Endothelium-journal of Endothelial Cell Research最新文献_第5页

Hypoxia-reoxygenation inhibits gap junctional communication in cultured human umbilical vein endothelial cells. 缺氧复氧抑制培养人脐静脉内皮细胞间隙连接通讯。

Endothelium-journal of Endothelial Cell Research Pub Date : 2000-01-01 DOI: 10.3109/10623320009072214

M. Nishida, S. Futami, I. Morita, Kazuhiko Maekawa, Sci-itsu Murota

{"title":"Hypoxia-reoxygenation inhibits gap junctional communication in cultured human umbilical vein endothelial cells.","authors":"M. Nishida, S. Futami, I. Morita, Kazuhiko Maekawa, Sci-itsu Murota","doi":"10.3109/10623320009072214","DOIUrl":"https://doi.org/10.3109/10623320009072214","url":null,"abstract":"We studied the change in gap junctional intercellular communication (GJIC) on human umbilical vein endothelial cells (HUVEC) under hypoxia-reoxygenation (H-R) conditions by the fluorescence redistribution after photobleaching (FRAP) method. Confluent HUVEC monolayers were exposed to hypoxia (pO2<0.1%) for 12 hours, and then were returned to normal atmospheric conditions for reoxygenation. Contrast microscopic observation showed no significant changes in the morphology of the HUVEC at any times after H-R. Reoxygenation following hypoxia caused time-dependent decrease in GJIC, that is, GJIC reduction was induced after 2 hours and reached maximum at 4-6 hours which recovered to normal levels after 18 hours. Oxidant sensitive fluorescence dye assay revealed that the generation of intracellular free radicals increased during the first 2 hours after reoxygenation. Hydroxyl radical scavengers (MCI-186, DMSO) and an iron chelator (deferoxamine) abolished the reduction of GJIC due to H-R. However, SOD, catalase and probucol were essentially inactive on this reduction. These data suggest that ischemia-reperfusion injury may be caused by a functional defect of GJIC induced by reactive oxygen radicals.","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"95 1","pages":"279-86"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76365522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 19

Second Symposium: Signal Transduction in the Blood-Brain Barrier: Congress Centre IBC Bogensee, Bogensee near Berlin, Germany 第二届研讨会:血脑屏障中的信号转导:会议中心IBC Bogensee，德国柏林附近的Bogensee

Endothelium-journal of Endothelial Cell Research Pub Date : 2000-01-01 DOI: 10.3109/10623320009165318

I. Blasig, R. Haseloff

引用次数: 0

Regulation of endothelial barrier function by the cAMP-dependent protein kinase. camp依赖性蛋白激酶对内皮屏障功能的调控。

Endothelium-journal of Endothelial Cell Research Pub Date : 2000-01-01 DOI: 10.3109/10623320009072215

Carolyn E. Patterson, Hazel Lum, K. Schaphorst, A. Verin, J. G. Garcia

{"title":"Regulation of endothelial barrier function by the cAMP-dependent protein kinase.","authors":"Carolyn E. Patterson, Hazel Lum, K. Schaphorst, A. Verin, J. G. Garcia","doi":"10.3109/10623320009072215","DOIUrl":"https://doi.org/10.3109/10623320009072215","url":null,"abstract":"Elevation of cAMP promotes the endothelial cell (EC) barrier and protects the lung from edema development. Thus, we tested the hypothesis that both increases and decreases in PKA modulate EC function and coordinate distribution of regulatory, adherence, and cytoskeletal proteins. Inhibition of PKA activity by RpcAMPS and activation by cholera toxin was verified by assay of kemptide phosphorylation in digitonin permeabilized EC. Inhibition of PKA by RpcAMPS or overexpression of the endogenous inhibitor, PKI, decreased monolayer electrical impedance and exacerbated the decreases produced by agonists (thrombin and PMA). RpcAMPS directly increased F-actin content and organization into stress fibers, increased co-staining of actin with both phosphatase 2B and myosin light chain kinase (MLCK), caused reorganization of focal adhesions, and decreased catenin at cell borders. These findings are similar to those evoked by thrombin. In contrast, cholera toxin prevented the agonist-induced resistance decrease and protein redistribution. Although PKA activation attenuated thrombin-induced myosin light chain (MLC) phosphorylation, PKA inhibition per se did not cause MLC phosphorylation or affect [Ca2+]i. These studies indicate that a decrease in PKA activity alone can produce disruption of barrier function via mechanisms not involving MLCK and support a central role for cAMP/PKA in regulation of cytoskeletal and adhesive protein function in EC which correlates with altered barrier function.","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"45 1","pages":"287-308"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76929435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 104

Effect of high blood flow on the expression of endothelial constitutive nitric oxide synthase in rats with femoral arteriovenous shunts. 高血流量对股动静脉分流术后大鼠内皮型一氧化氮合酶表达的影响。

Endothelium-journal of Endothelial Cell Research Pub Date : 2000-01-01 DOI: 10.3109/10623320009072211

B. Jeon, S. Chang, J. W. Kim, Y. Hong, S. Yoon, I. Choe

{"title":"Effect of high blood flow on the expression of endothelial constitutive nitric oxide synthase in rats with femoral arteriovenous shunts.","authors":"B. Jeon, S. Chang, J. W. Kim, Y. Hong, S. Yoon, I. Choe","doi":"10.3109/10623320009072211","DOIUrl":"https://doi.org/10.3109/10623320009072211","url":null,"abstract":"The effect of high blood flow on the expression of endothelial nitric oxide synthase has been investigated in the femoral arteriovenous shunt (AVS) rats created by inserting U-shaped polyurethane tubes in the left femoral arteries and veins. Three days after inserting the femoral AVS, the mean aortic blood flow rate in the abdominal aorta of the AVS rats was about 2.0 times higher than that in the control rats (110.0 +/- 8.4 ml/min vs 52.7 +/- 2.7 ml/min, p < 0.001). The competitive reverse transcriptase-polymerase chain reaction (RT-PCR) data revealed that the mRNA expression level of the endothelial constitutive nitric oxide synthase (ecNOS) was increased in the aortas of the femoral AVS rats compared to that in the control rats. Western blot analysis using a monoclonal antibody against ecNOS revealed that the ecNOS protein levels were markedly increased in the aortas of femoral AVS rats, but ecNOS protein levels in aortas without endothelium were not significantly increased. Inducible nitric oxide synthase (iNOS) protein was not expressed in the aortic tissues with and without endothelium in the control rats. This iNOS expression was not increased by the high blood flow in the femoral AVS rats. These findings suggest that high blood flow could up-regulate the expression levels of ecNOS mRNA and proteins in femoral arteriovenous shunt rats.","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"61 1","pages":"243-52"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90590367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 9

Highlights of the 9th Endothelium Symposium, Rotterdam, the Netherlands 荷兰鹿特丹第九届内皮细胞研讨会的亮点

Endothelium-journal of Endothelial Cell Research Pub Date : 1997-01-01 DOI: 10.3109/10623329709052600

W. Sluiter, R. W. D. Waal, M. D. Ruiter

引用次数: 0

Protein Kinase C Inhibitors Prevent Cultured Human Endothelial Cell Stress Fiber Formation, but not Heightened Endocytosis 蛋白激酶C抑制剂阻止培养的人内皮细胞应激纤维的形成，但不增加内吞作用

Endothelium-journal of Endothelial Cell Research Pub Date : 1996-01-01 DOI: 10.3109/10623329609024697

V. Patel, Jamie W. Meyer, David K. Johnson, R. Abdul-karim, L. M. Ziegler, L. Kauffman, K. Schillinger, L. Lemanski, J. Holland

{"title":"Protein Kinase C Inhibitors Prevent Cultured Human Endothelial Cell Stress Fiber Formation, but not Heightened Endocytosis","authors":"V. Patel, Jamie W. Meyer, David K. Johnson, R. Abdul-karim, L. M. Ziegler, L. Kauffman, K. Schillinger, L. Lemanski, J. Holland","doi":"10.3109/10623329609024697","DOIUrl":"https://doi.org/10.3109/10623329609024697","url":null,"abstract":"In order to study the signal transduction mechanism of endothelial perturbation, the effects of phorbol 12-myristate 13-acetate (PMA) and phorbol 12,13-dibutyrate (PDBu), both protein kinase C (PKC) activators, on cultured human endothelial cell (EC) hydrogen peroxide (H2O2) generation, endocytotic activity, and cytoskeletal structure have been investigated. EC were incubated with 1-100 nM PMA, or PDBu, and cellular H2O2 generation and endocytotic activity measured. PMA and PDBu exposure caused dose-dependent rises in EC H2O2 production. Likewise, EC incubated with PMA and PDBu had dose-related endocytosis increases. Cytoskeletal inspection of 10 nM PMA-perturbed EC revealed structural remodeling with stress fiber formation. Similar cellular functional changes occur in EC exposed to high low-density lipoprotein (LDL) concentrations. Protein kinase C (PKC) inhibition with 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7) prevented cytoskeletal remodeling in PMA-stimulated EC. In differenc...","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"35 1","pages":"207-218"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76156778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 5

Relationship Between Perfusion Pressure and Coronary Vasoreactivity in Saline Perfused Hearts Isolated from Normotensive and Spontaneously Hypertensive Rats: Role of Endothelium 正常和自发性高血压大鼠生理盐水灌注心脏灌注压与冠状动脉血管反应性的关系:内皮的作用

Endothelium-journal of Endothelial Cell Research Pub Date : 1996-01-01 DOI: 10.3109/10623329609024703

H. Mertens, G. Rubanyi

引用次数: 0

Superoxide Anions Contribute to Impaired Endothelium-Dependent Relaxation in Coronary Arteries of Young Cardiomyopathic Hamsters 超氧阴离子导致幼龄心肌病仓鼠冠状动脉内皮依赖性松弛受损

Endothelium-journal of Endothelial Cell Research Pub Date : 1996-01-01 DOI: 10.3109/10623329609024690

L. Fuchs

引用次数: 7

Multiple Ionic Mechanisms Activated by Bradykinin in Coronary Venular Endothelial Cells 缓激肽在冠状静脉内皮细胞中激活的多种离子机制

Endothelium-journal of Endothelial Cell Research Pub Date : 1996-01-01 DOI: 10.3109/10623329609024679

Jianben Song, D. Zawieja, H. Granger, A. H. Goodman, M. Davis

引用次数: 2

An atherogenic level of native LDL increases endothelial cell vulnerability to shear-induced plasma membrane wounding and consequent release of basic fibroblast growth factor 天然低密度脂蛋白的致动脉粥样硬化水平增加内皮细胞对剪切诱导的质膜损伤的脆弱性，并随之释放碱性成纤维细胞生长因子

Endothelium-journal of Endothelial Cell Research Pub Date : 1996-01-01 DOI: 10.3109/10623329609024689

M. Clarke, K. Pritchard, M. Medow, P. McNeil

引用次数: 8