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Pesquisa : A11.620.520 [Categoria DeCS]
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[PMID]:28449099
[Au] Autor:Allagnat F; Dubuis C; Lambelet M; Le Gal L; Alonso F; Corpataux JM; Déglise S; Haefliger JA
[Ad] Endereço:Department of Vascular Surgery, Centre Hospitalier Universitaire Vaudois (CHUV), Lausanne, Switzerland.
[Ti] Título:Connexin37 reduces smooth muscle cell proliferation and intimal hyperplasia in a mouse model of carotid artery ligation.
[So] Source:Cardiovasc Res;113(7):805-816, 2017 Jun 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aims: Intimal hyperplasia (IH) is an abnormal response to vessel injury characterized by the dedifferentiation, migration, and proliferation of quiescent vascular smooth muscle cells (VSMC) to form a neointima layer. Vascular connexins (Cx) are involved in the pathophysiology of various vascular diseases, and Cx43, the main Cx expressed in VSMC, has been shown to promote VSMC proliferation and IH. The aim of this study was to investigate the participation of another Cx, namely Cx37, in the formation of the neointima layer. Methods and results: Wild-type (WT) and Cx37-deficient (Cx37-/-) C57BL/6J mice were subjected to carotid artery ligation (CAL), a model of vessel injury and IH. The neointima developed linearly in WT until 28 days post surgery. In contrast, the neointima layer was almost absent 14 days after surgery in Cx37-/- mice, and twice as more developed after 28 days compared to WT mice. This large neointima formation correlated with a two-fold increase in cell proliferation in the media and neointima regions between 14 and 28 days in Cx37-/- mice compared to WT mice. The CAL triggered Cx43 overexpression in the media and neointima layers of ligated carotids in WT mice, and selectively up-regulated Cx37 expression in the media layer, but not in the neointima layer. The de novo expression of Cx37 in human primary VSMC reduced cell proliferation and P-Akt levels, in association with lower Cx43 levels, whereas Cx43 overexpression increased P-Akt levels. Conclusion: The presence of Cx37 in the media layer of injured arteries restrains VSMC proliferation and limits the development of IH, presumably by interfering with the pro-proliferative effect of Cx43 and the Akt pathway.
[Mh] Termos MeSH primário: Lesões das Artérias Carótidas/metabolismo
Estenose das Carótidas/metabolismo
Proliferação Celular
Conexinas/metabolismo
Músculo Liso Vascular/metabolismo
Miócitos de Músculo Liso/metabolismo
Neointima
[Mh] Termos MeSH secundário: Idoso
Animais
Artérias Carótidas/metabolismo
Artérias Carótidas/patologia
Artérias Carótidas/cirurgia
Lesões das Artérias Carótidas/genética
Lesões das Artérias Carótidas/patologia
Estenose das Carótidas/genética
Estenose das Carótidas/patologia
Células Cultivadas
Conexina 43/metabolismo
Conexinas/deficiência
Conexinas/genética
Modelos Animais de Doenças
Feminino
Seres Humanos
Hiperplasia
Ligadura
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Músculo Liso Vascular/patologia
Miócitos de Músculo Liso/patologia
Fosforilação
Proteínas Proto-Oncogênicas c-akt/metabolismo
Transdução de Sinais
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexin 43); 0 (Connexins); 0 (connexin 37); 0 (connexin 43 protein, rat); 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:170428
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvx079


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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


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[PMID]:29409796
[Au] Autor:Li H; Shin SE; Seo MS; An JR; Choi IW; Jung WK; Firth AL; Lee DS; Yim MJ; Choi G; Lee JM; Na SH; Park WS
[Ad] Endereço:Institute of Medical Sciences, Department of Physiology, Kangwon National University School of Medicine, Chuncheon 24341, South Korea.
[Ti] Título:The anti-diabetic drug dapagliflozin induces vasodilation via activation of PKG and Kv channels.
