1
40
2
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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/10.1152/ajpheart.00077.2013" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00077.2013</a>
Pages
H1275–1280
Issue
9
Volume
305
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
The role of mitochondrial bioenergetics and reactive oxygen species in coronary collateral growth.
Publisher
An entity responsible for making the resource available
American journal of physiology. Heart and circulatory physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-11
Subject
The topic of the resource
*Collateral Circulation; *Coronary Circulation; *Energy Metabolism; *Neovascularization; angiogenesis; Animals; arteriogenesis; Coronary Vessels/metabolism; Humans; mitochondria; Mitochondria; Mitochondrial Proteins/metabolism; Muscle; Muscle/*metabolism; Myocytes; Oxidative Stress; Phenotype; Physiologic; Reactive Oxygen Species/*metabolism; redox-dependent signaling; Signal Transduction; Smooth; Smooth Muscle/*metabolism; Vascular/*metabolism
Creator
An entity primarily responsible for making the resource
Pung Yuh Fen; Sam Wai Johnn; Hardwick James P; Yin Liya; Ohanyan Vahagn; Logan Suzanna; Di Vincenzo Lola; Chilian William M
Description
An account of the resource
Coronary collateral growth is a process involving coordination between growth factors expressed in response to ischemia and mechanical forces. Underlying this response is proliferation of vascular smooth muscle and endothelial cells, resulting in an enlargement in the caliber of arterial-arterial anastomoses, i.e., a collateral vessel, sometimes as much as an order of magnitude. An integral element of this cell proliferation is the process known as phenotypic switching in which cells of a particular phenotype, e.g., contractile vascular smooth muscle, must change their phenotype to proliferate. Phenotypic switching requires that protein synthesis occurs and different kinase signaling pathways become activated, necessitating energy to make the switch. Moreover, kinases, using ATP to phosphorylate their targets, have an energy requirement themselves. Mitochondria play a key role in the energy production that enables phenotypic switching, but under conditions where mitochondrial energy production is constrained, e.g., mitochondrial oxidative stress, this switch is impaired. In addition, we discuss the potential importance of uncoupling proteins as modulators of mitochondrial reactive oxygen species production and bioenergetics, as well as the role of AMP kinase as an energy sensor upstream of mammalian target of rapamycin, the master regulator of protein synthesis.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00077.2013" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00077.2013</a>
Rights
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).
*Collateral Circulation
*Coronary Circulation
*Energy Metabolism
*Neovascularization
2013
American journal of physiology. Heart and circulatory physiology
angiogenesis
Animals
Arteriogenesis
Chilian William M
Coronary Vessels/metabolism
Department of Integrative Medical Sciences
Di Vincenzo Lola
Hardwick James P
Humans
Logan Suzanna
Mitochondria
Mitochondrial Proteins/metabolism
Muscle
Muscle/*metabolism
Myocytes
NEOMED College of Medicine
Ohanyan Vahagn
Oxidative Stress
Phenotype
Physiologic
Pung Yuh Fen
Reactive Oxygen Species/*metabolism
Redox-dependent signaling
Sam Wai Johnn
Signal Transduction
Smooth
Smooth Muscle/*metabolism
Vascular/*metabolism
Yin Liya
-
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/CIRCRESAHA.111.250126" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/CIRCRESAHA.111.250126</a>
Pages
241–252
Issue
2
Volume
110
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
Induction of vascular progenitor cells from endothelial cells stimulates coronary collateral growth.
