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[PMID]:29040313
[Au] Autor:Dale M; Fitzgerald MP; Liu Z; Meisinger T; Karpisek A; Purcell LN; Carson JS; Harding P; Lang H; Koutakis P; Batra R; Mietus CJ; Casale G; Pipinos I; Baxter BT; Xiong W
[Ad] Endereço:Department of Surgery, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.
[Ti] Título:Premature aortic smooth muscle cell differentiation contributes to matrix dysregulation in Marfan Syndrome.
[So] Source:PLoS One;12(10):e0186603, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thoracic aortic aneurysm and dissection are life-threatening complications of Marfan syndrome (MFS). Studies of human and mouse aortic samples from late stage MFS demonstrate increased TGF-ß activation/signaling and diffuse matrix changes. However, the role of the aortic smooth muscle cell (SMC) phenotype in early aneurysm formation in MFS has yet to be fully elucidated. As our objective, we investigated whether an altered aortic SMC phenotype plays a role in aneurysm formation in MFS. We describe previously unrecognized concordant findings in the aortas of a murine model of MFS, mgR, during a critical and dynamic phase of early development. Using Western blot, gelatin zymography, and histological analysis, we demonstrated that at postnatal day (PD) 7, before aortic TGF-ß levels are increased, there is elastic fiber fragmentation/disorganization and increased levels of MMP-2 and MMP-9. Compared to wild type (WT) littermates, aortic SMCs in mgR mice express higher levels of contractile proteins suggesting a switch to a more mature contractile phenotype. In addition, tropoelastin levels are decreased in mgR mice, a finding consistent with a premature switch to a contractile phenotype. Proliferation assays indicate a decrease in the proliferation rate of mgR cultured SMCs compared to WT SMCs. KLF4, a regulator of smooth muscle cell phenotype, was decreased in aortic tissue of mgR mice. Finally, overexpression of KLF4 partially reversed this phenotypic change in the Marfan SMCs. This study indicates that an early phenotypic switch appears to be associated with initiation of important metabolic changes in SMCs that contribute to subsequent pathology in MFS.
[Mh] Termos MeSH primário: Aorta Torácica/patologia
Aneurisma da Aorta Torácica/patologia
Matriz Extracelular/patologia
Síndrome de Marfan/patologia
Miócitos de Músculo Liso/patologia
[Mh] Termos MeSH secundário: Animais
Aorta Torácica/metabolismo
Aneurisma da Aorta Torácica/genética
Aneurisma da Aorta Torácica/metabolismo
Diferenciação Celular
Proliferação Celular
Tecido Elástico/metabolismo
Tecido Elástico/patologia
Matriz Extracelular/metabolismo
Regulação da Expressão Gênica
Seres Humanos
Fatores de Transcrição Kruppel-Like/genética
Fatores de Transcrição Kruppel-Like/metabolismo
Síndrome de Marfan/genética
Síndrome de Marfan/metabolismo
Metaloproteinase 2 da Matriz/genética
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/genética
Metaloproteinase 9 da Matriz/metabolismo
Camundongos
Camundongos Transgênicos
Miócitos de Músculo Liso/metabolismo
Fenótipo
Cultura Primária de Células
Transdução de Sinais
Fator de Crescimento Transformador beta/genética
Fator de Crescimento Transformador beta/metabolismo
Tropoelastina/genética
Tropoelastina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GKLF protein); 0 (Kruppel-Like Transcription Factors); 0 (Transforming Growth Factor beta); 0 (Tropoelastin); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.24 (Mmp2 protein, mouse); EC 3.4.24.35 (Matrix Metalloproteinase 9); EC 3.4.24.35 (Mmp9 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171018
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186603


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[PMID]:28954103
[Au] Autor:Almeida HL; Almeida MG; Jorge VM; Abreu LB
[Ad] Endereço:Department of Dermatology, Universidade Federal de Pelotas (UFPel) - Pelotas (RS), Brazil.
