Endothelium-journal of Endothelial Cell Research最新文献

Science Never Sleeps: Tucker Collins, MD, PhD 科学永不眠:塔克·柯林斯，医学博士，博士

Endothelium-journal of Endothelial Cell Research Pub Date : 2007-01-01 DOI: 10.1080/10623320701670026

L. Khachigian

引用次数: 0

Molecular Mechanism of Angiogenesis—Preface 血管生成的分子机制

Endothelium-journal of Endothelial Cell Research Pub Date : 2006-01-01 DOI: 10.1080/10623320600705840

Yasufumi Sato

引用次数: 0

The Endothelium and Cardiovascular Disease: New Developments, New Challenges 内皮与心血管疾病:新进展，新挑战

Endothelium-journal of Endothelial Cell Research Pub Date : 2006-01-01 DOI: 10.1080/10623320601125303

H. Lowe, L. Khachigian

引用次数: 0

Regulation of tie2 expression by angiopoietin--potential feedback system. 血管生成素-电位反馈系统对tie2表达的调控。

Endothelium-journal of Endothelial Cell Research Pub Date : 2004-10-01 DOI: 10.1097/00008506-200410000-00033

T. Hashimoto, Yongqin Wu, N. Boudreau, Jenny F Li, M. Matsumoto, W. Young

引用次数: 31

Oxidative Stress and Endothelial Dysfunction 氧化应激与内皮功能障碍

Endothelium-journal of Endothelial Cell Research Pub Date : 2004-01-01 DOI: 10.1080/10623320490492339

L. Khachigian

引用次数: 1

pH-dependent oxidant production following inhibition of the mitochondrial electron transport chain in pulmonary endothelial cells. 肺内皮细胞线粒体电子传递链抑制后ph依赖性氧化剂的产生。

Endothelium-journal of Endothelial Cell Research Pub Date : 2002-01-01 DOI: 10.1080/10623320212007

M. Cutaia, J. Kroczyński, K. Tollefson

{"title":"pH-dependent oxidant production following inhibition of the mitochondrial electron transport chain in pulmonary endothelial cells.","authors":"M. Cutaia, J. Kroczyński, K. Tollefson","doi":"10.1080/10623320212007","DOIUrl":"https://doi.org/10.1080/10623320212007","url":null,"abstract":"We investigated the effect of changes in intracellular pH (pHi) and Na/H antiport activity on intracellular oxidant production in human pulmonary artery endothelial cells (HPAEC) following disruption of cellular metabolism. Oxidant production was measured with oxidant-sensitive probes (2',7'-dichlorofluorescein diacetate [H2DCF], dihydroethidium [DHE]) following treatment with inhibitors of mitochondrial electron transport and glycolysis (antimycin/2-deoxyglucose, A/D). A/D treatment increased oxidant production in a dose-dependent fashion over 2 hours. Omission of 2-deoxyglucose did not alter the magnitude of oxidant production. Inhibition at more proximal sites in the mitochondrial electron transport chain inhibited oxidant production. These data suggested that the mitochondrial electron transport chain was the source of oxidant production. Fluorescent imaging experiments confirmed the mitochondrial origin of the increased oxidant production under these conditions. Maneuvers that reduced pHi and inhibited Na/H exchange (acidosis, specific Na/H exchange inhibitors) attenuated oxidant production, whereas maneuvers that raised pHi (monensin) potentiated oxidant production. The results with the pH-insensitive probe (DHE) confirmed that oxidant production was pH-dependent. Oxidant production preceded significant loss of cell viability at 6 h following A/D treatment. These results demonstrate that oxidant production following inhibition of mitochondrial electron transport in HPAEC is pH-dependent and may contribute to endothelial cell injury by increasing endogenous oxidative stress.","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"52 1","pages":"109-21"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78029225","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: 13

Mechanisms of endothelial survival under shear stress. 内皮细胞在剪切应力下存活的机制。

Endothelium-journal of Endothelial Cell Research Pub Date : 2002-01-01 DOI: 10.1080/10623320212004

