1
40
2
-
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/10.1007/s00395-017-0626-1" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s00395-017-0626-1</a>
Pages
36–36
Issue
4
Volume
112
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
Impairment of pH gradient and membrane potential mediates redox dysfunction in the mitochondria of the post-ischemic heart.
Publisher
An entity responsible for making the resource available
Basic research in cardiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-07
Subject
The topic of the resource
*Energy Metabolism; *Membrane potential; *Membrane Potential; *Mitochondria; *Myocardial ischemia and reperfusion; *Oxidative Stress; *pH gradient; *Redox dysfunction; Aconitate Hydratase/metabolism; Animal; Animals; Cell Line; Disease Models; Electron Transport Chain Complex Proteins/metabolism; Heart/*metabolism/pathology; Hydrogen Peroxide/metabolism; Hydrogen-Ion Concentration; Ionophores/pharmacology; Male; Mitochondria; Mitochondrial; Myocardial Infarction/*metabolism/pathology; Myocardium/*metabolism/pathology; Oxidation-Reduction; Potassium/metabolism; Rats; Sprague-Dawley; Superoxides/metabolism
Creator
An entity primarily responsible for making the resource
Kang Patrick T; Chen Chwen-Lih; Lin Paul; Chilian William M; Chen Yeong-Renn
Description
An account of the resource
The mitochondrial electrochemical gradient (Deltap), which comprises the pH gradient (DeltapH) and the membrane potential (DeltaPsi), is crucial in controlling energy transduction. During myocardial ischemia and reperfusion (IR), mitochondrial dysfunction mediates superoxide ((.)O2(-)) and H2O2 overproduction leading to oxidative injury. However, the role of DeltapH and DeltaPsi in post-ischemic injury is not fully established. Here we studied mitochondria from the risk region of rat hearts subjected to 30 min of coronary ligation and 24 h of reperfusion in vivo. In the presence of glutamate, malate and ADP, normal mitochondria (mitochondria of non-ischemic region, NR) exhibited a heightened state 3 oxygen consumption rate (OCR) and reduced (.)O2(-) and H2O2 production when compared to state 2 conditions. Oligomycin (increases DeltapH by inhibiting ATP synthase) increased (.)O2(-) and H2O2 production in normal mitochondria, but not significantly in the mitochondria of the risk region (IR mitochondria or post-ischemic mitochondria), indicating that normal mitochondrial (.)O2(-) and H2O2 generation is dependent on DeltapH and that IR impaired the DeltapH of normal mitochondria. Conversely, nigericin (dissipates DeltapH) dramatically reduced (.)O2(-) and H2O2 generation by normal mitochondria under state 4 conditions, and this nigericin quenching effect was less pronounced in IR mitochondria. Nigericin also increased mitochondrial OCR, and predisposed normal mitochondria to a more oxidized redox status assessed by increased oxidation of cyclic hydroxylamine, CM-H. IR mitochondria, although more oxidized than normal mitochondria, were not responsive to nigericin-induced CM-H oxidation, which is consistent with the result that IR induced DeltapH impairment in normal mitochondria. Valinomycin, a K(+) ionophore used to dissipate DeltaPsi, drastically diminished (.)O2(-) and H2O2 generation by normal mitochondria, but less pronounced effect on IR mitochondria under state 4 conditions, indicating that DeltaPsi also contributed to (.)O2(-) generation by normal mitochondria and that IR mediated DeltaPsi impairment. However, there was no significant difference in valinomycin-induced CM-H oxidation between normal and IR mitochondria. In conclusion, under normal conditions the proton backpressure imposed by DeltapH restricts electron flow, controls a limited amount of (.)O2(-) generation, and results in a more reduced myocardium; however, IR causes DeltapH impairment and prompts a more oxidized myocardium.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s00395-017-0626-1" target="_blank" rel="noreferrer noopener">10.1007/s00395-017-0626-1</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).
*Energy Metabolism
*Membrane potential
*Mitochondria
*Myocardial ischemia and reperfusion
*Oxidative Stress
*pH gradient
*Redox dysfunction
2017
Aconitate Hydratase/metabolism
Animal
Animals
Basic research in cardiology
Cell Line
Chen Chwen-Lih
Chen Yeong-Renn
Chilian William M
Department of Family & Community Medicine
Department of Integrative Medical Sciences
Disease Models
Electron Transport Chain Complex Proteins/metabolism
Heart/*metabolism/pathology
Hydrogen Peroxide/metabolism
Hydrogen-Ion Concentration
Ionophores/pharmacology
Kang Patrick T
Lin Paul
Male
Mitochondria
Mitochondrial
Myocardial Infarction/*metabolism/pathology
Myocardium/*metabolism/pathology
NEOMED College of Medicine
Oxidation-Reduction
Potassium/metabolism
Rats
Sprague-Dawley
Superoxides/metabolism
-
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