[So] Source:Life Sci;197:46-55, 2018 Mar 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIM: Considering the clinical efficacy of dapagliflozin in patients with type 2 DM and the pathophysiological relevance of Kv channels for vascular reactivity. We investigate the vasodilatory effect of dapagliflozin and related mechanisms using phenylephrine (Phe)-induced contracted aortic rings. MATERIAL AND METHODS: Arterial tone measurement was performed in aortic smooth muscle. KEY FINDINGS: Application of dapagliflozin induced vasodilation in a concentration-dependent manner. Pre-treatment with the BK channel inhibitor paxilline, the K channel inhibitor glibenclamide, and the Kir channel inhibitor Ba did not change dapagliflozin-induced vasodilation. However, application of the Kv channels inhibitor 4-AP effectively inhibited dapagliflozin-induced vasodilation. Application of the Ca channel inhibitor nifedipine and the sarcoplasmic/endoplasmic reticulum Ca -ATPase (SERCA) pump inhibitor thapsigargin did not alter the vasodilatory effect of dapagliflozin. Moreover, the adenylyl cyclase inhibitor SQ 22536 and the protein kinase A (PKA) inhibitor KT 5720 had no effect on dapagliflozin-induced vasodilation. Although guanylyl cyclase inhibitors, NS 2028 and ODQ, did not reduce the vasodilatory effect of dapagliflozin, the protein kinase G (PKG) inhibitor KT 5823 effectively inhibited dapagliflozin-induced vasodilation. The vasodilatory effect of dapagliflozin was not affected by elimination of the endothelium. Furthermore, pretreatment with the nitric oxide synthase inhibitor L-NAME or the small-conductance Ca -activated K (SKCa) channel inhibitor apamin did not change the vasodilatory effect of dapagliflozin. SIGNIFICANCE: We concluded that dapagliflozin induced vasodilation via the activation of Kv channels and PKG, and was independent of other K channels, Ca channels, intracellular Ca , and the endothelium.
[Mh] Termos MeSH primário: Aorta/metabolismo
Compostos Benzidrílicos/farmacologia
Proteínas Quinases Dependentes de GMP Cíclico/metabolismo
Glucosídeos/farmacologia
Hipoglicemiantes/farmacologia
Músculo Liso Vascular/metabolismo
Miócitos de Músculo Liso/metabolismo
Canais de Potássio de Abertura Dependente da Tensão da Membrana/metabolismo
Vasodilatação/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Aorta/fisiopatologia
Ativação Enzimática/efeitos dos fármacos
Masculino
Músculo Liso Vascular/fisiopatologia
Coelhos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-(3-(4-ethoxybenzyl)-4-chlorophenyl)-6-hydroxymethyltetrahydro-2H-pyran-3,4,5-triol); 0 (Benzhydryl Compounds); 0 (Glucosides); 0 (Hypoglycemic Agents); 0 (Potassium Channels, Voltage-Gated); EC 2.7.11.12 (Cyclic GMP-Dependent Protein Kinases)
[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:180208
[St] Status:MEDLINE


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[PMID]:29360846
[Au] Autor:Yu X; Stallone JN; Heaps CL; Han G
[Ad] Endereço:Veterinary Physiology & Pharmacology, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX, United States of America.
[Ti] Título:The activation of G protein-coupled estrogen receptor induces relaxation via cAMP as well as potentiates contraction via EGFR transactivation in porcine coronary arteries.
