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1. |
Physiological Levels ofS-Nitrosothiols in Human Plasma |
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Circulation Research: Journal of the American Heart Association,
Volume 89,
Issue 12,
2001,
Page 47-47
Ranieri,
Rossi Daniela,
Giustarini Aldo,
Milzani Roberto,
Colombo Isabella,
Dalle-Donne Paolo,
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ISSN:0009-7330
出版商:OVID
年代:2001
数据来源: OVID
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2. |
Ischemic Preconditioning Through Opening of Swelling-Activated Chloride Channels? |
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Circulation Research: Journal of the American Heart Association,
Volume 89,
Issue 12,
2001,
Page 48-48
Gerd,
Heusch Michael,
Cohen James,
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ISSN:0009-7330
出版商:OVID
年代:2001
数据来源: OVID
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3. |
Acknowledgment to Reviewers |
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Circulation Research: Journal of the American Heart Association,
Volume 89,
Issue 12,
2001,
Page 1081-1083
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ISSN:0009-7330
出版商:OVID
年代:2001
数据来源: OVID
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4. |
Molecular Clock Mechanisms and Circadian Rhythms Intrinsic to the Heart |
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Circulation Research: Journal of the American Heart Association,
Volume 89,
Issue 12,
2001,
Page 1084-1086
Michael,
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ISSN:0009-7330
出版商:OVID
年代:2001
数据来源: OVID
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5. |
Road RageCardiac Rab1 and ER-to-Golgi Traffic |
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Circulation Research: Journal of the American Heart Association,
Volume 89,
Issue 12,
2001,
Page 1087-1088
Anthony,
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ISSN:0009-7330
出版商:OVID
年代:2001
数据来源: OVID
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6. |
Recent Fibrillation StudiesAttempts to Wrest Order From Disorder |
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Circulation Research: Journal of the American Heart Association,
Volume 89,
Issue 12,
2001,
Page 1089-1091
Raymond,
Ideker Jian,
Huang Vladimir,
Fast William,
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ISSN:0009-7330
出版商:OVID
年代:2001
数据来源: OVID
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7. |
CD40 Signaling and Plaque Instability |
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Circulation Research: Journal of the American Heart Association,
Volume 89,
Issue 12,
2001,
Page 1092-1103
Uwe,
Schönbeck Peter,
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摘要:
Today, multiple lines of evidence support the view of atherosclerosis as a chronic inflammatory disease and implicate components of the immune system in atherogenesis. Recent work has documented overexpression of the potent immune mediator CD40 and its counterpart CD40 ligand (CD40L) in experimental and human atherosclerotic lesions. Notably, interruption of CD40/CD40L interactions not only diminished the formation and progression of mouse atheroma, but also fostered changes in lesion biology and structure, which are associated in humans with “plaque stabilization.” In accordance with the hypothesis that CD40 signaling promotes plaque instability, in vitro studies demonstrated that ligation of CD40 on atheroma-associated cell types, namely endothelial cells, smooth muscle cells, and macrophages, mediates functions considered crucial to the process of atherogenesis, such as the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, and procoagulants. The combination of the broad gamut of proatherogenic biological responses triggered by ligation of CD40 on endothelial cells, smooth muscle cells, and macrophages in vitro and the results of in vivo studies of interruption of CD40 signaling suggests a central role for this receptor/ligand dyad during atherogenesis, proposing CD40/CD40L interactions as a novel potential therapeutic target for this prevalent human disease.
ISSN:0009-7330
出版商:OVID
年代:2001
数据来源: OVID
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8. |
Integrin and Growth Factor Receptor Crosstalk |
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Circulation Research: Journal of the American Heart Association,
Volume 89,
Issue 12,
2001,
Page 1104-1110
Brian,
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摘要:
Crosstalk between integrins and growth factor receptors are an important signaling mechanism to provide specificity during normal development and pathological processes in vascular biology. Evidence from several model systems demonstrates the physiological importance of the coordination of signals from growth factors and the extracellular matrix to support cell proliferation, migration, and invasion in vivo. Several examples of crosstalk between these two important classes of receptors indicate that integrin ligation is required for growth factor–induced biological processes. Furthermore, integrins can directly associate with growth factor receptors, thereby regulating the capacity of integrin/growth factor receptor complexes to propagate downstream signaling. Recent data suggest that antagonists of &agr;vintegrins can provide a therapeutic benefit in human cancer patients, whereas knockout mice lacking specific integrins can provide an interesting insight into the role of integrins during development. This review will focus on the biological importance of integrin and growth factor receptor crosstalk that occurs during cell growth, migration, and invasion as well as in endothelial cells during angiogenesis.