[Ti] Título:Ultrastructural aspects of pseudoxanthoma elasticum.
[So] Source:An Bras Dermatol;92(4):527-530, 2017 Jul-Aug.
[Is] ISSN:1806-4841
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:We report the ultrastructural findings in a case of a 72-year-old black woman with confluent yellowish papules in the cervical region. She had no comorbidities. Ophthalmological examination, electrocardiogram, and echocardiogram were normal. Hematoxylin-eosin staining of the affected skin showed strong alterations in the mid-dermis with irregular clumps of eosinophilic material and loss of the normal parallel arrangement of collagen bundles. Orcein staining revealed that the elastic fibers lost their normal linear configuration, showing clump fragmentation, sometimes forming square structures. Transmission electron microscopy showed aberrant elastic fibers with an irregular outline and heterogenic inner structures. We also observed small elastic fibers. Collagen fibers showed a normal structure with irregular distribution. Scanning electron microscopy revealed important disorganization of collagen fibers and small stone-like deposits measuring around 5 µm associated with bigger structures ranging from 10-16 µm. Higher magnification revealed that these small stone-like structures were sometimes polyhedral-shaped or squared.
[Mh] Termos MeSH primário: Derme/ultraestrutura
Tecido Elástico/ultraestrutura
Pseudoxantoma Elástico/patologia
[Mh] Termos MeSH secundário: Idoso
Colágeno/ultraestrutura
Feminino
Seres Humanos
Microscopia Eletrônica de Varredura
Microscopia Eletrônica de Transmissão
Pele/patologia
Coluna Vertebral
Coloração e Rotulagem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
9007-34-5 (Collagen)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170928
[St] Status:MEDLINE


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[PMID]:28922187
[Au] Autor:Rodriguez IM; Cuevas M; Silvero A; Cañete-Portillo S; Sanchez DF; Barreto J; Cubilla AL
[Ad] Endereço:*Pathology and Research Institute †School of Medicine, National University of Asunción, Asunción, Paraguay.
[Ti] Título:Novel Histologic Finding: Adipose Tissue Is Prevalent Within Penile Tunica Albuginea and Corpora Cavernosa: An Anatomic Study of 63 Specimens and Considerations for Cancer Invasion.
[So] Source:Am J Surg Pathol;41(11):1542-1546, 2017 Nov.
[Is] ISSN:1532-0979
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Adipose tissue, along with arteries, veins, and peripheral nerves, is a normal constituent of mesenchymal tissues encasing the corpora cavernosa at the level of the penile shaft, variously designated as penile fascia or Bucks fascia. To our knowledge, the presence of fat has not been previously reported within the corpora cavernosa. One or 2 transversal histologic sections at the level of the surgical margin at the shaft of 63 consecutive partial penectomy specimens for squamous cell carcinoma were evaluated. From outer to inner tissues, 3 anatomic levels were identified: (1) outer fascia composed of a loose fibrovascular mesenchyme containing some nerve branches. Adipose tissue was present in the majority of the cases. (2) The tunica albuginea, a thick and dense fibroelastic band of tissue separating the outer fascia from the erectile tissues of the corpora cavernosa. Adipose tissue within the albuginea was present in 21 specimens (19%). (3) Erectile tissues of corpora cavernosa. Besides the typical erectile tissues, adipose tissue was present in 33 cases (52%). The fatty tissue was focal or multifocal and scant and peripherally located at the junction of the tunica albuginea with the corpora. In some cases, it was associated with small amounts of fibrous tissue, small vessels, and nerves. We are reporting the presence of adipose tissue in the tunica albuginea and the corpora cavernosa. It is possible that adipose tissue, along with small nutritional vessels and nerves perforates from the fascia, in which fat is usually present, through the tunica albuginea to reach the corpora. In a previous examination of the local routes of cancer spread, we found this pathway to be one of the mechanisms of cancer invading the penile corpora from the penile fascia.
