Base de dados : LILACS
Pesquisa : A11.620.520 [Categoria DeCS]
Referências encontradas : 35 [refinar]
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Id: biblio-838973
Autor: Seo, Hyang-Hee; Kim, Sang Woo; Lee, Chang Youn; Lim, Kyu Hee; Lee, Jiyun; Choi, Eunhyun; Lim, Soyeon; Lee, Seahyoung; Hwang, Ki-Chul.
Título: A spleen tyrosine kinase inhibitor attenuates the proliferation and migration of vascular smooth muscle cells
Fonte: Biol. Res;50:1, 2017. tab, graf.
Idioma: en.
Projeto: Future Planning; . Future Planning.
Resumo: BACKGROUND: Pathologic vascular smooth muscle cell (VSMC) proliferation and migration after vascular injury promotes the development of occlusive vascular disease. Therefore, an effective chemical agent to suppress aberrant proliferation and migration of VSMCs can be a potential therapeutic modality for occlusive vascular disease such as atherosclerosis and restenosis. To find an anti-proliferative chemical agent for VSMCs, we screened an in-house small molecule library, and the selected small molecule was further validated for its anti-proliferative effect on VSMCs using multiple approaches, such as cell proliferation assays, wound healing assays, transwell migration assays, and ex vivo aortic ring assay. RESULTS: Among 43 initially screened small molecule inhibitors of kinases that have no known anti-proliferative effect on VSMCs, a spleen tyrosine kinase (Syk) inhibitor (BAY61-3606) showed significant anti-proliferative effect on VSMCs. Further experiments indicated that BAY61 attenuated the VSMC proliferation in both concentration- and time-dependent manner, and it also significantly suppressed the migration of VSMCs as assessed by both wound healing assays and transwell assays. Additionally, BAY61 suppressed the sprouting of VSMCs from endothelium-removed aortic rings. CONCLUSION: The present study identified a Syk kinase inhibitor as a potent VSMC proliferation and migration inhibitor and warrants further studies to elucidate its underlying molecular mechanisms, such as its primary target, and to validate its in vivo efficacy as a therapeutic agent for restenosis and atherosclerosis.
Descritores: Pirimidinas/farmacologia
Movimento Celular/efeitos dos fármacos
Niacinamida/análogos & derivados
Miócitos de Músculo Liso/efeitos dos fármacos
Proliferação de Células/efeitos dos fármacos
Quinase Syk/antagonistas & inibidores
Músculo Liso Vascular/efeitos dos fármacos
-Aorta Torácica/efeitos dos fármacos
Fatores de Tempo
Cicatrização/efeitos dos fármacos
Células Cultivadas
Western Blotting
Reprodutibilidade dos Testes
Ratos Sprague-Dawley
Niacinamida/farmacologia
Relação Dose-Resposta a Droga
Avaliação Pré-Clínica de Medicamentos
Ensaios de Migração Celular
Músculo Liso Vascular/citologia
Limites: Animais
Ratos
Tipo de Publ: Estudo de Avaliação
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-950771
Autor: Yin, Lei-Miao; Wei, Ying; Wang, Wen-Qian; Wang, Yu; Xu, Yu-Dong; Yang, Yong-Qing.
Título: Simultaneous application of BrdU and WST-1 measurements for detection of the proliferation and viability of airway smooth muscle cells
Fonte: Biol. Res;47:1-5, 2014. ilus, graf.
Idioma: en.
Projeto: National Natural Science Foundation of China; . The Scientific Research Funds for Young Scholar of the Health System in Shanghai. Shanghai Rising-Star Program.
