Pub Date : 2007-01-01DOI: 10.1080/10623320701670026
L. Khachigian
Tucker Collins, MD, PhDTucker Collins, S. Burt Wolbach Professor of Pathology at Harvard Medical School, died on 8 June 2007, 6 months after being diagnosed with an aggressive brain tumor. He was o...
{"title":"Science Never Sleeps: Tucker Collins, MD, PhD","authors":"L. Khachigian","doi":"10.1080/10623320701670026","DOIUrl":"https://doi.org/10.1080/10623320701670026","url":null,"abstract":"Tucker Collins, MD, PhDTucker Collins, S. Burt Wolbach Professor of Pathology at Harvard Medical School, died on 8 June 2007, 6 months after being diagnosed with an aggressive brain tumor. He was o...","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"1 1","pages":"173-174"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88162871","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}
Pub Date : 2006-01-01DOI: 10.1080/10623320601125303
H. Lowe, L. Khachigian
{"title":"The Endothelium and Cardiovascular Disease: New Developments, New Challenges","authors":"H. Lowe, L. Khachigian","doi":"10.1080/10623320601125303","DOIUrl":"https://doi.org/10.1080/10623320601125303","url":null,"abstract":"","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"159 1","pages":"365-365"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76968235","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}
Pub Date : 2004-10-01DOI: 10.1097/00008506-200410000-00033
T. Hashimoto, Yongqin Wu, N. Boudreau, Jenny F Li, M. Matsumoto, W. Young
To study a potential feedback system in the angiopoietin (Ang)-Tie2 system, the authors examined effects of Ang1 and Ang2 on Tie2 expression on human umbilical vein endothelial cells (HUVECs) with or without stimulation by a potent inflammatory cytokine, tumor necrosis factor-alpha (TNF-alpha). Ang1, but not Ang2, down-regulated Tie2 expression on HUVECs without TNF-alpha stimulation. Both Ang1 and Ang2 attenuated TNF-alpha-induced Tie2 up-regulation. Regulation of Tie2 expression by Ang1 or Ang2 was not dependent on phosphatidylinositol 3-kinase. The Ang-Tie2 system appears to have an autoregulatory feedback system that may be regulating the overall activity of the Tie2 system in both physiological and pathological conditions.
{"title":"Regulation of tie2 expression by angiopoietin--potential feedback system.","authors":"T. Hashimoto, Yongqin Wu, N. Boudreau, Jenny F Li, M. Matsumoto, W. Young","doi":"10.1097/00008506-200410000-00033","DOIUrl":"https://doi.org/10.1097/00008506-200410000-00033","url":null,"abstract":"To study a potential feedback system in the angiopoietin (Ang)-Tie2 system, the authors examined effects of Ang1 and Ang2 on Tie2 expression on human umbilical vein endothelial cells (HUVECs) with or without stimulation by a potent inflammatory cytokine, tumor necrosis factor-alpha (TNF-alpha). Ang1, but not Ang2, down-regulated Tie2 expression on HUVECs without TNF-alpha stimulation. Both Ang1 and Ang2 attenuated TNF-alpha-induced Tie2 up-regulation. Regulation of Tie2 expression by Ang1 or Ang2 was not dependent on phosphatidylinositol 3-kinase. The Ang-Tie2 system appears to have an autoregulatory feedback system that may be regulating the overall activity of the Tie2 system in both physiological and pathological conditions.","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"320 ","pages":"207-10"},"PeriodicalIF":0.0,"publicationDate":"2004-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91447216","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}
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.
{"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}
Shailesh Y. Desai, M. Marroni, L. Cucullo, L. Križanac-Bengez, M. Mayberg, Mohammed Hossain, Gerald G Grant, D. Janigro
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.
{"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}
{"title":"Editorial Comment: A New Beginning","authors":"P. Lelkes","doi":"10.1080/10623320210717","DOIUrl":"https://doi.org/10.1080/10623320210717","url":null,"abstract":"","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"22 1","pages":"1-2"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82329445","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}
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.
{"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}
Pub Date : 2002-01-01DOI: 10.1007/978-90-481-3741-1_18
Domenico Ribatti, Marco Presta
{"title":"Pietro M. Gullino and angiogenesis.","authors":"Domenico Ribatti, Marco Presta","doi":"10.1007/978-90-481-3741-1_18","DOIUrl":"https://doi.org/10.1007/978-90-481-3741-1_18","url":null,"abstract":"","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"31 5","pages":"227-30"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91432296","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}
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