Publisher
An entity responsible for making the resource available
Circulation research
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-01
Subject
The topic of the resource
*Collateral Circulation; *Coronary Circulation; Animal; Animals; Biomarkers/metabolism; Cell Differentiation; Cell Lineage; Cells; Coronary Occlusion/genetics/metabolism/pathology/physiopathology/*surgery; Coronary Vessels/metabolism/pathology/*physiopathology; Cultured; Developmental; Disease Models; Endothelial Cells/metabolism/pathology/*transplantation; Epigenesis; Gene Expression Profiling; Gene Expression Regulation; Genetic; Induced Pluripotent Stem Cells/metabolism/*transplantation; Mice; Muscle; Myocytes; Neovascularization; Physiologic; Rats; Regenerative Medicine/methods; Regional Blood Flow; Reverse Transcriptase Polymerase Chain Reaction; SCID; Smooth; Smooth Muscle/metabolism/pathology/*transplantation; Sprague-Dawley; Teratoma/metabolism/pathology; Time Factors; Transcription Factors/genetics/metabolism; Transduction; Vascular/metabolism/pathology/*physiopathology
Creator
An entity primarily responsible for making the resource
Yin Liya; Ohanyan Vahagn; Pung Yuh Fen; Delucia Angelo; Bailey Erin; Enrick Molly; Stevanov Kelly; Kolz Christopher L; Guarini Giacinta; Chilian William M
Description
An account of the resource
RATIONALE: A well-developed coronary collateral circulation improves the morbidity and mortality of patients following an acute coronary occlusion. Although regenerative medicine has great potential in stimulating vascular growth in the heart, to date there have been mixed results, and the ideal cell type for this therapy has not been resolved. OBJECTIVE: To generate induced vascular progenitor cells (iVPCs) from endothelial cells, which can differentiate into vascular smooth muscle cells (VSMCs) or endothelial cells (ECs), and test their capability to stimulate coronary collateral growth. METHODS AND RESULTS: We reprogrammed rat ECs with the transcription factors Oct4, Klf4, Sox2, and c-Myc. A population of reprogrammed cells was derived that expressed pluripotent markers Oct4, SSEA-1, Rex1, and AP and hemangioblast markers CD133, Flk1, and c-kit. These cells were designated iVPCs because they remained committed to vascular lineage and could differentiate into vascular ECs and VSMCs in vitro. The iVPCs demonstrated better in vitro angiogenic potential (tube network on 2-dimensional culture, tube formation in growth factor reduced Matrigel) than native ECs. The risk of teratoma formation in iVPCs is also reduced in comparison with fully reprogrammed induced pluripotent stem cells (iPSCs). When iVPCs were implanted into myocardium, they engrafted into blood vessels and increased coronary collateral flow (microspheres) and improved cardiac function (echocardiography) better than iPSCs, mesenchymal stem cells, native ECs, and sham treatments. CONCLUSIONS: We conclude that iVPCs, generated by partially reprogramming ECs, are an ideal cell type for cell-based therapy designed to stimulate coronary collateral growth.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/CIRCRESAHA.111.250126" target="_blank" rel="noreferrer noopener">10.1161/CIRCRESAHA.111.250126</a>
Rights
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).
*Collateral Circulation
*Coronary Circulation
2012
Animal
Animals
Bailey Erin
Biomarkers/metabolism
Cell Differentiation
Cell Lineage
Cells
Chilian William M
Circulation research
Coronary Occlusion/genetics/metabolism/pathology/physiopathology/*surgery
Coronary Vessels/metabolism/pathology/*physiopathology
Cultured
Delucia Angelo
Department of Integrative Medical Sciences
Developmental
Disease Models
Endothelial Cells/metabolism/pathology/*transplantation
Enrick Molly
Epigenesis
Gene Expression Profiling
Gene Expression Regulation
Genetic
Guarini Giacinta
Induced Pluripotent Stem Cells/metabolism/*transplantation
Kolz Christopher L
Mice
Muscle
Myocytes
NEOMED College of Medicine
Neovascularization
Ohanyan Vahagn
Physiologic
Pung Yuh Fen
Rats
Regenerative Medicine/methods
Regional Blood Flow
Reverse Transcriptase Polymerase Chain Reaction
SCID
Smooth
Smooth Muscle/metabolism/pathology/*transplantation
Sprague-Dawley
Stevanov Kelly
Teratoma/metabolism/pathology
Time Factors
Transcription Factors/genetics/metabolism
Transduction
Vascular/metabolism/pathology/*physiopathology
Yin Liya