Resumo: BACKGROUND: BrdU is a commonly used reagent in cell proliferation assays, and WST-1 measurement is widely used to detect cell viability. However, no previous study has formally reported the combination of the two assays, which may be used to detect the proliferation and viability simultaneously. In this study, we examined the effect of adding BrdU 2 h prior to the WST-1 assay and tried to test the possibility of the combined detection using rat airway smooth muscle cells. RESULTS: The WST-1 measurements obtained from the combined detection were consistent with those obtained from the separate detection, which suggested that the addition of BrdU 2 h prior to the WST-1 analysis did not affect the WST-1 results. The BrdU measurements obtained from the combined detection also demonstrated the same trend as that obtained from the separate detection, and dosages of 200, 400 and 800 ng/ml testing reagent significantly inhibited the proliferation of rat airway smooth muscle cells. CONCLUSIONS: Our study suggests that the BrdU and WST-1 measurements can be applied simultaneously without mutual interference, which may increase the efficacy and consistency of these measurements to a certain extent.
Descritores: Avaliação da Tecnologia Biomédica/métodos
Sais de Tetrazólio/farmacologia
Traqueia/citologia
Bromodesoxiuridina/farmacologia
Miócitos de Músculo Liso/fisiologia
Proliferação de Células/fisiologia
-Kit de Reagentes para Diagnóstico
Traqueia/crescimento & desenvolvimento
Ensaio de Imunoadsorção Enzimática
Sobrevivência Celular/fisiologia
Calgranulina B/administração & dosagem
Cultura Primária de Células
Limites: Animais
Ratos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-1131888
Autor: Liu, Yi; Cui, Xiyun; Wang, Cong; Zhao, Sihai.
Título: LncRNA HCG11 regulates proliferation and apoptosis of vascular smooth muscle cell through targeting miR-144-3p/FOXF1 axis in atherosclerosis
Fonte: Biol. Res;53:44, 2020. graf.
Idioma: en.
Resumo: BACKGROUND: Atherosclerosis (AS) is the main pathological basis of coronary heart disease, cerebral infarction and peripheral vascular disease, which seriously endanger people's life and health. In recent years, long non-coding RNA (lncRNA) has been found to be involved in gene expression regulation, but the research on AS is still in the initial stage. In this study, we mainly studied the role of HCG11 in patients with AS. Quantitative Real-time Polymerase Chain Reaction (QRT-PCR) was used to detect the expression of HCG11 and miR-144 in the serum of AS patients and healthy volunteers. Oxidation Low Lipoprotein (Ox-LDL), interleukin-6 (IL-6) and tumor necrosis factor α (TNF α) radiation were used to establish human vascular smooth muscle cells (VSMCs) in vitro model. Cell proliferation was determined by Cell Counting Kit-8 (CCK-8) assay. The apoptosis rate was determined by flow cytometry (FACS) and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL) staining. The expression levels of Forkhead box protein F1 (FOXF1), B cell lymphoma-2 (Bcl-2) and BCL2-Associated X (Bax) were detected by qRT-PCR. Luciferase gene reporter and RNA pull down experiments confirmed the relationship between HCG11 and miR-144, miR-144 and FOXF1. RESULTS: This study showed that HCG11 was significantly upregulated in patients with AS, while miR-144 was down-regulated in patients with AS. Ox-LDL and IL-6 in VSMCs induced up-regulation of HCG11 and down-regulation of miR-144. Overexpression of HCG11 promoted the proliferation and inhibited apoptosis of VSMCs. Luciferase gene reporter gene assay showed that HCG11 could bind to miR-144, and miR-144 could bind to FOXF1. Overexpression of miR-144 reversed the effect of HCG11 on VSMCs. CONCLUSIONS: LncRNA HCG11 regulates proliferation and apoptosis of vascular smooth muscle cell through targeting miR-144-3p/FOXF1 axis.
Descritores: Miócitos de Músculo Liso/citologia
MicroRNAs/genética
Aterosclerose/genética
Fatores de Transcrição Forkhead/genética
RNA Longo não Codificante/genética
-Apoptose/genética
Proliferação de Células/genética
Músculo Liso Vascular/citologia
Limites: Humanos
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-956455
Autor: Yu, Wen-Cheng; Cong, Jin-Peng; Mi, Li-Yun.