[Mh] Termos MeSH primário: Tecido Adiposo/patologia
Carcinoma de Células Escamosas/patologia
Tecido Elástico/patologia
Neoplasias Penianas/patologia
[Mh] Termos MeSH secundário: Tecido Adiposo/cirurgia
Biópsia
Carcinoma de Células Escamosas/cirurgia
Tecido Elástico/cirurgia
Fáscia/patologia
Seres Humanos
Masculino
Invasividade Neoplásica
Neoplasias Penianas/cirurgia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE
[do] DOI:10.1097/PAS.0000000000000953


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[PMID]:28905442
[Au] Autor:Kielty CM
[Ad] Endereço:Wellcome Trust Centre for Cell-Matrix Research, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK.
[Ti] Título:Fell-Muir Lecture: Fibrillin microfibrils: structural tensometers of elastic tissues?
[So] Source:Int J Exp Pathol;98(4):172-190, 2017 Aug.
[Is] ISSN:1365-2613
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Fibrillin microfibrils are indispensable structural elements of connective tissues in multicellular organisms from early metazoans to humans. They have an extensible periodic beaded organization, and support dynamic tissues such as ciliary zonules that suspend the lens. In tissues that express elastin, including blood vessels, skin and lungs, microfibrils support elastin deposition and shape the functional architecture of elastic fibres. The vital contribution of microfibrils to tissue form and function is underscored by the heritable fibrillinopathies, especially Marfan syndrome with severe elastic, ocular and skeletal tissue defects. Research since the early 1990s has advanced our knowledge of biology of microfibrils, yet understanding of their mechanical and homeostatic contributions to tissues remains far from complete. This review is a personal reflection on key insights, and puts forward the conceptual hypothesis that microfibrils are structural 'tensometers' that direct cells to monitor and respond to altered tissue mechanics.
[Mh] Termos MeSH primário: Tecido Elástico/patologia
Matriz Extracelular/patologia
Fibrilinas/metabolismo
Síndrome de Marfan/patologia
Microfibrilas/patologia
Proteínas dos Microfilamentos/metabolismo
[Mh] Termos MeSH secundário: Animais
Tecido Elástico/metabolismo
Matriz Extracelular/metabolismo
Seres Humanos
Síndrome de Marfan/metabolismo
Microfibrilas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Fibrillins); 0 (Microfilament Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1111/iep.12239


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[PMID]:28684544
[Au] Autor:Bultmann-Mellin I; Dinger K; Debuschewitz C; Loewe KMA; Melcher Y; Plum MTW; Appel S; Rappl G; Willenborg S; Schauss AC; Jüngst C; Krüger M; Dressler S; Nakamura T; Wempe F; Alejandre Alcázar MA; Sterner-Kock A
[Ad] Endereço:Center for Experimental Medicine, Medical Faculty, University of Cologne, Cologne, Germany.
[Ti] Título:Role of LTBP4 in alveolarization, angiogenesis, and fibrosis in lungs.
[So] Source:Am J Physiol Lung Cell Mol Physiol;313(4):L687-L698, 2017 Oct 01.
[Is] ISSN:1522-1504
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Deficiency of the extracellular matrix protein latent transforming growth factor-ß (TGF-ß)-binding protein-4 (LTBP4) results in lack of intact elastic fibers, which leads to disturbed pulmonary development and lack of normal alveolarization in humans and mice. Formation of alveoli and alveolar septation in pulmonary development requires the concerted interaction of extracellular matrix proteins, growth factors such as TGF-ß, fibroblasts, and myofibroblasts to promote elastogenesis as well as vascular formation in the alveolar septae. To investigate the role of LTBP4 in this context, lungs of LTBP4-deficient ( ) mice were analyzed in close detail. We elucidate the role of LTBP4 in pulmonary alveolarization and show that three different, interacting mechanisms might contribute to alveolar septation defects in lungs: ) absence of an intact elastic fiber network, ) reduced angiogenesis, and ) upregulation of TGF-ß activity resulting in profibrotic processes in the lung.
