1
40
5
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Text
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URL Address
<a href="http://doi.org/10.1161/ATVBAHA.114.303929" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/ATVBAHA.114.303929</a>
Pages
1854–1859
Issue
9
Volume
34
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
A brief etymology of the collateral circulation.
Publisher
An entity responsible for making the resource available
Arteriosclerosis, thrombosis, and vascular biology
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
2014-09
Subject
The topic of the resource
*Cardiology; *Collateral Circulation/physiology; *Terminology as Topic; Blood Vessels/embryology/growth & development; collateral circulation; Humans; myocardial ischemia; Neovascularization; peripheral arterial disease; Physiologic/physiology; stroke
Creator
An entity primarily responsible for making the resource
Faber James E; Chilian William M; Deindl Elisabeth; van Royen Niels; Simons Michael
Description
An account of the resource
It is well known that the protective capacity of the collateral circulation falls short in many individuals with ischemic disease of the heart, brain, and lower extremities. In the past 15 years, opportunities created by molecular and genetic tools, together with disappointing outcomes in many angiogenic trials, have led to a significant increase in the number of studies that focus on: understanding the basic biology of the collateral circulation; identifying the mechanisms that limit the collateral circulation's capacity in many individuals; devising methods to measure collateral extent, which has been found to vary widely among individuals; and developing treatments to increase collateral blood flow in obstructive disease. Unfortunately, accompanying this increase in reports has been a proliferation of vague terms used to describe the disposition and behavior of this unique circulation, as well as the increasing misuse of well-ensconced ones by new (and old) students of collateral circulation. With this in mind, we provide a brief glossary of readily understandable terms to denote the formation, adaptive growth, and maladaptive rarefaction of collateral circulation. We also propose terminology for several newly discovered processes that occur in the collateral circulation. Finally, we include terms used to describe vessels that are sometimes confused with collaterals, as well as terms describing processes active in the general arterial-venous circulation when ischemic conditions engage the collateral circulation. We hope this brief review will help unify the terminology used in collateral research.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/ATVBAHA.114.303929" target="_blank" rel="noreferrer noopener">10.1161/ATVBAHA.114.303929</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Cardiology
*Collateral Circulation/physiology
*Terminology as Topic
2014
Arteriosclerosis, thrombosis, and vascular biology
Blood Vessels/embryology/growth & development
Chilian William M
Collateral Circulation
Deindl Elisabeth
Department of Integrative Medical Sciences
Faber James E
Humans
myocardial ischemia
NEOMED College of Medicine
Neovascularization
peripheral arterial disease
Physiologic/physiology
Simons Michael
stroke
van Royen Niels
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1161/atvbaha.109.186189" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/atvbaha.109.186189</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
802-U56
Issue
6
Volume
29
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Amplification of Coronary Arteriogenic Capacity of Multipotent Stromal Cells by Epidermal Growth Factor
Publisher
An entity responsible for making the resource available
Arteriosclerosis Thrombosis and Vascular Biology
Date
A point or period of time associated with an event in the lifecycle of the resource
2009
2009-06
Subject
The topic of the resource
coronary circulation; angiogenesis; collateral circulation; Cardiovascular System & Cardiology; Myocardial infarction; expression; binding; Hematology; mesenchymal stem-cells; smooth-muscle-cells; rat model; endothelial-cells; collateral growth; improve heart function
Creator
An entity primarily responsible for making the resource
Belmadani S; Matrougui K; Kolz C; Pung Y F; Palen D; Prockop D J; Chilian W M
Description
An account of the resource
Objective-We determined whether increasing adherence of multipotent stromal cells (MSCs) would amplify their effects on coronary collateral growth (CCG). Methods and Results-Adhesion was established in cultured coronary endothelials cells (CECs) or MSCs treated with epidermal growth factor (EGF). EGF increased MSCs adhesion to CECs, and increased intercellular adhesion molecule (ICAM-1) or vascular cell adhesion molecule (VCAM-1) expression. Increased adherence was blocked by EGF receptor antagonism or antibodies to the adhesion molecules. To determine whether adherent MSCs, treated with EGF, would augment CCG, repetitive episodes of myocardial ischemia (RI) were introduced and CCG was measured from the ratio of collateral-dependent (CZ) and normal zone (NZ) flows. CZ/NZ was increased by MSCs without treatment versus RI-control and was further increased by EGF-treated MSCs. EGF-treated MSCs significantly improved myocardial function versus RI or RI + MSCs demonstrating that the increase in collateral flow was functionally significant. Engraftment of MSCs into myocardium was also increased by EGF treatment. Conclusions-These results reveal the importance of EGF in MSCs adhesion to endothelium and suggest that MSCs may be effective therapies for the stimulation of coronary collateral growth when interventions are used to increase their adhesion and homing (in vitro EGF treatment) to the jeopardized myocardium. (Arterioscler Thromb Vasc Biol. 2009; 29: 802-808.)