Título: Expressions of TOLL-like receptor 4 (TLR-4) and matrix metalloproteinase 9 (MMP-9)/Tissue inhibitor of metalloproteinase 1 (TIMP-1) in pulmonary blood vessels with chronic obstructive pulmonary diseases and their relationships with pulmonary vascular remodelling
Fonte: Rev. Assoc. Med. Bras. (1992);64(4):361-367, Apr. 2018. tab, graf.
Idioma: en.
Resumo: SUMMARY OBJECTIVE: This study aims at investigating the expressions of TOLL-like receptor 4 (TLR-4) and matrix metalloproteinase 9 (MMP-9)/ tissue inhibitor of metalloproteinase 1 (TIMP-1) in pulmonary blood vessels with chronic obstructive pulmonary disease (COPD) and their relationships with pulmonary vascular remodelling (PVR). METHODS: 60 para-tumour tissues were divided into the COPD group and the control group (n=30); the inflammations, pulmonary artery wall area/total artery area (WA%), and wall thickness/vascular outer diameter (WT%) were compared. The expressions of TLR-4, MMP-9/TIMP-1, and PCNA in pulmonary vascular smooth muscle cells were detected, and their relationships with PVR were then analysed. RESULTS: The inflammations (1.6±0.8), WA% (44.0±6.4), and WT% (27.3±3.3) in the COPD group were higher than in the control group (0.3±0.5, 26.1±2.8, 15.6±1.8), and the expressions of TLR-4 (31.4±147) and MMP-9/TIMP-1 (2.2±2.6) were increased compared to the control group (4.7±4.5, 1.9±12). Correlation analysis: TLR-4 and MMP-9/TIMP-1 were positively correlated with the inflammations (r=0.18, P<0.01), WA% (r=0.68, P<0.01), and WT% (r=0.73, P<0.01), as well as positively correlated with the expression of PCNA (r=0.44, P<0.01); the upregulation of TLR-4 was positively correlated with the expressions of MMP-9 and TIMP-1. CONCLUSIONS: The upregulation of TLR-4 in the pulmonary arterial smooth muscle cells of COPD patients could promote the inflammations and the MMP-9 expression, thus causing abnormal degradation of extracellular matrix, so it played an important role in the process of PVR.

RESUMO OBJETIVO: Este estudo tem como objetivo investigar as expressões de TOLL-like receptor 4 (TLR-4) e metaloproteinase 9 da matriz (MMP-9)/inibidor de tecido da metaloproteinase 1 (TIMP-1) em vasos sanguíneos pulmonares com doença pulmonar obstrutiva crônica (DPOC) e suas relações com o remodelamento vascular pulmonar (PVR). MÉTODOS: Sessenta tecidos paratumorais foram divididos em grupo COPD e o grupo controle (n = 30). Foram comparadas as inflamações, área da parede da artéria pulmonar/área da artéria total (WA%) e espessura da parede/diâmetro externo vascular (WT%). As expressões de TLR-4, MMP-9/TIMP-1 e PCNA em células de músculo liso vascular pulmonar foram detectadas, e suas relações com PVR foram então analisadas. RESULTADOS: As inflamações (1,6 ± 0,8), WA% (44,0 ± 6,4) e WT% (27,3 ± 3,3) no grupo COPD foram maiores que no grupo controle (0,3 ± 0,5; 26,1 ± 2,8; 15,6 ± 1,8). E as expressões de TLR-4 (31,4 ± 14,7) e MMP-9/TIMP-1 (2,2 ± 2,6) foram aumentadas em relação ao grupo controle (4,7 ± 4,5, 1,9 ± 1,2). Na análise de correlação, TLR-4 e MMP-9/TIMP-1 foram positivamente correlacionadas com as inflamações (r = 0,18; P <0,01), WA% (r = 0,68; P <0,01) e WT% (r = 0,73; P <0,01), bem como correlacionadas positivamente com a expressão de PCNA (r = 0,44; P <0,01). A elevação da TLR-4 foi correlacionada positivamente com as expressões de MMP-9 e TIMP-1. CONCLUSÕES: A regulação positiva do TLR-4 nas células do músculo liso arterial pulmonar de pacientes com DPOC poderia promover as inflamações e a expressão de MMP-9, causando assim uma degradação anormal da matriz extracelular, por isso desempenhou um papel importante no processo de PVR.