Shailesh Y. Desai, M. Marroni, L. Cucullo, L. Križanac-Bengez, M. Mayberg, Mohammed Hossain, Gerald G Grant, D. Janigro

{"title":"Mechanisms of endothelial survival under shear stress.","authors":"Shailesh Y. Desai, M. Marroni, L. Cucullo, L. Križanac-Bengez, M. Mayberg, Mohammed Hossain, Gerald G Grant, D. Janigro","doi":"10.1080/10623320212004","DOIUrl":"https://doi.org/10.1080/10623320212004","url":null,"abstract":"Endothelial cells (ECs) are exposed to cytotoxic reactive oxygen species and oxidation products of NO, yet they are characterized by low apoptotic rates and have an average life span of many years. EC exposure to flow has been shown to downregulate cell cycle-related genes and cause cytoskeletal rearrangement. We hypothesized that exposure to flow also causes molecular and physiological changes that induce antioxidant properties in ECs. We used cDNA array expression profiling and protein analysis to study the responses of human ECs exposed to flow in a hollow fiber apparatus or the same ECs grown under static conditions. Our results show that shear-induced synchronized expression of processes control oxidant production; these changes included upregulation of NADH-producing enzymes (Krebs cycle dehydrogenases and glyceraldehyde-3-phosphate dehydrogenase [GAPDH]) accompanied by simultaneous decrease in NADH-depleting pathways (e.g., lactate dehydrogenase [LDH]) and diminished production of lactate. Exposure to flow upregulated cytoskeletal genes. Our results suggest that, in addition to inhibition of cell cycle, exposure to flow influences ECs by controlling expression of enzymes involved in the generation of antioxidant intermediates and in adaptive control of cell shape. These changes may explain longevity and antioxidant efficiency of ECs and may provide insight in mechanisms leading to pathological conditions such as arteriosclerosis.","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"31 1","pages":"89-102"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82524046","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: 73

Editorial Comment: A New Beginning 编者按:一个新的开始

Endothelium-journal of Endothelial Cell Research Pub Date : 2002-01-01 DOI: 10.1080/10623320210717

P. Lelkes

引用次数: 0

Vessel co-option: how tumors obtain blood supply in the absence of sprouting angiogenesis. 血管共选择:肿瘤如何在没有新生血管生成的情况下获得血液供应。

Endothelium-journal of Endothelial Cell Research Pub Date : 2002-01-01 DOI: 10.1080/10623320212006

W. Leenders, B. Küsters, R. D. de Waal

{"title":"Vessel co-option: how tumors obtain blood supply in the absence of sprouting angiogenesis.","authors":"W. Leenders, B. Küsters, R. D. de Waal","doi":"10.1080/10623320212006","DOIUrl":"https://doi.org/10.1080/10623320212006","url":null,"abstract":"The hypothesis that solid tumors are dependent on angiogenesis, the formation of new vessels, for outgrowth and metastasis has acquired a central position in cancer research and has since inspired many scientists for several decades. Among the various angiogenic stimuli that are secreted by tumor cells, members of the Vascular Endothelial Growth Factor (VEGF) family are most prominent. More recently it has become clear, however, that tumors may use alternative ways to obtain blood supply. Vessel co-option, the use of pre-existent vessels, was described first in the brain, one of the most densely vascularized organs in the body. Thus, brain tumors may develop without the need of an angiogenic switch to occur. Obviously, this way of blood supply will not be affected by angiogenesis inhibition. In addition, it is predicted that tumors with this type of behavior will be less visible in contrast-enhanced MRI. In this article we present our recently developed mouse brain model of vessel co-option in melanoma. The effects of expression of VEGF on tumor vascularity, and on MRI visualization of these brain lesions are described. Possible consequences of anti-angiogenesis therapy are discussed.","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"33 1","pages":"83-7"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85102259","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: 154

Pietro M. Gullino and angiogenesis. Pietro M. Gullino和血管生成。

Endothelium-journal of Endothelial Cell Research Pub Date : 2002-01-01 DOI: 10.1007/978-90-481-3741-1_18

Domenico Ribatti, Marco Presta

引用次数: 2