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/atvbaha.109.186189" target="_blank" rel="noreferrer noopener">10.1161/atvbaha.109.186189</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2009
angiogenesis
Arteriosclerosis Thrombosis and Vascular Biology
Belmadani S
Binding
Cardiovascular System & Cardiology
Chilian W M
Collateral Circulation
collateral growth
Coronary Circulation
endothelial-cells
expression
Hematology
improve heart function
Journal Article or Conference Abstract Publication
Kolz C
Matrougui K
mesenchymal stem-cells
myocardial infarction
Palen D
Prockop D J
Pung Y F
rat model
smooth-muscle-cells
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
n/a
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
2-2
Issue
21
Volume
126
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Title
A name given to the resource
Failure Of Regenerative Cell-based Therapy To Stimulate Coronary Collateral Growth In A Rat Model Of Metabolic Syndrome
Publisher
An entity responsible for making the resource available
Circulation
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-11
Subject
The topic of the resource
Arteriogenesis; Cardiovascular System & Cardiology; Collateral circulation; Metabolic; oxidative stress; Stem cell therapy; syndrome
Creator
An entity primarily responsible for making the resource
Logan S; Chilian W M; Ohanyan V A; Stevanov K; Enrick M; Kolz C L; Yin L Y
Identifier
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n/a
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2012
Arteriogenesis
Cardiovascular System & Cardiology
Chilian W M
Circulation
Collateral Circulation
Enrick M
Journal Article or Conference Abstract Publication
Kolz C L
Logan S
Metabolic
Ohanyan V A
Oxidative Stress
Stem cell therapy
Stevanov K
Syndrome
Yin L Y
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
n/a
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
1-1
Issue
21
Volume
124
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Induced Vascular Progenitor Cells Derived From Endothelial Cells Stimulate Coronary Collateral Growth
Publisher
An entity responsible for making the resource available
Circulation
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-11
Subject
The topic of the resource
Cardiovascular System & Cardiology; Collateral circulation
Creator
An entity primarily responsible for making the resource
Yin L Y; Ohanyan V; Pung Y F; Delucia A L; Bailey E; Enrick M; Stevanov K; Kolz C L; Guarini G; Chilian W
Identifier
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n/a
Format
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Journal Article
2011
Bailey E
Cardiovascular System & Cardiology
Chilian W
Circulation
Collateral Circulation
DeLucia A L
Enrick M
Guarini G
Journal Article
Kolz C L
Ohanyan V
Pung Y F
Stevanov K
Yin L Y
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1161/ATVBAHA.113.301591" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/ATVBAHA.113.301591</a>
Pages
1911–1919
Issue
8
Volume
33
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Mitochondrial oxidative stress corrupts coronary collateral growth by activating adenosine monophosphate activated kinase-alpha signaling.