Descritores: Artéria Pulmonar/metabolismo
Inibidor Tecidual de Metaloproteinase-1/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
Doença Pulmonar Obstrutiva Crônica/metabolismo
Receptor 4 Toll-Like/metabolismo
Remodelação Vascular
-Valores de Referência
Imuno-Histoquímica
Estudos de Casos e Controles
Capacidade Vital/fisiologia
Volume Expiratório Forçado/fisiologia
Doença Pulmonar Obstrutiva Crônica/fisiopatologia
Miócitos de Músculo Liso/metabolismo
Hematoxilina
Pulmão/irrigação sanguínea
Pessoa de Meia-Idade
Limites: Humanos
Masculino
Responsável: BR1.1 - BIREME


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Id: biblio-950874
Autor: Xu, Yu-Dong; Wang, Yu; Yin, Lei-Miao; Peng, Ling-Ling; Park, Gyoung-Hee; Yang, Yong-Qing.
Título: S100A8 inhibits PDGF-induced proliferation of airway smooth muscle cells dependent on the receptor for advanced glycation end-products
Fonte: Biol. Res;50:23, 2017. graf.
Idioma: en.
Projeto: National Natural Science Foundation of China; . National Natural Science Foundation of China; . National Natural Science Foundation of China; . Shanghai Municipal Commission of Health and Family Planning; . Shanghai Municipal Commission of Health and Family Planning.
Resumo: BACKGROUND: Airway remodeling is a key feature of asthma, characterized by increased proliferation of airway smooth muscle cells (ASMCs). S100A8 is a calcium-binding protein with a potential to regulate cell proliferation. Here, the effect of exogenous S100A8 protein on the proliferation of ASMCs induced by platelet-derived growth factor (PDGF) and the underlying molecular mechanism was investigated. METHODS: Rat ASMCs were cultured with or without a neutralizing antibody to the receptor for advanced glycation end-products (RAGE), a potential receptor for S100A8 protein. Purified recombinant rat S100A8 protein was then added into the cultured cells, and the proliferation of ASMCs induced by PDGF was detected by colorimetric-based WST-8 assay and ampedance-based xCELLigence proliferation assay. The expression levels of RAGE in ASMCs were analyzed using western blotting assay. RESULTS: Results showed that exogenous S100A8 inhibited the PDGF-induced proliferation of rat ASMCs in a dose- dependent manner with the maximal effect at 1 µg/ml in vitro. Furthermore, when ASMCs was pre-treated with anti-RAGE neutralizing antibody, the inhibitory effect of S100A8 on PDGF-induced proliferation was significantly suppressed. In addition, neither the treatment with S100A8 or PDGF alone nor the pre-treatment with rS100A8 followed by PDGF stimulation affected the expression levels of RAGE. CONCLUSIONS: Our study demonstrated that S100A8 inhibits PDGF-induced ASMCs proliferation in a manner dependent on membrane receptor RAGE.
Descritores: Fator de Crescimento Derivado de Plaquetas/agonistas
Miócitos de Músculo Liso/efeitos dos fármacos
Calgranulina A/administração & dosagem
Proliferação de Células/efeitos dos fármacos
Receptor para Produtos Finais de Glicação Avançada/efeitos dos fármacos
-Células Cultivadas
Limites: Animais
Ratos
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-1100911
Autor: Zhang, Chuang; Li, Huixiang; Guo, Xueli.
Título: FOXC2-AS1 regulates phenotypic transition, proliferation and migration of human great saphenous vein smooth muscle cells
Fonte: Biol. Res;52:59, 2019. graf.
Idioma: en.