[So] Source:PLoS One;13(1):e0191418, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Estrogen exerts protective effects against cardiovascular diseases in premenopausal women, but is associated with an increased risk of both coronary heart disease and stroke in older postmenopausal women. Studies have shown that activation of the G-protein-coupled estrogen receptor 1 (GPER) can cause either relaxation or contraction of arteries. It is highly likely that these dual actions of GPER may contribute to the seemingly paradoxical effects of estrogen in regulating coronary artery function. The objective of this study was to test the hypothesis that activation of GPER enhances agonist-stimulated porcine coronary artery contraction via epidermal growth factor receptor (EGFR) transactivation and its downstream extracellular signal-regulated kinases (ERK1/2) pathway. Isometric tension studies and western blot were performed to determine the effect of GPER activation on coronary artery contraction. Our findings demonstrated that G-1 caused concentration-dependent relaxation of ET-1-induced contraction, while pretreatment of arterial rings with G-1 significantly enhanced ET-1-induced contraction. GPER antagonist, G-36, significantly inhibited both the G-1-induced relaxation effect and G-1-enhanced ET-1 contraction. Gallein, a Gßγ inhibitor, significantly increased G-1-induced relaxation, yet inhibited G-1-enhanced ET-1-mediated contraction. Similarly, inhibition of EGFR with AG1478 or inhibition of Src with phosphatase 2 further increased G-1-induced relaxation responses in coronary arteries, but decreased G-1-enhanced ET-1-induced contraction. Western blot experiments in porcine coronary artery smooth muscle cells (PCASMC) showed that G-1 increased tyrosine phosphorylation of EGFR, which was inhibited by AG-1478. Furthermore, enzyme-linked immunosorbent assays showed that the level of heparin-binding EGF (HB-EGF) released by ET-1 treatment increased two-fold; whereas pre-incubation with G-1 further increased ET-1-induced HB-EGF release to four-fold over control conditions. Lastly, the role of ERK1/2 was determined by applying the MEK inhibitor, PD98059, in isometric tension studies and detecting phospho-ERK1/2 in immunoblotting. PD98059 potentiated G-1-induced relaxation response, but blocked G-1-enhanced ET-1-induced contraction. By western blot, G-1 treatment decreased phospho-ERK1/2, however, in the presence of the adenylyl cyclase inhibitor, SQ22536, G-1 significantly increased ERK1/2 phosphorylation in PCASMC. These data demonstrate that activation of GPER induces relaxation via cAMP as well as contraction via a mechanism involving transactivation of EGFR and the phosphorylation of ERK1/2 in porcine coronary arteries.
[Mh] Termos MeSH primário: Vasos Coronários/fisiologia
Receptor do Fator de Crescimento Epidérmico/genética
Receptores Estrogênicos/metabolismo
Receptores Acoplados a Proteínas-G/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Vasos Coronários/efeitos dos fármacos
Ciclopentanos/farmacologia
Flavonoides/farmacologia
Seres Humanos
Técnicas In Vitro
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Modelos Cardiovasculares
Miócitos de Músculo Liso/metabolismo
Quinazolinas/farmacologia
Quinolinas/farmacologia
Receptores Acoplados a Proteínas-G/agonistas
Suínos
Ativação Transcricional
Tirfostinas/farmacologia
Vasodilatação/efeitos dos fármacos
Vasodilatação/genética
Vasodilatação/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (1-(4-(6-bromobenzo(1,3)dioxol-5-yl)-3a,4,5,9b-tetrahydro-3H-cyclopenta(c)quinolin-8-yl)ethanone); 0 (2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one); 0 (Cyclopentanes); 0 (Flavonoids); 0 (Quinazolines); 0 (Quinolines); 0 (Receptors, Estrogen); 0 (Receptors, G-Protein-Coupled); 0 (Tyrphostins); 170449-18-0 (tyrphostin AG 1478); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180124
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191418


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[PMID]:29388834
[Au] Autor:Oldham WM
[Ad] Endereço:1 Department of Medicine Brigham and Women's Hospital and Harvard Medical School Boston, Massachusetts.
[Ti] Título:The Long Noncoding RNA LnRPT Puts the Brakes on Pulmonary Artery Smooth Muscle Cell Proliferation.
[So] Source:Am J Respir Cell Mol Biol;58(2):138-139, 2018 02.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Hipertensão Pulmonar/patologia
Miócitos de Músculo Liso/citologia
Artéria Pulmonar/citologia
RNA Longo não Codificante/genética
Resistência Vascular/fisiologia
[Mh] Termos MeSH secundário: Proliferação Celular/genética
Insuficiência Cardíaca/patologia
Insuficiência Cardíaca/prevenção & controle
Seres Humanos
Pulmão/irrigação sanguínea
Músculo Liso Vascular/citologia
Receptores do Fator de Crescimento Derivado de Plaquetas/fisiologia
[Pt] Tipo de publicação:EDITORIAL
[Nm] Nome de substância:
0 (RNA, Long Noncoding); EC 2.7.10.1 (Receptors, Platelet-Derived Growth Factor)
[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:180202
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2017-0342ED


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[PMID]:29381285
[Au] Autor:Wu T; Zhang J; Wang Y; Sun B; Guo X; Morsi Y; El-Hamshary H; El-Newehy M; Mo X
[Ti] Título:Development of Dynamic Liquid and Conjugated Electrospun Poly(L-lactide-co-caprolactone)/Collagen Nanoyarns for Regulating Vascular Smooth Muscle Cells Growth.
[So] Source:J Biomed Nanotechnol;13(3):303-12, 2017 Mar.
[Is] ISSN:1550-7033
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Simulating the modeling of smooth muscle layer in the vascular structure makes a great difference for vascular tissue regeneration. A functional tissue engineered vascular media shall promote the aligned organization and three-dimensional penetration of smooth muscle cells (SMCs) into the scaffold. To this aim, dynamic liquid and conjugated nanoyarns based on poly(L-lactide-co-caprolactone) (P(LLA-CL)) and collagen (COL) with a weight ratio at 3:1 were fabricated by electrospinning methods, with random and aligned nanofibers as control groups. The Fourier transform infrared spectroscopy and X-ray diffraction analyses confirmed the preservation of P(LLA-CL)/COL components and structure. Scanning electron microscope (SEM) results indicated a significant increase of yarn diameters at 19.27 ± 6.16 µm (dynamic liquid) and 10.24 ± 3.09 µm (conjugated), and both of the nanoyarns had improved mechanical tensile properties than the random nanofibers. Compared with random and aligned nanofibers, the nanoyarns presented significant higher porosity and larger pore diameter, leading to a decrease of water contact angle and a promotion of SMCs proliferation and migration. Better SMCs orientation was observed on the conjugated nanoyarns, while superior SMCs penetration was achieved on the dynamic liquid nanoyarns, owing to the differences in yarns microstructure. Herein, this study demonstrated that the aligned and porous P(LLA-CL)/COL nanoyarns fabricated by dynamic liquid and conjugated electrospinning were beneficial to regulating vascular SMCs outgrowth, which had important implications for functional reconstruction of vascular media.
[Mh] Termos MeSH primário: Materiais Biocompatíveis/síntese química
Colágeno/química
Músculo Liso Vascular/citologia
Miócitos de Músculo Liso/citologia
Nanoconjugados/química
Poliésteres/química
Tecidos Suporte
[Mh] Termos MeSH secundário: Proliferação Celular/fisiologia
Células Cultivadas
Galvanoplastia/métodos
Desenho de Equipamento
Análise de Falha de Equipamento
Seres Humanos
Músculo Liso Vascular/fisiologia
Miócitos de Músculo Liso/fisiologia
Nanoconjugados/ultraestrutura
Rotação
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biocompatible Materials); 0 (Nanoconjugates); 0 (Polyesters); 0 (poly(lactic acid-co-epsilon-caprolactone)); 9007-34-5 (Collagen)
[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:180131
[St] Status:MEDLINE


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[PMID]:28456475
[Au] Autor:Molinuevo MS; Fernández JM; Cortizo AM; McCarthy AD; Schurman L; Sedlinsky C
[Ad] Endereço:Laboratorio de Investigación en Osteopatías y Metabolismo Mineral, Facultad de Ciencias Exactas, Universidad Nacional de La Plata. 47 y 115, (1900) La Plata, Argentina.
[Ti] Título:Advanced glycation end products and strontium ranelate promote osteogenic differentiation of vascular smooth muscle cells in vitro: Preventive role of vitamin D.
[So] Source:Mol Cell Endocrinol;450:94-104, 2017 Jul 15.
[Is] ISSN:1872-8057
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Advanced glycation end products (AGE) have been demonstrated to induce the osteogenic trans-differentiation of vascular smooth muscle cells (VSMC). Strontium ranelate (SR) is an anti-osteoporotic agent that has both anti-catabolic and anabolic actions on bone tissue. However, in the last years SR has been associated with an increase of cardiovascular risk. We hypothesize that SR can increase the osteoblastic trans-differentiation of VSMC and the induction of extracellular calcifications, an effect that could be potentiated in the presence of AGE and inhibited by simultaneous administration of vitamin D. The present results of our in vitro experiments demonstrate that AGE and SR alone or in combination, stimulate L-type calcium channels, causing an increase in reactive oxygen species and activation of both ERK and NFkB, with the final effect of promoting the osteogenic shift of VSMC. Importantly, these in vitro effects of AGE and/or SR can be prevented by co-incubation with vitamin D.
[Mh] Termos MeSH primário: Diferenciação Celular/efeitos dos fármacos
Produtos Finais de Glicação Avançada/farmacologia
Músculo Liso Vascular/citologia
Miócitos de Músculo Liso/citologia
Osteogênese/efeitos dos fármacos
Tiofenos/farmacologia
Vitamina D/farmacologia
[Mh] Termos MeSH secundário: Animais
Ácido Ascórbico/farmacologia
Contagem de Células
Movimento Celular/efeitos dos fármacos
Subunidade alfa 1 de Fator de Ligação ao Core/metabolismo
Masculino
Modelos Biológicos
Miócitos de Músculo Liso/efeitos dos fármacos
Miócitos de Músculo Liso/metabolismo
Nifedipino/farmacologia
Estresse Oxidativo/efeitos dos fármacos
Ratos Sprague-Dawley
Espécies Reativas de Oxigênio/metabolismo
Sulfassalazina/farmacologia
Vitamina E/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Core Binding Factor Alpha 1 Subunit); 0 (Glycation End Products, Advanced); 0 (Reactive Oxygen Species); 0 (Thiophenes); 04NQ160FRU (strontium ranelate); 1406-16-2 (Vitamin D); 1406-18-4 (Vitamin E); 3XC8GUZ6CB (Sulfasalazine); I9ZF7L6G2L (Nifedipine); PQ6CK8PD0R (Ascorbic Acid)
[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:170501
[St] Status:MEDLINE


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[PMID]:29311554
[Au] Autor:Frudd K; Burgoyne T; Burgoyne JR
[Ad] Endereço:King's College London, Cardiovascular Division, The British Heart Foundation, Centre of Excellence, The Rayne Institute, St Thomas' Hospital, London, SE1 7EH, UK.
[Ti] Título:Oxidation of Atg3 and Atg7 mediates inhibition of autophagy.
[So] Source:Nat Commun;9(1):95, 2018 01 08.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Macroautophagy (autophagy) is a crucial cellular stress response for degrading defective macromolecules and organelles, as well as providing bioenergetic intermediates during hypoxia and nutrient deprivation. Here we report a thiol-dependent process that may account for impaired autophagy during aging. This is through direct oxidation of key autophagy-related (Atg) proteins Atg3 and Atg7. When inactive Atg3 and Atg7 are protected from oxidation due to stable covalent interaction with their substrate LC3. This interaction becomes transient upon activation of Atg3 and Atg7 due to transfer of LC3 to phosphatidylethanolamine (lipidation), a process crucial for functional autophagy. However, loss in covalent-bound LC3 also sensitizes the catalytic thiols of Atg3 and Atg7 to inhibitory oxidation that prevents LC3 lipidation, observed in vitro and in mouse aorta. Here findings provide a thiol-dependent process for negatively regulating autophagy that may contribute to the process of aging, as well as therapeutic targets to regulate autophagosome maturation.
[Mh] Termos MeSH primário: Envelhecimento/metabolismo
Proteína 7 Relacionada à Autofagia/química
Proteínas Relacionadas à Autofagia/química
Autofagia/efeitos dos fármacos
Peróxido de Hidrogênio/farmacologia
Proteínas Associadas aos Microtúbulos/química
Enzimas de Conjugação de Ubiquitina/química
[Mh] Termos MeSH secundário: Animais
Aorta/citologia
Aorta/efeitos dos fármacos
Aorta/metabolismo
Autofagossomos/efeitos dos fármacos
Autofagossomos/metabolismo
Proteína 7 Relacionada à Autofagia/metabolismo
Proteínas Relacionadas à Autofagia/metabolismo
Células HEK293
Seres Humanos
Masculino
Camundongos Endogâmicos C57BL
Proteínas Associadas aos Microtúbulos/metabolismo
Miócitos de Músculo Liso/citologia
Miócitos de Músculo Liso/efeitos dos fármacos
Miócitos de Músculo Liso/metabolismo
Oxirredução
Fosfatidiletanolaminas/química
Fosfatidiletanolaminas/metabolismo
Cultura Primária de Células
Ratos
Compostos de Sulfidrila/química
Enzimas de Conjugação de Ubiquitina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Atg7 protein, mouse); 0 (Autophagy-Related Proteins); 0 (MAP1LC3 protein, mouse); 0 (Microtubule-Associated Proteins); 0 (Phosphatidylethanolamines); 0 (Sulfhydryl Compounds); 39382-08-6 (phosphatidylethanolamine); BBX060AN9V (Hydrogen Peroxide); EC 2.3.2.23 (Ubiquitin-Conjugating Enzymes); EC 6.2.1.45 (Autophagy-Related Protein 7); EC 6.3.2.- (Atg3 protein, mouse)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180110
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02352-z


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[PMID]:28450296
[Au] Autor:Tian H; Ketova T; Hardy D; Xu X; Gao X; Zijlstra A; Blobe GC
[Ad] Endereço:From the Division of Medical Oncology, Department of Medicine (H.T., D.H., G.C.B.) and Department of Pharmacology and Cancer Biology (G.C.B.), Duke University Medical Center, Durham, NC; Department of Pathology, Microbiology, and Immunology (T.K., A.Z.) and Department of Cancer Biology (A.Z.), Vande
[Ti] Título:Endoglin Mediates Vascular Maturation by Promoting Vascular Smooth Muscle Cell Migration and Spreading.
[So] Source:Arterioscler Thromb Vasc Biol;37(6):1115-1126, 2017 Jun.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Endoglin, a transforming growth factor-ß superfamily coreceptor, is predominantly expressed in endothelial cells and has essential roles in vascular development. However, whether endoglin is also expressed in vascular smooth muscle cells (VSMCs), especially in vivo, remains controversial. Furthermore, the roles of endoglin in VSMC biology remain largely unknown. Our objective was to examine the expression and determine the function of endoglin in VSMCs during angiogenesis. APPROACH AND RESULTS: Here, we determine that endoglin is robustly expressed in VSMCs. Using CRISPR/CAS9 knockout and short hairpin RNA knockdown in the VSMC/endothelial coculture model system, we determine that endoglin in VSMCs, but not in endothelial cells, promotes VSMCs recruitment by the endothelial cells both in vitro and in vivo. Using an unbiased bioinformatics analysis of RNA sequencing data and further study, we determine that, mechanistically, endoglin mediates VSMC recruitment by promoting VSMC migration and spreading on endothelial cells via increasing integrin/FAK pathway signaling, whereas endoglin has minimal effects on VSMC adhesion to endothelial cells. In addition, we further determine that loss of endoglin in VSMCs inhibits VSMC recruitment in vivo. CONCLUSIONS: These studies demonstrate that endoglin has an important role in VSMC recruitment and blood vessel maturation during angiogenesis and also provide novel insights into how discordant endoglin function in endothelial and VSMCs may regulate vascular maturation and angiogenesis.
[Mh] Termos MeSH primário: Movimento Celular
Forma Celular
Endoglina/metabolismo
Músculo Liso Vascular/metabolismo
Miócitos de Músculo Liso/metabolismo
[Mh] Termos MeSH secundário: Animais
Sistemas CRISPR-Cas
Células Cultivadas
Técnicas de Cocultura
Endoglina/genética
Células Endoteliais/metabolismo
Quinase 1 de Adesão Focal/metabolismo
Regulação da Expressão Gênica
Seres Humanos
Integrinas/metabolismo
Camundongos Endogâmicos C57BL
Fenótipo
Interferência de RNA
Transdução de Sinais
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ENG protein, human); 0 (Endoglin); 0 (Eng protein, mouse); 0 (Integrins); EC 2.7.10.2 (Focal Adhesion Kinase 1); EC 2.7.10.2 (PTK2 protein, human); EC 2.7.10.2 (Ptk2 protein, mouse)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.116.308859


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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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