[Mh] Termos MeSH primário: Tecido Elástico/patologia
Fibroblastos/patologia
Fibrose/patologia
Proteínas de Ligação a TGF-beta Latente/fisiologia
Pulmão/patologia
Neovascularização Patológica/patologia
Alvéolos Pulmonares/patologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Tecido Elástico/metabolismo
Matriz Extracelular/metabolismo
Feminino
Fibroblastos/metabolismo
Fibrose/metabolismo
Pulmão/irrigação sanguínea
Pulmão/metabolismo
Masculino
Camundongos
Camundongos Knockout
Neovascularização Patológica/metabolismo
Organogênese/fisiologia
Alvéolos Pulmonares/metabolismo
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Latent TGF-beta Binding Proteins); 0 (Transforming Growth Factor beta)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE
[do] DOI:10.1152/ajplung.00031.2017


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[PMID]:28619995
[Au] Autor:Tojais NF; Cao A; Lai YJ; Wang L; Chen PI; Alcazar MAA; de Jesus Perez VA; Hopper RK; Rhodes CJ; Bill MA; Sakai LY; Rabinovitch M
[Ad] Endereço:From the Department of Pediatrics (N.F.T., A.C., Y.-J.L., L.W., P.I.C., M.A.A.A., R.K.H., C.J.R., M.R.) and Department of Medicine (V.A.d.J.P., M.A.B.), the Vera Moulton Wall Center for Pulmonary Vascular Disease and the Cardiovascular Institute, Stanford University School of Medicine, CA; and Shrin
[Ti] Título:Codependence of Bone Morphogenetic Protein Receptor 2 and Transforming Growth Factor-ß in Elastic Fiber Assembly and Its Perturbation in Pulmonary Arterial Hypertension.
[So] Source:Arterioscler Thromb Vasc Biol;37(8):1559-1569, 2017 Aug.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: We determined in patients with pulmonary arterial (PA) hypertension (PAH) whether in addition to increased production of elastase by PA smooth muscle cells previously reported, PA elastic fibers are susceptible to degradation because of their abnormal assembly. APPROACH AND RESULTS: Fibrillin-1 and elastin are the major components of elastic fibers, and fibrillin-1 binds bone morphogenetic proteins (BMPs) and the large latent complex of transforming growth factor-ß1 (TGFß1). Thus, we considered whether BMPs like TGFß1 contribute to elastic fiber assembly and whether this process is perturbed in PAH particularly when the BMP receptor, BMPR2, is mutant. We also assessed whether in mice with compound heterozygosity, elastic fibers are susceptible to degradation. In PA smooth muscle cells and adventitial fibroblasts, TGFß1 increased elastin mRNA, but the elevation in elastin protein was dependent on BMPR2; TGFß1 and BMP4, via BMPR2, increased extracellular accumulation of fibrillin-1. Both BMP4- and TGFß1-stimulated elastic fiber assembly was impaired in idiopathic (I) PAH-PA adventitial fibroblast versus control cells, particularly those with hereditary (H) PAH and a mutation. This was related to profound reductions in elastin and fibrillin-1 mRNA. Elastin protein was increased in IPAH PA adventitial fibroblast by TGFß1 but only minimally so in mutant cells. Fibrillin-1 protein increased only modestly in IPAH or HPAH PA adventitial fibroblasts stimulated with BMP4 or TGFß1. In heterozygote mice, reduced PA fibrillin-1 was associated with elastic fiber susceptibility to degradation and more severe pulmonary hypertension. CONCLUSIONS: Disrupting BMPR2 impairs TGFß1- and BMP4-mediated elastic fiber assembly and is of pathophysiologic significance in PAH.
[Mh] Termos MeSH primário: Receptores de Proteínas Morfogenéticas Ósseas Tipo II/metabolismo
Tecido Elástico/metabolismo
Hipertensão Pulmonar Primária Familiar/metabolismo
Hipertensão Pulmonar/metabolismo
Artéria Pulmonar/efeitos dos fármacos
Fator de Crescimento Transformador beta/farmacologia
Remodelação Vascular
[Mh] Termos MeSH secundário: Animais
Proteína Morfogenética Óssea 4/farmacologia
Receptores de Proteínas Morfogenéticas Ósseas Tipo I/deficiência
Receptores de Proteínas Morfogenéticas Ósseas Tipo I/genética
Receptores de Proteínas Morfogenéticas Ósseas Tipo II/deficiência
Receptores de Proteínas Morfogenéticas Ósseas Tipo II/genética
Estudos de Casos e Controles
Células Cultivadas
Modelos Animais de Doenças
Tecido Elástico/patologia
Tecido Elástico/fisiopatologia
Elastina/genética
Elastina/metabolismo
Hipertensão Pulmonar Primária Familiar/genética
Hipertensão Pulmonar Primária Familiar/patologia
Hipertensão Pulmonar Primária Familiar/fisiopatologia
Fibrilina-1/genética
Fibrilina-1/metabolismo
Fibroblastos/efeitos dos fármacos
Fibroblastos/metabolismo
Fibroblastos/patologia
Predisposição Genética para Doença
Seres Humanos
Hipertensão Pulmonar/genética
Hipertensão Pulmonar/patologia
Hipertensão Pulmonar/fisiopatologia
Camundongos da Linhagem 129
Camundongos Endogâmicos C57BL
Camundongos Knockout
Mutação
Miócitos de Músculo Liso/efeitos dos fármacos
Miócitos de Músculo Liso/metabolismo
Miócitos de Músculo Liso/patologia
Fenótipo
Artéria Pulmonar/metabolismo
Artéria Pulmonar/patologia
Artéria Pulmonar/fisiopatologia
Interferência de RNA
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bone Morphogenetic Protein 4); 0 (FBN1 protein, human); 0 (Fbn1 protein, mouse); 0 (Fibrillin-1); 0 (Transforming Growth Factor beta); 9007-58-3 (Elastin); EC 2.7.11.30 (BMPR2 protein, human); EC 2.7.11.30 (Bmpr1a protein, mouse); EC 2.7.11.30 (Bmpr2 protein, mouse); EC 2.7.11.30 (Bone Morphogenetic Protein Receptors, Type I); EC 2.7.11.30 (Bone Morphogenetic Protein Receptors, Type II)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170913
[Lr] Data última revisão:
170913
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170617
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309696


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[PMID]:28504204
[Au] Autor:Lei G; Yang H; Hong T; Zhou C; Li J; Liu W; Hu J; Zeng L; Chen G; Chen Q; Zhang Y; Yang N
[Ad] Endereço:Department of Medical Oncology, Lung Cancer and Gastrointestinal Unit, Hunan Cancer Hospital, Affiliated Cancer Hospital of Xiangya School of Medicine, Changsha, China, 410013; Graduate School, University of South China, Hunan Hengyang, China, 421001.
[Ti] Título:Elastic staining-a rejuvenated method to reassess prognosis and serosal invasion in patients with pT3N0M0 gastric cancer.
[So] Source:Hum Pathol;65:79-84, 2017 Jul.