Resumo: OBJECTIVES: In varicose veins, vascular smooth muscle cells (VSMCs) often shows phenotypic transition and abnormal proliferation and migration. Evidence suggests the FOXC2-Notch pathway may be involved in the pathogenesis of varicose veins. Here, this study aimed to explore the role of long non-coding RNA FOXC2-AS1 (FOXC2 antisense RNA 1) in phenotypic transition, proliferation, and migration of varicose vein-derived VSMCs and to explore whether the FOXC2-Notch pathway was involved in this process. METHODS: The effect of FOXC2-AS1 on the proliferation and migration of human great saphenous vein smooth muscle cells (SV-SMCs) was analyzed using MTT assay and Transwell migration assay, respectively. The levels of contractile marker SM22α and synthetic marker osteopontin were measured by immunohistochemistry and Western blot to assess the phenotypic transition. RESULTS: The human varicose veins showed thickened intima, media and adventitia layers, increased synthetic VSMCs, as well as upregulated FOXC2-AS1 and FOXC2 expression. In vitro assays showed that FOXC2-AS1 overexpression promoted phenotypic transition, proliferation, and migration of SV-SMCs. However, the effect of FOXC2-AS1 overexpression could be abrogated by both FOXC2 silencing and the Notch signaling inhibitor FLI-06. Furthermore, FOXC2-AS1 overexpression activated the Notch pathway by upregulating FOXC2. CONCLUSION: FOXC2-AS1 overexpression promotes phenotypic transition, proliferation, and migration of SV-SMCs, at least partially, by activating the FOXC2-Notch pathway.
Descritores: Veia Safena/metabolismo
Movimento Celular/fisiologia
Miócitos de Músculo Liso/metabolismo
Proliferação de Células/fisiologia
Fatores de Transcrição Forkhead/metabolismo
-Fenótipo
Veia Safena/patologia
Transdução de Sinais
Regulação para Cima
Células Cultivadas
Miócitos de Músculo Liso/patologia
Limites: Humanos
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-837705
Autor: Jia, Peng; Hu, Yu; Li, Gang; Sun, Yuqin; Zhao, Jian; Fu, Jie; Lu, Cuixia; Liu, Bin.
Título: Roles of the ERK1/2 and PI3K/PKB signaling pathways in regulating the expression of extracellular matrix genes in rat pulmonary artery smooth muscle cells
Fonte: Acta cir. bras;32(5):350-358, May 2017. tab, graf.
Idioma: en.
Projeto: Science and Technology Research Foundation of Sichuan Provincial Health Department.
Resumo: Abstract Purpose: To investigate the mechanisms by which PD98059 and LY294002 interfere with the abnormal deposition of extracellular matrix regulated by connective tissue growth factor (CTGF) of rat pulmonary artery smooth muscle cells (PASMCs). Methods: Rat PASMCs were cultured and separated into a control group. Real-time fluorescence quantitative PCR was performed to detect the expression of collagen III and fibronectin mRNA. Immunohistochemistry and western blot analyses were performed to detect the expression of collagen III protein. Results: The expression of collagen III and fibronectin mRNA was greater in PASMCs stimulated with CTGF for 48 h, than in the control group. After 72h of stimulation, the expression of collagen III protein in the PASMCs was greater than in the control. The equivalent gene and protein expression of the CPL group were much more significant. Conclusions: CTGF can stimulate the gene expression of collagen III and fibronectin in PASMCs, which may be one of the factors that promote pulmonary vascular remodeling (PVR) under the conditions of pulmonary arterial hypertension (PAH). PD98059 and LY294002 can inhibit the ERK1/2 and PI3K/PKB signaling pathways, respectively, thus interfering with the biological effects of CTGF. This may be a new way to reduce PAH-PVR.