Publisher
An entity responsible for making the resource available
Arteriosclerosis, thrombosis, and vascular biology
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-08
Subject
The topic of the resource
AMP-Activated Protein Kinases/*metabolism; Animal; Animals; Body Weight/physiology; Cells; collateral circulation; coronary circulation; Coronary Vessels/cytology/*enzymology; Cultured; Disease Models; Endothelial Cells/cytology/*enzymology; Humans; Inbred WKY; Ischemia/metabolism/pathology; mitochondria; Mitochondria/drug effects/*metabolism; Myocardium/enzymology/pathology; Oxidative Stress/*physiology; Rats; reactive oxygen species; Rotenone/pharmacology; Signal Transduction/*physiology; TOR Serine-Threonine Kinases/metabolism; Uncoupling Agents/pharmacology
Creator
An entity primarily responsible for making the resource
Pung Yuh Fen; Sam Wai Johnn; Stevanov Kelly; Enrick Molly; Chen Chwen-Lih; Kolz Christopher; Thakker Prashanth; Hardwick James P; Chen Yeong-Renn; Dyck Jason R B; Yin Liya; Chilian William M
Description
An account of the resource
OBJECTIVE: Our goal was to determine the mechanism by which mitochondrial oxidative stress impairs collateral growth in the heart. APPROACH AND RESULTS: Rats were treated with rotenone (mitochondrial complex I inhibitor that increases reactive oxygen species production) or sham-treated with vehicle and subjected to repetitive ischemia protocol for 10 days to induce coronary collateral growth. In control rats, repetitive ischemia increased flow to the collateral-dependent zone; however, rotenone treatment prevented this increase suggesting that mitochondrial oxidative stress compromises coronary collateral growth. In addition, rotenone also attenuated mitochondrial complex I activity and led to excessive mitochondrial aggregation. To further understand the mechanistic pathway(s) involved, human coronary artery endothelial cells were treated with 50 ng/mL vascular endothelial growth factor, 1 micromol/L rotenone, and rotenone/vascular endothelial growth factor for 48 hours. Vascular endothelial growth factor induced robust tube formation; however, rotenone completely inhibited this effect (P\textless0.05 rotenone versus vascular endothelial growth factor treatment). Inhibition of tube formation by rotenone was also associated with significant increase in mitochondrial superoxide generation. Immunoblot analyses of human coronary artery endothelial cells with rotenone treatment showed significant activation of adenosine monophosphate activated kinase (AMPK)-alpha and inhibition of mammalian target of rapamycin and p70 ribosomal S6 kinase. Activation of AMPK-alpha suggested impairments in energy production, which was reflected by decrease in O2 consumption and bioenergetic reserve capacity of cultured cells. Knockdown of AMPK-alpha (siRNA) also preserved tube formation during rotenone, suggesting the negative effects were mediated by the activation of AMPK-alpha. Conversely, expression of a constitutively active AMPK-alpha blocked tube formation. CONCLUSIONS: We conclude that activation of AMPK-alpha during mitochondrial oxidative stress inhibits mammalian target of rapamycin signaling, which impairs phenotypic switching necessary for the growth of blood vessels.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/ATVBAHA.113.301591" target="_blank" rel="noreferrer noopener">10.1161/ATVBAHA.113.301591</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2013
AMP-Activated Protein Kinases/*metabolism
Animal
Animals
Arteriosclerosis, thrombosis, and vascular biology
Body Weight/physiology
Cells
Chen Chwen-Lih
Chen Yeong-Renn
Chilian William M
Collateral Circulation
Coronary Circulation
Coronary Vessels/cytology/*enzymology
Cultured
Department of Integrative Medical Sciences
Disease Models
Dyck Jason R B
Endothelial Cells/cytology/*enzymology
Enrick Molly
Hardwick James P
Humans
Inbred WKY
Ischemia/metabolism/pathology
Kolz Christopher
Mitochondria
Mitochondria/drug effects/*metabolism
Myocardium/enzymology/pathology
NEOMED College of Medicine
Oxidative Stress/*physiology
Pung Yuh Fen
Rats
reactive oxygen species
Rotenone/pharmacology
Sam Wai Johnn
Signal Transduction/*physiology
Stevanov Kelly
Thakker Prashanth
TOR Serine-Threonine Kinases/metabolism
Uncoupling Agents/pharmacology
Yin Liya