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Adiponectin is protective against endoplasmic reticulum stress-induced apoptosis of endothelial cells in sepsis BJMBR
Hou,Yun; Wang,Xi Feng; Lang,Zhi Qiang; Jin,Yin Chuan; Fu,Jia Rong; Xv,Xiao Min; Sun,Shi Tian; Xin,Xin; Zhang,Lian Shuang.
Endoplasmic reticulum (ER) stress is a critical molecular mechanism involved in the pathogenesis of sepsis. Hence, strategies for alleviating this stress may be essential for preventing cardiovascular injuries under sepsis. Adiponectin is secreted by adipocytes and its levels are decreased in sepsis. The purpose of this study was to investigate the protective effects of adiponectin treatment on endothelial cells and its mechanism. Male Wistar rats underwent cecal ligation and puncture (CLP) before being treated with adiponectin (72 and 120 μg/kg). The levels of malondialdehyde (MDA) in plasma, histological structure, and apoptosis of endothelial cells were evaluated. In vitro, human umbilical vein endothelial cells (HUVECs) were treated with adiponectin at...
Tipo: Info:eu-repo/semantics/article Palavras-chave: Adiponectin; Apoptosis; Endoplasmic reticulum stress; Endothelial cell; Sepsis.
Ano: 2018 URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2018001200609
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Endothelial cell oxidative stress and signal transduction Biol. Res.
FONCEA,ROCIO; CARVAJAL,CRISTIAN; ALMARZA,CAROLINA; LEIGHTON,FEDERICO.
Endothelial dysfunction (ED) is an early event in atherosclerotic disease, preceding clinical manifestations and complications. Increased reactive oxygen species (ROS) have been implicated as important mechanisms that contribute to ED, and ROS’s may function as intracellular messengers that modulate signaling pathways. Several intracellular signal events stimulated by ROS have been defined, including the identification of two members of the mitogen activated protein kinase family (ERK1/2 and big MAP kinase, BMK1), tyrosine kinases (Src and Syk) and different isoenzymes of PKC as redox-sensitive kinases. ROS regulation of signal transduction components include the modification in the activity of transcriptional factors such as NFkB and others that result in...
Tipo: Journal article Palavras-chave: Oxidative stress; Signal transduction; Gene expression; Endothelial cell; Atherosclerosis; Antioxidants.
Ano: 2000 URL: http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602000000200008
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Endothelial cells, tissue factor and infectious diseases BJMBR
Lopes-Bezerra,L.M.; Filler,S.G..
Tissue factor is a transmembrane procoagulant glycoprotein and a member of the cytokine receptor superfamily. It activates the extrinsic coagulation pathway, and induces the formation of a fibrin clot. Tissue factor is important for both normal homeostasis and the development of many thrombotic diseases. A wide variety of cells are able to synthesize and express tissue factor, including monocytes, granulocytes, platelets and endothelial cells. Tissue factor expression can be induced by cell surface components of pathogenic microorganisms, proinflammatory cytokines and membrane microparticles released from activated host cells. Tissue factor plays an important role in initiating thrombosis associated with inflammation during infection, sepsis, and organ...
Tipo: Info:eu-repo/semantics/article Palavras-chave: Tissue factor; Endothelial cell; Fungus; Infectious diseases; Procoagulant activity.
Ano: 2003 URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2003000800004
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Low molecular weight fucoidan promotes FGF-2-induced vascular tube formation by human endothelial cells, with decreased PAI-1 release and ICAM-1 downregulation ArchiMer
Chabut, D; Fischer, A; Helley, D; Colliec-jouault, Sylvia.
Tipo: Text Palavras-chave: Fucoidan; Vascularization; Endothelial cell; Human therapy.
Ano: 2004 URL: http://archimer.ifremer.fr/doc/2004/publication-2115.pdf
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The blockade of cyclooxygenases-1 and -2 reduces the effects of hypoxia on endothelial cells BJMBR
Gloria,M.A.; Cenedeze,M.A.; Pacheco-Silva,A.; Câmara,N.O.S..
Hypoxia activates endothelial cells by the action of reactive oxygen species generated in part by cyclooxygenases (COX) production enhancing leukocyte transmigration. We investigated the effect of specific COX inhibition on the function of endothelial cells exposed to hypoxia. Mouse immortalized endothelial cells were subjected to 30 min of oxygen deprivation by gas exchange. Acridine orange/ethidium bromide dyes and lactate dehydrogenase activity were used to monitor cell viability. The mRNA of COX-1 and -2 was amplified and semi-quantified before and after hypoxia in cells treated or not with indomethacin, a non-selective COX inhibitor. Expression of RANTES (regulated upon activation, normal T cell expressed and secreted) protein and the protective role...
Tipo: Info:eu-repo/semantics/article Palavras-chave: Endothelial cell; Hypoxia; Indomethacin; Cyclooxygenase; Heme oxygenase 1.
Ano: 2006 URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2006000900006
Registros recuperados: 5
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