Descritores: Flavonoides/farmacologia
Cromonas/farmacologia
Fibronectinas/metabolismo
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Colágeno Tipo III/metabolismo
Fator de Crescimento do Tecido Conjuntivo/farmacologia
-Artéria Pulmonar/citologia
Expressão Gênica/efeitos dos fármacos
Células Cultivadas
Regulação da Expressão Gênica
Fibronectinas/genética
Ratos Sprague-Dawley
Fosfatidilinositol 3-Quinases/metabolismo
Modelos Animais
Colágeno Tipo III/genética
Miócitos de Músculo Liso/citologia
Miócitos de Músculo Liso/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Fator de Crescimento do Tecido Conjuntivo/metabolismo
Limites: Animais
Masculino
Responsável: BR1.1 - BIREME


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Id: biblio-900479
Autor: Yañez, Julian; Duque, Angélica; Beltrán, María Isleña.
Título: Leiomiosarcoma de ovario: tumor infrecuente y de comportamiento agresivo / Leiomyosarcoma ovarian cancer: a rare tumour with aggressive behaviour
Fonte: Rev. colomb. cancerol;21(4):230-235, oct.-dic. 2017. graf.
Idioma: es.
Resumo: Resumen Los leiomyosarcomas pueden originarse en la mayor parte de los órganos desarrollados fuera del sistema nervioso central. Se han documentado casos de leiomyosarcomas de origen: intestinal, mesentérico, uterino, retroperitoneal, de tejidos blandos y vascular. Sin embargo, los casos de leiomyosarcomas primarios de ovario son extremadamente infrecuentes y pocos casos han sido descritos en la literatura. Se cree que estos leiomyosarcomas se originan en el músculo liso alrededor de los folículos o a partir de remanentes del conducto de Wolff a partir de las paredes de la vasculatura existente en el parénquima ovárico. La mayor parte de los casos se presentan en pacientes postmenopáusicas y con un pronóstico a corto plazo desfavo rable. El pilar del tratamiento continúa siendo la citorreducción tumoral completa obteniendo márgenes quirúrgicos negativos con miras a disminuir el potencial de recidiva. El beneficio de la utilización de quimioterapia adyuvante como parte del tratamiento de esta patología sigue siendo incierto.

Abstract Leiomyosarcomas may originate in most of the organs developed outside the central nervous system. There are documented cases of leiomyosarcomas of intestinal, mesenteric, ute rine, retroperitoneal, and of soft and vascular tissue origin. However, cases of primary ovarian leiomyosarcoma are extremely rare, with few cases reported in the international literature. Leiomyosarcomas are believed to be those that originate from the walls of existing vasculature in ovarian parenchyma, in the smooth muscle around the follicles, or from remnants of the Wolff duct. Most cases occur in post-menopausal patients, and have an unfavourable prognosis in the short term. The mainstay of treatment remains the complete tumour debulking, with negative surgical margins in order to reduce the potential for recurrence. The benefit of the use of adjuvant chemotherapy as part of treatment of this condition remains uncertain.
Descritores: Leiomiossarcoma
-Quimioterapia Adjuvante
Miócitos de Músculo Liso
Ovário
Limites: Humanos
Tipo de Publ: Relatos de Casos
Responsável: CO304.1 - Biblioteca Arturo Aparicio Jaramillo


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Id: lil-792523
Autor: Chai, SD; Liu, T; Dong, MF; Li, ZK; Tang, PZ; Wang, JT; Ma, SJ.
Título: Inactivated Pseudomonas aeruginosa inhibits hypoxia-induced pulmonary hypertension by preventing TGF-beta1/Smad signaling
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;49(10):e5526, 2016. graf.
Idioma: en.