ISSN:0009-7330
出版商:OVID
年代:2001
数据来源: OVID
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9. |
Contribution of Adventitial Fibroblasts to Neointima Formation and Vascular RemodelingFrom Innocent Bystander to Active Participant |
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Circulation Research: Journal of the American Heart Association,
Volume 89,
Issue 12,
2001,
Page 1111-1121
Saverio,
Sartore Angela,
Chiavegato Elisabetta,
Faggin Rafaella,
Franch Massimo,
Puato Simonetta,
Ausoni Paolo,
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摘要:
The adventitial layer surrounding the blood vessels has long been exclusively considered a supporting tissue the main function of which is to provide adequate nourishment to the muscle layers of tunica media. Although functionally interconnected, the adventitial and medial layers are structurally interfaced at the external elastic lamina level, clearly distinguishable at the maturational phase of vascular morphogenesis. Over the last few years the “passive” role that the adventitia seemed to play in experimental and spontaneous vascular pathologies involving proliferation, migration, differentiation, and apoptosis of vascular smooth muscle cells (VSMCs) has been questioned. It has been demonstrated that fibroblasts from the adventitia display an important partnership with the resident medial VSMCs in terms of phenotypic conversion, proliferation, apoptotic, and migratory properties the result of which is neointima formation and vascular remodeling. This article is an attempt at reviewing the major themes and more recent findings dealing with the phenotypic conversion process that leads adventitial “passive” (static) fibroblasts to become “activated” (mobile) myofibroblasts. This event shows some facets in common with vascular morphogenesis, ie, the process of recruitment, incorporation, and phenotypic conversion of cells surrounding the primitive endothelial tube in the definitive vessel wall. We hypothesize that during the response to vascular injuries in the adult, “activation” of adventitial fibroblasts is, at least in part, reminiscent of a developmental program that also invests, although with distinct spatiotemporal features, medial VSMCs.
ISSN:0009-7330
出版商:OVID
年代:2001
数据来源: OVID
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10. |
Inducible Activation of c-Myc in Adult Myocardium In Vivo Provokes Cardiac Myocyte Hypertrophy and Reactivation of DNA Synthesis |
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Circulation Research: Journal of the American Heart Association,
Volume 89,
Issue 12,
2001,
Page 1122-1129
Guishan,
Xiao Songyan,
Mao Georg,
Baumgarten Jennifer,
Serrano Maria,
Jordan Kenneth,
Roos Michael,
Fishbein W.,
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PDF (375KB)
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摘要:
c-Myc, a protooncogene, mediates both proliferative and cellular growth in many cell types. Although not expressed in the adult heart under normal physiological conditions, Myc expression is rapidly upregulated in response to hypertrophic stimuli. Although Myc is capable of sustaining hyperplastic growth in fetal myocytes, the effects of its re-expression in adult postmitotic myocardium and its role in mediating cardiac hypertrophy are unknown. To determine the effects of de novo Myc activity in adult postmitotic myocardium in vivo, we created a novel transgenic model in which Myc is expressed and inducibly activated specifically in cardiac myocytes. Activation of Myc in adult myocardium was sufficient to reproduce the characteristic changes in myocyte size, protein synthesis, and cardiac-specific gene expression seen in cardiac hypertrophy. Despite the increased cardiac mass, left ventricular function remained normal. Activation of Myc also provoked cell cycle reentry in postmitotic myocytes, which led to increased nuclei per myocyte and DNA content per nuclei.
ISSN:0009-7330
出版商:OVID
年代:2001
数据来源: OVID
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