[Is] ISSN:1532-8392
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Prognosis of pT3N0M0 gastric cancer (GC) varies greatly, though the major factor conferring poor prognosis is unclear. Subserosal elastic lamina invasion (ELI+) is closely associated with poor outcomes in pT3 colorectal cancer, but related research on GC is unavailable. This study aimed to identify the influence of ELI+ on the prognosis of patients with pT3N0M0 GC and its relationship with serosal invasion using elastic staining. We retrospectively reviewed 94 and 28 patients with pT3N0M0 and pT4aN0M0 GC who underwent gastrectomy between 1994 and 2005. For the former, one section with invasion depth closest to the peritoneal surface and one corresponding paraffin block for each specimen were selected for conventional elastic staining to assess the relationship between ELI+ and patients' clinical characteristics and survival. pT3N0M0 GC specimens were divided into 3 groups based on staining results: ELI+ (N=51), non-invasion (N=31), and unidentified (N=12). ELI+ was closely related to recurrence and lymphovascular invasion. Five-year disease-free (DFS) (46%) and overall (OS) (36%) survival rates were significantly lower in the ELI+ than in the non-invasion or unidentified groups (P<.0001); no obvious difference was found between the ELI+ and pT4aN0M0 groups (P=.25). Multivariate analysis showed ELI+ and recurrence as independent prognostic factors for DFS in pT3 GC patients. In conclusion, elastic staining is an effective and highly feasible method for predicting prognosis and evaluating the serosal invasion depth of pT3 GC. pT3 GC accompanied with ELI+ is an obvious adverse prognostic factor and could be considered a treatment for pT4a GC.
[Mh] Termos MeSH primário: Tecido Elástico/patologia
Coloração e Rotulagem/métodos
Neoplasias Gástricas/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Distribuição de Qui-Quadrado
Progressão da Doença
Intervalo Livre de Doença
Estudos de Viabilidade
Feminino
Gastrectomia
Seres Humanos
Estimativa de Kaplan-Meier
Masculino
Meia-Idade
Análise Multivariada
Invasividade Neoplásica
Recidiva Local de Neoplasia
Estadiamento de Neoplasias
Valor Preditivo dos Testes
Modelos de Riscos Proporcionais
Estudos Retrospectivos
Fatores de Risco
Neoplasias Gástricas/mortalidade
Neoplasias Gástricas/cirurgia
Fatores de Tempo
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170516
[St] Status:MEDLINE


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[PMID]:28485217
[Au] Autor:Uehara E; Hokazono H; Hida M; Sasaki T; Yoshioka H; Matsuo N
[Ad] Endereço:a Sanwa Shurui Co., Ltd. , Usa , Japan.
[Ti] Título:GABA promotes elastin synthesis and elastin fiber formation in normal human dermal fibroblasts (HDFs).
[So] Source:Biosci Biotechnol Biochem;81(6):1198-1205, 2017 Jun.
[Is] ISSN:1347-6947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The multiple physiological effects of γ-aminobutyric acid (GABA) as a functional food component have been recently reported. We previously reported that GABA upregulated the expression of type I collagen in human dermal fibroblasts (HDFs), and that oral administration of GABA significantly increased skin elasticity. However, details of the regulatory mechanism still remain unknown. In this study, we further examined the effects of GABA on elastin synthesis and elastin fiber formation in HDFs. Real-time PCR indicated that GABA significantly increased the expression of tropoelastin transcript in a dose-dependent manner. Additionally, the expression of fibrillin-1, fibrillin-2, and fibulin-5/DANCE, but not lysyl oxidase and latent transforming factor-ß-binding protein 4, were also significantly increased in HDFs. Finally, immunohistochemical analysis confirmed that treatment with GABA dramatically increased the formation of elastic fibers in HDFs. Taken together, our results showed that GABA improves skin elasticity in HDFs by upregulating elastin synthesis and elastin fiber formation.