Resumo: Pseudomonas aeruginosa is one of the common colonizing bacteria of the human body and is an opportunistic pathogen frequently associated with respiratory infections. Inactivated P. aeruginosa (IPA) have a variety of biological effects against inflammation and allergy. Transforming growth factor-β (TGF-β) signaling plays a critical role in the regulation of cell growth, differentiation, and development in a wide range of biological systems. The present study was designed to investigate the effects of IPA on TGF-β/Smad signaling in vivo, using a hypoxia-induced pulmonary hypertension (PH) rat model. Sprague Dawley rats (n=40) were exposed to 10% oxygen for 21 days to induce PH. At the same time, IPA was administered intravenously from day 1 to day 14. Mean pulmonary artery pressure (mPAP) and the right ventricle (RV) to left ventricle plus the interventricular septum (LV+S) mass ratio were used to evaluate the development of PH. Vessel thickness and density were measured using immunohistochemistry. Primary arterial smooth muscle cells (PASMCs) were isolated and the proliferation of PASMCs was assayed by flow cytometry. The production of TGF-β1 in cultured supernatant of PASMCs was assayed by ELISA. The expression levels of α-smooth muscle actin (α-SMA), TGF-β1 and phospho-Smad 2/3 in PASMCs were assayed by western blot. Our data indicated that IPA attenuated PH, RV hypertrophy and pulmonary vascular remodeling in rats, which was probably mediated by restraining the hypoxia-induced overactive TGF-β1/Smad signaling. In conclusion, IPA is a promising protective treatment in PH due to the inhibiting effects on TGF-β1/Smad 2/3 signaling.
Descritores: Hipertensão Pulmonar/metabolismo
Hipertensão Pulmonar/prevenção & controle
Hipóxia/metabolismo
Miócitos de Músculo Liso/fisiologia
Pseudomonas aeruginosa/fisiologia
Proteínas Smad/metabolismo
Fator de Crescimento Transformador beta1/metabolismo
-Actinas/análise
Actinas/metabolismo
Western Blotting
Proliferação de Células/fisiologia
Ensaio de Imunoadsorção Enzimática
Citometria de Fluxo
Hipertensão Pulmonar/etiologia
Hipóxia/complicações
Imuno-Histoquímica
Ratos Sprague-Dawley
Reprodutibilidade dos Testes
Transdução de Sinais/fisiologia
Proteínas Smad/análise
Fator de Crescimento Transformador beta1/análise
Limites: Animais
Masculino
Tipo de Publ: Estudo de Avaliação
Responsável: BR1.1 - BIREME


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Id: lil-774551
Autor: Yuan, Shi-Min.
Título: α-Smooth Muscle Actin and ACTA2 Gene Expressions in Vasculopathies
Fonte: Rev. bras. cir. cardiovasc = Braz. j. cardiovasc. surg. (impr.);30(6):644-649, Nov.-Dec. 2015. tab, graf.
Idioma: en.
Resumo: ABSTRACT α-smooth muscle actin, encoded by ACTA2 gene, is an isoform of the vascular smooth muscle actins, typically expressed in the vascular smooth muscle cells contributing to vascular motility and contraction. ACTA2 gene mutations cause a diversity of diffuse vasculopathies such as thoracic aortic aneurysms and dissections as well as occlusive vascular diseases, including premature coronary artery disease and ischemic stroke. Dynamics of differentiation-specific α-smooth muscle actin in arterial smooth muscle cells and proliferation of the proteins have been well described. Although a variety of research works have been undertaken in terms of modifications of α-smooth muscle actin and mutations of ACTA2 gene and myosin, the underlying mechanisms towards the pathological processes by way of gene mutations are yet to be clarified. The purpose of the present article is to describe the phenotypes of α-smooth muscle actin and implications of ACTA2 mutations in vasculopathies in order to enhance the understanding of potential mechanisms of aortic and coronary disorders.
Descritores: Actinas/genética
Doenças da Aorta/metabolismo
Doença das Coronárias/metabolismo
Músculo Liso Vascular/metabolismo
Miócitos de Músculo Liso/metabolismo
-Actinas/metabolismo
Doenças da Aorta/genética
Doença das Coronárias/genética
Expressão Gênica
Contração Muscular/fisiologia
Mutação/genética
Fenótipo
Limites: Humanos
Tipo de Publ: Revisão
Responsável: BR1.1 - BIREME



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BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde