized that erosion and rupture are associated with significant differences in intracoronary cytokines in vivo. METHODS AND RESULTS: Forty ST-segment elevation myocardial infarction patients with <6 hours of chest pain were classified as ruptured fibrous cap (RFC) or intact fibrous cap (IFC) using optical coherence tomography. Plasma samples from the infarct-related artery and a peripheral artery were analyzed for expression of 102 cytokines using arrays; results were confirmed with ELISA. Thrombectomy samples were analyzed for differential mRNA expression using quantitative real-time polymerase chain reaction. Twenty-three lesions were classified as RFC (58%), 15 as IFC (38%), and 2 were undefined (4%). In addition, 12% (12 of 102) of cytokines were differentially expressed in both coronary and peripheral plasma. I-TAC was preferentially expressed in RFC (significance analysis of microarrays adjusted <0.001; ELISA IFC 10.2 versus RFC 10.8 log pg/mL; =0.042). IFC was associated with preferential expression of epidermal growth factor (significance analysis of microarrays adjusted <0.001; ELISA IFC 7.42 versus RFC 6.63 log pg/mL, =0.036) and thrombospondin 1 (significance analysis of microarrays adjusted =0.03; ELISA IFC 10.4 versus RFC 8.65 log ng/mL, =0.0041). Thrombectomy mRNA showed elevated I-TAC in RFC ( =0.0007) epidermal growth factor expression in IFC ( =0.0264) but no differences in expression of thrombospondin 1. CONCLUSIONS: These results demonstrate differential intracoronary cytokine expression in RFC and IFC. Elevated thrombospondin 1 and epidermal growth factor may play an etiological role in erosion.
[Mh] Termos MeSH primário: Doença da Artéria Coronariana/complicações
Citocinas/sangue
Mediadores da Inflamação/sangue
Placa Aterosclerótica
Infarto do Miocárdio com Supradesnível do Segmento ST/etiologia
[Mh] Termos MeSH secundário: Idoso
Biomarcadores/sangue
Angiografia Coronária
Doença da Artéria Coronariana/sangue
Doença da Artéria Coronariana/diagnóstico por imagem
Doença da Artéria Coronariana/terapia
Citocinas/genética
Ensaio de Imunoadsorção Enzimática
Fator de Crescimento Epidérmico/sangue
Feminino
Fibrose
Perfilação da Expressão Gênica/métodos
Seres Humanos
Masculino
Meia-Idade
Análise de Sequência com Séries de Oligonucleotídeos
Intervenção Coronária Percutânea
Estudos Prospectivos
Reação em Cadeia da Polimerase em Tempo Real
Fatores de Risco
Ruptura Espontânea
Infarto do Miocárdio com Supradesnível do Segmento ST/sangue
Infarto do Miocárdio com Supradesnível do Segmento ST/diagnóstico por imagem
Infarto do Miocárdio com Supradesnível do Segmento ST/terapia
Trombectomia
Trombospondina 1/sangue
Tomografia de Coerência Óptica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cytokines); 0 (Inflammation Mediators); 0 (Thrombospondin 1); 0 (thrombospondin-1, human); 62229-50-9 (Epidermal Growth Factor)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


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[PMID]:28458469
[Au] Autor:Ryu J; Lee JW
[Ad] Endereço:Department of Pharmacy, Research Institute of Pharmaceutical Sciences, Tumor Microenvironment Global Core Research Center, Medicinal Bioconvergence Research Center, College of Pharmacy, Seoul National University, Seoul 08826, Republic of Korea.
[Ti] Título:TM4SF5-Mediated Roles in the Development of Fibrotic Phenotypes.
[So] Source:Mediators Inflamm;2017:5108525, 2017.
[Is] ISSN:1466-1861
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Transmembrane 4 L six family member 5 (TM4SF5) can form tetraspanin-enriched microdomains (TERMs) on the cell's surface. TERMs contain protein-protein complexes comprised of tetraspanins, growth factor receptors, and integrins. These complexes regulate communication between extracellular and intracellular spaces to control diverse cellular functions. TM4SF5 influences the epithelial-mesenchymal transition (EMT), aberrant multilayer cellular growth, drug resistance, enhanced migration and invasion, circulation through the bloodstream, tumor-initiation property, metastasis, and muscle development in zebrafish. Here, current data on TM4SF5's roles in the development of fibrotic phenotypes are reviewed. TM4SF5 is induced by transforming growth factor 1 (TGF 1) signaling via a collaboration with epidermal growth factor receptor (EGFR) activation. TM4SF5, by itself or in concert with other receptors, transduces signals intracellularly. In hepatocytes, TM4SF5 expression regulates cell cycle progression, migration, and expression of extracellular matrix components. In CCl -treated mice, TM4SF5, -smooth muscle actin ( -SMA), and collagen I expression are observed together along the fibrotic septa regions of the liver. These fibrotic phenotypes are diminished by anti-TM4SF5 reagents, such as a specific small compound [TSAHC, 4'-( -toluenesulfonylamido)-4-hydroxychalcone] or a chimeric antibody. This review discusses the antifibrotic strategies that target TM4SF5 and its associated protein networks that regulate the intracellular signaling necessary for fibrotic functions of hepatocytes.
[Mh] Termos MeSH primário: Fibrose/metabolismo
Proteínas de Membrana/metabolismo
[Mh] Termos MeSH secundário: Actinas/metabolismo
Animais
Fibrose/genética
Hepatócitos/metabolismo
Seres Humanos
Proteínas de Membrana/genética
Camundongos
Receptor do Fator de Crescimento Epidérmico/genética
Receptor do Fator de Crescimento Epidérmico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Actins); 0 (Membrane Proteins); 0 (TM4SF5 protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1155/2017/5108525


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[PMID]:29334924
[Au] Autor:Zhao C; Dong F; Gao F; Liu X; Pei M; Jia S; Zhang M
[Ad] Endereço:Ophthalmology Department, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, 1 Shuaifuyuan, Wangfujing, Dongcheng District, Beijing, 100730, China.
[Ti] Título:Longitudinal observation of subretinal fibrosis in Vogt-Koyanagi-Harada disease.
[So] Source:BMC Ophthalmol;18(1):6, 2018 Jan 15.
[Is] ISSN:1471-2415
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Subretinal fibrosis (SRF) is a vision-threatening complication of Vogt-Koyanagi-Harada disease (VKH). It has long been recognized as a sequela of chronic inflammation. The developmental process of SRF, however, has not been described. The purpose of this study is to provide longitudinal observations of SRF in VKH. METHODS: Retrospective chart review of 10 VKH patients referred to our group between January 2008 and September 2015 at acute uveitic stage with SRF at presentation or who developed SRF during follow up. RESULTS: Ten patients (6 males and 4 females) with a median age of 39.0 (range, 23 to 58) years old were included. The median disease duration at presentation and median duration of follow up were 25.5 (range 5 to 60) days and 32.5 (range 13 to 61) months respectively. At presentation, all patients except one had been inappropriately treated with glucocorticosteroid (insufficiently dosed or tapered too fast) for longer than 2 weeks. Despite large dose oral glucocorticosteroid (1 mg/kg/d prednisone or equivalent) with slow tapering in combination with at least one immunomodulatory agent (cyclosporin A, cyclophosphamide or azathioprine) after presentation, all patients developed bilateral SRF within the first 4 months of disease course and 7 patients within the first 2 months. In 8 patients, shape-change/migration and progressive proliferation/pigmentation of SRF was observed over a period of several months after its formation, and then became quiescent but may further underwent depigmentation or pigmentation. SRF involved macula in 12 eyes (7 patients) and caused treatment resistant macular detachment and severe visual impairment in 6 eyes (4 patients). At the last visit, eyes with macular involvement were more common to had worse final best corrected visual acuity (≤20/50) than those without (9/12 vs. 0/8, p = 0.001). CONCLUSIONS: SRF usually develop early in the disease course in VKH patients who are not adequately controlled; it usually undergoes a highly dynamic process within the subretinal space and may involve the macula and resulted in poor final visual outcome.
[Mh] Termos MeSH primário: Macula Lutea/patologia
Doenças Retinianas/etiologia
Síndrome Uveomeningoencefálica/complicações
Acuidade Visual
[Mh] Termos MeSH secundário: Adulto
Feminino
Fibrose/diagnóstico
Fibrose/etiologia
Angiofluoresceinografia
Seguimentos
Fundo de Olho
Seres Humanos
Masculino
Meia-Idade
Prognóstico
Doenças Retinianas/diagnóstico
Doenças Retinianas/fisiopatologia
Estudos Retrospectivos
Fatores de Tempo
Tomografia de Coerência Óptica/métodos
Síndrome Uveomeningoencefálica/diagnóstico
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE
[do] DOI:10.1186/s12886-018-0670-0


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[PMID]:29184405
[Au] Autor:Hureaux J; Lacoeuille F; Lagarce F; Rousselet MC; Contini A; Saulnier P; Benoit JP; Urban T
[Ad] Endereço:Unité Micro et Nanomédecines Biomimétiques (MINT), Université d'Angers, INSERM 1066, CNRS 6021, Université Bretagne Loire.
[Ti] Título:Absence of lung fibrosis after a single pulmonary delivery of lipid nanocapsules in rats.
[So] Source:Int J Nanomedicine;12:8159-8170, 2017.
[Is] ISSN:1178-2013
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:Lipid nanocapsules (LNCs) are potential drug carriers for pulmonary delivery since they can be nebulized without any structural or functional changes, and the aerosols produced are highly compatible with pulmonary drug delivery in human beings. The alveolar surface tension, in vitro cytotoxicity, biodistribution and pulmonary toxicity in rats of a single endotracheal spray of LNCs or paclitaxel-loaded LNCs were studied. In vitro cytotoxicity of LNCs after a spray remained unchanged. Biodistribution study showed a homogeneous repartition in the lungs in rats with an improvement in lung retention of the radiolabeled tracer loaded in LNCs compared to the absence of LNCs with a lung half-time of 8.8±0.7 hours. Bronchoalveolar fluid analysis revealed transient 7-day alveolar inflammation, reaching a maximum between days 2 and 4, characterized by a peak of granulocytes at day 1 followed by a peak of lymphocytes at day 3. Alveolar protein levels were increased at days 3 and 7. Acute inflammation was increased with paclitaxel-loaded LNCs in comparison with blank LNCs but dropped out at day 7. No histological pulmonary lesion was observed at day 60. LNCs lowered surface tension to a greater degree than Curosurf in a physicochemical model of the pulmonary alveolus. A single pulmonary delivery of LNCs induces a short-term alveolar inflammation with no residual lesions in rats at day 60. These data permit to start the study of LNCs in surfactant replacement therapy.
[Mh] Termos MeSH primário: Portadores de Fármacos/efeitos adversos
Portadores de Fármacos/farmacocinética
Pulmão/efeitos dos fármacos
Pulmão/patologia
Nanocápsulas/efeitos adversos
[Mh] Termos MeSH secundário: Aerossóis/administração & dosagem
Aerossóis/efeitos adversos
Aerossóis/química
Animais
Produtos Biológicos
Linhagem Celular
Portadores de Fármacos/administração & dosagem
Sistemas de Liberação de Medicamentos/efeitos adversos
Sistemas de Liberação de Medicamentos/métodos
Feminino
Fibrose
Seres Humanos
Lipídeos/química
Nanocápsulas/administração & dosagem
Nanocápsulas/química
Paclitaxel/química
Paclitaxel/farmacocinética
Fosfolipídeos
Alvéolos Pulmonares/efeitos dos fármacos
Alvéolos Pulmonares/fisiopatologia
Ratos Sprague-Dawley
Tensão Superficial/efeitos dos fármacos
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aerosols); 0 (Biological Products); 0 (Drug Carriers); 0 (Lipids); 0 (Nanocapsules); 0 (Phospholipids); KE3U2023NP (poractant alfa); P88XT4IS4D (Paclitaxel)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S146740


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[PMID]:28460481
[Au] Autor:Kang HJ; Chung DH; Sung CO; Yoo SH; Yu E; Kim N; Lee SH; Song JY; Kim CJ; Choi J
[Ad] Endereço:Department of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
[Ti] Título:SHP2 is induced by the HBx-NF-κB pathway and contributes to fibrosis during human early hepatocellular carcinoma development.
[So] Source:Oncotarget;8(16):27263-27276, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The non-receptor tyrosine phosphatase SHP2 has scaffolding functions in signal transduction cascades downstream of growth receptors. A recent study suggested that SHP2 acts as a tumor suppressor during hepatocellular carcinoma (HCC) development. Herein we examined whether SHP2 links the HBx-NF-κB pathway to EGFR signaling during HCC development. The overexpression of HBx or NF-κB led to increased SHP2 expression via NF-κB binding to the Shp2 promoter. EGF treatment induced ERK activation as well as the rapid assembly of SHP2, EGFR, and Gab1. Upon LPS stimulation, NF-κB-SHP2-ERK activation and phosphorylated STAT3 levels exhibited a negative correlation in vitro. By contrast, in patients with HBV-associated HCC, NF-κB-SHP2-ERK and IL-6-JAK-STAT3 pathway activity levels were concomitantly higher in adjacent non-neoplastic tissues than in HCC tissues. The immunohistochemical analysis of 162 tissues of patients with HCC revealed that SHP2 levels were significantly higher in non-neoplastic background tissues than in corresponding HCC tissues and considerably increased in background liver tissues with advanced fibrosis (P < 0.001). SHP2 expression increased gradually from normal liver to chronic hepatitis, cirrhosis, and background liver with a dysplastic nodule, but was decreased or lost in dysplastic nodules and HCC. This is the first report to describe the existence of the HBx-NF-κB-SHP2 pathway, linking HBV infection to the EGFR-RAS-RAF-MAPK pathway in the liver. SHP2 depletion from the negative crosstalk between NF-κB and STAT3 accelerates HCC development.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/etiologia
Carcinoma Hepatocelular/metabolismo
Neoplasias Hepáticas/etiologia
Neoplasias Hepáticas/metabolismo
NF-kappa B/metabolismo
Proteína Tirosina Fosfatase não Receptora Tipo 11/genética
Transativadores/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Carcinoma Hepatocelular/patologia
Carcinoma Hepatocelular/cirurgia
Linhagem Celular Tumoral
Feminino
Fibrose
Regulação Neoplásica da Expressão Gênica
Vírus da Hepatite B/fisiologia
Seres Humanos
Cirrose Hepática/etiologia
Cirrose Hepática/metabolismo
Cirrose Hepática/patologia
Neoplasias Hepáticas/patologia
Neoplasias Hepáticas/cirurgia
Masculino
Meia-Idade
Modelos Biológicos
Gradação de Tumores
Estadiamento de Neoplasias
Regiões Promotoras Genéticas
Ligação Proteica
Proteína Tirosina Fosfatase não Receptora Tipo 11/metabolismo
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais
Proteínas ras/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B); 0 (STAT3 Transcription Factor); 0 (Trans-Activators); 0 (hepatitis B virus X protein); EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 11); EC 3.6.5.2 (ras Proteins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15930



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