[Mh] Termos MeSH primário: Tecido Elástico/efeitos dos fármacos
Elastina/genética
Fibroblastos/efeitos dos fármacos
Tropoelastina/agonistas
Ácido gama-Aminobutírico/farmacologia
[Mh] Termos MeSH secundário: Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Derme/citologia
Derme/efeitos dos fármacos
Derme/metabolismo
Tecido Elástico/metabolismo
Elastina/agonistas
Elastina/metabolismo
Proteínas da Matriz Extracelular/agonistas
Proteínas da Matriz Extracelular/genética
Proteínas da Matriz Extracelular/metabolismo
Fibrilina-1/agonistas
Fibrilina-1/genética
Fibrilina-1/metabolismo
Fibrilina-2/agonistas
Fibrilina-2/genética
Fibrilina-2/metabolismo
Fibroblastos/citologia
Fibroblastos/metabolismo
Regulação da Expressão Gênica
Seres Humanos
Proteínas de Ligação a TGF-beta Latente/genética
Proteínas de Ligação a TGF-beta Latente/metabolismo
Proteína-Lisina 6-Oxidase/genética
Proteína-Lisina 6-Oxidase/metabolismo
Transdução de Sinais
Tropoelastina/genética
Tropoelastina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Extracellular Matrix Proteins); 0 (FBLN5 protein, human); 0 (FBN1 protein, human); 0 (Fibrillin-1); 0 (Fibrillin-2); 0 (LTBP1 protein, human); 0 (Latent TGF-beta Binding Proteins); 0 (Tropoelastin); 56-12-2 (gamma-Aminobutyric Acid); 9007-58-3 (Elastin); EC 1.4.3.13 (Protein-Lysine 6-Oxidase)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170703
[Lr] Data última revisão:
170703
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170510
[St] Status:MEDLINE
[do] DOI:10.1080/09168451.2017.1290518


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[PMID]:28475442
[Au] Autor:Westra I; Verhaegen PDHM; Ibrahim Korkmaz H; Braam KI; Kaspers GJL; Niessen HWM; Niessen FB
[Ad] Endereço:Department of Plastic, Reconstructive and Hand Surgery, VU Medical Centre, Amsterdam, the Netherlands.
[Ti] Título:Investigating histological aspects of scars in children.
[So] Source:J Wound Care;26(5):256-265, 2017 May 02.
[Is] ISSN:0969-0700
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Very little is known about histological aspects of paediatric scars and the possible role of the immune system during their formation. In this study, the histology thoracic scars caused by the placement of an implantable central venous access device in children who underwent treatment for cancer was assessed. METHOD: The amount and type of collagen, the collagen orientation, the type of elastic fibres, the vascularsation, and the count of neutrophils, macrophages, and lymphocytes were analysed. The severity of scarring was assessed using the Vancouver scar scale (VSS). To evaluate the role of the immune system on scar severity and histology, the scars of children suffering from acute lymphoblastic leukaemia (ALL) were compared with the scars of children suffering from other types of childhood cancer. RESULTS: Our results showed an extremely random orientation of the collagen fibres of the paediatric scars with a mean collagen orientation index of 0.22 (standard deviation (SD) 0.10, zero indicating a perfectly random orientation and a perfectly parallel orientation). A lower collagen orientation index was seen in scars with a lower VSS score (VSS score <3: 0.19 versus VSS score ≥3 0.29, p=0.037). A higher total VSS score, resembling a worse scar, was assessed to the scars in the non-ALL group compared with the children with ALL (mean ALL: 0.91 (0-3) versus mean non-ALL: 2.50 (0-6), p=0.037). CONCLUSION: To our knowledge, this is the first study investigating a wide array of histological aspects in paediatric scars. Compared with adult scars, an extremely random collagen orientation was found (0.22 in children versus 0.41 and 0.46 adult normotrophic and hypertrophic scars, respectively). A lower collagen orientation index was found in scars with a lower VSS score. In addition, less severe scarring was measured in children suffering from ALL compared with children suffering from other types of childhood cancer. This suggests that the immune system could play a role in the development of aberrant scarring and should be a target for future research.
[Mh] Termos MeSH primário: Cicatriz/patologia
Colágeno/metabolismo
Tecido Elástico/patologia
Linfócitos/patologia
Macrófagos/patologia
Neovascularização Fisiológica
Neutrófilos/patologia
Leucemia-Linfoma Linfoblástico de Células Precursoras/imunologia
[Mh] Termos MeSH secundário: Adolescente
Contagem de Células
Criança
Pré-Escolar
Cicatriz/complicações
Cicatriz/imunologia
Cicatriz/metabolismo
Colágeno Tipo I/metabolismo
Colágeno Tipo II/metabolismo
Estudos Transversais
Feminino
Seres Humanos
Imuno-Histoquímica
Linfócitos/imunologia
Macrófagos/imunologia
Masculino
Neoplasias/complicações
Neoplasias/imunologia
Neutrófilos/imunologia
Leucemia-Linfoma Linfoblástico de Células Precursoras/complicações
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type I); 0 (Collagen Type II); 9007-34-5 (Collagen)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:N
[Da] Data de entrada para processamento:170506
[St] Status:MEDLINE
[do] DOI:10.12968/jowc.2017.26.5.256


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[PMID]:28395026
[Au] Autor:White TL; Lewis P; Hayes S; Fergusson J; Bell J; Farinha L; White NS; Pereira LV; Meek KM
[Ad] Endereço:Structural Biophysics Research Group, School of Optometry and Vision Sciences, Cardiff University, Maindy Road, Cardiff, United Kingdom.
[Ti] Título:The Structural Role of Elastic Fibers in the Cornea Investigated Using a Mouse Model for Marfan Syndrome.
[So] Source:Invest Ophthalmol Vis Sci;58(4):2106-2116, 2017 Apr 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: The presence of fibrillin-rich elastic fibers in the cornea has been overlooked in recent years. The aim of the current study was to elucidate their functional role using a mouse model for Marfan syndrome, defective in fibrillin-1, the major structural component of the microfibril bundles that constitute most of the elastic fibers. Methods: Mouse corneas were obtained from animals with a heterozygous fibrillin-1 mutation (Fbn1+/-) and compared to wild type controls. Corneal thickness and radius of curvature were calculated using optical coherence tomography microscopy. Elastic microfibril bundles were quantified and visualized in three-dimensions using serial block face scanning electron microscopy. Transmission electron microscopy was used to analyze stromal ultrastructure and proteoglycan distribution. Center-to-center average interfibrillar spacing was determined using x-ray scattering. Results: Fbn1+/- corneas were significantly thinner than wild types and displayed a higher radius of curvature. In the Fbn1+/- corneas, elastic microfibril bundles were significantly reduced in density and disorganized compared to wild-type controls, in addition to containing a higher average center-to-center collagen interfibrillar spacing in the center of the cornea. No other differences were detected in stromal ultrastructure or proteoglycan distribution between the two groups. Proteoglycan side chains appeared to colocalize with the microfibril bundles. Conclusions: Elastic fibers have an important, multifunctional role in the cornea as highlighted by the differences observed between Fbn1+/- and wild type animals. We contend that the presence of normal quantities of structurally organized elastic fibers are required to maintain the correct geometry of the cornea, which is disrupted in Marfan syndrome.
[Mh] Termos MeSH primário: Córnea/ultraestrutura
Tecido Elástico/ultraestrutura
Síndrome de Marfan/diagnóstico
[Mh] Termos MeSH secundário: Animais
Córnea/metabolismo
DNA/genética
Análise Mutacional de DNA
Modelos Animais de Doenças
Fibrilina-1/genética
Fibrilina-1/metabolismo
Síndrome de Marfan/genética
Síndrome de Marfan/metabolismo
Camundongos
Camundongos Mutantes
Microfibrilas/ultraestrutura
Microscopia Eletrônica de Varredura
Microscopia Eletrônica de Transmissão
Mutação
Tomografia de Coerência Óptica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fbn1 protein, mouse); 0 (Fibrillin-1); 9007-49-2 (DNA)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171123
[Lr] Data última revisão:
171123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170411
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.16-21358



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