1
40
4
-
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.00099.2002" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00099.2002</a>
Pages
H2062–2073
Issue
5
Volume
283
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
Sexual dimorphism in prostanoid-potentiated vascular contraction: roles of endothelium and ovarian steroids.
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
2002
2002-11
Subject
The topic of the resource
*Sex Characteristics; Animals; Aorta/drug effects/physiology; Bridged Bicyclo Compounds; Cyclooxygenase Inhibitors/pharmacology; Endothelium; Enzyme Inhibitors/pharmacology; Estrogens/*physiology; Fatty Acids; Female; Heterocyclic; Hydrazines/pharmacology; Imidazoles/pharmacology; Indomethacin/pharmacology; Male; Ovariectomy; Phenylephrine/pharmacology; Progesterone/*physiology; Prostaglandins/*metabolism; Rats; Sprague-Dawley; Thromboxanes/metabolism; Unsaturated; Vascular/*metabolism; Vasoconstriction/drug effects/*physiology; Vasoconstrictor Agents/pharmacology; Vasopressins/pharmacology
Creator
An entity primarily responsible for making the resource
Fulton Clifford T; Stallone John N
Description
An account of the resource
The effects of constrictor prostanoid (CP) pathway inhibitors on vascular reactivity to vasopressin (VP) and phenylephrine (PE) were examined in thoracic aortas of male, female, and ovariectomized (OVX) female Sprague-Dawley rats. Maximal contractile response of control (Cont) aortas to VP was markedly higher in females (3,885 +/- 332 mg/mg ring wt) than in males (810 +/- 148 mg). Indomethacin (Indo; 10 microM) attenuated maximal response to VP in females (3,043 +/- 277 mg) but not in males. SQ-29,548 (SQ; 1 microM) attenuated maximal response to VP in females (3,042 +/- 290 mg) to a similar extent as Indo. Dazoxiben (Daz; 10 microM) alone had no effect, but Daz + SQ attenuated maximal contractile response to VP to a similar extent as SQ alone. Removal of the endothelium in female aortas attenuated contractile responses to VP in Cont aortas. OVX attenuated maximal contractile response to VP in Cont aortas (2,093 +/- 329 mg) and abolished the attenuating effects of Indo. Indo, SQ, and Daz exerted identical effects on contractile responses of male, female, and OVX female aortas to PE. These findings establish the following in the rat aorta: 1) CP, probably thromboxane and/or endoperoxide, is responsible for approximately
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00099.2002" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00099.2002</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).
*Sex Characteristics
2002
American journal of physiology. Heart and circulatory physiology
Animals
Aorta/drug effects/physiology
Bridged Bicyclo Compounds
Cyclooxygenase Inhibitors/pharmacology
Endothelium
Enzyme Inhibitors/pharmacology
Estrogens/*physiology
Fatty Acids
Female
Fulton Clifford T
Heterocyclic
Hydrazines/pharmacology
Imidazoles/pharmacology
Indomethacin/pharmacology
Male
Ovariectomy
Phenylephrine/pharmacology
Progesterone/*physiology
Prostaglandins/*metabolism
Rats
Sprague-Dawley
Stallone John N
Thromboxanes/metabolism
Unsaturated
Vascular/*metabolism
Vasoconstriction/drug effects/*physiology
Vasoconstrictor Agents/pharmacology
Vasopressins/pharmacology
-
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.115.306642" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/CIRCRESAHA.115.306642</a>
Pages
612–621
Issue
7
Volume
117
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
Requisite Role of Kv1.5 Channels in Coronary Metabolic Dilation.
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
2015
2015-09
Subject
The topic of the resource
129 Strain; Animals; cardiac function; contrast echocardiography; Coronary Circulation/*physiology; Coronary Vessels/*metabolism; hydrogen peroxide; Inbred C57BL; ion channel; Knockout; Kv1.5 Potassium Channel/*physiology; Mice; Muscle; Smooth; Transgenic; transgenic mice; Vascular/*metabolism; vasodilation; Vasodilation/*physiology; voltage-gated potassium channels
Creator
An entity primarily responsible for making the resource
Ohanyan Vahagn; Yin Liya; Bardakjian Raffi; Kolz Christopher; Enrick Molly; Hakobyan Tatevik; Kmetz John; Bratz Ian; Luli Jordan; Nagane Masaki; Khan Nadeem; Hou Huagang; Kuppusamy Periannan; Graham Jacqueline; Fu Frances Kwan; Janota Danielle; Oyewumi Moses O; Logan Suzanna; Lindner Jonathan R; Chilian William M
Description
An account of the resource
RATIONALE: In the working heart, coronary blood flow is linked to the production of metabolites, which modulate tone of smooth muscle in a redox-dependent manner. Voltage-gated potassium channels (Kv), which play a role in controlling membrane potential in vascular smooth muscle, have certain members that are redox-sensitive. OBJECTIVE: To determine the role of redox-sensitive Kv1.5 channels in coronary metabolic flow regulation. METHODS AND RESULTS: In mice (wild-type [WT], Kv1.5 null [Kv1.5(-/-)], and Kv1.5(-/-) and WT with inducible, smooth muscle-specific expression of Kv1.5 channels), we measured mean arterial pressure, myocardial blood flow, myocardial tissue oxygen tension, and ejection fraction before and after inducing cardiac stress with norepinephrine. Cardiac work was estimated as the product of mean arterial pressure and heart rate. Isolated arteries were studied to establish whether genetic alterations modified vascular reactivity. Despite higher levels of cardiac work in the Kv1.5(-/-) mice (versus WT mice at baseline and all doses of norepinephrine), myocardial blood flow was lower in Kv1.5(-/-) mice than in WT mice. At high levels of cardiac work, tissue oxygen tension dropped significantly along with ejection fraction. Expression of Kv1.5 channels in smooth muscle in the null background rescued this phenotype of impaired metabolic dilation. In isolated vessels from Kv1.5(-/-) mice, relaxation to H2O2 was impaired, but responses to adenosine and acetylcholine were normal compared with those from WT mice. CONCLUSIONS: Kv1.5 channels in vascular smooth muscle play a critical role in coupling myocardial blood flow to cardiac metabolism. Absence of these channels disassociates metabolism from flow, resulting in cardiac pump dysfunction and tissue hypoxia.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/CIRCRESAHA.115.306642" target="_blank" rel="noreferrer noopener">10.1161/CIRCRESAHA.115.306642</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).
129 Strain
2015
Animals
Bardakjian Raffi
Bratz Ian
Cardiac function
Chilian William M
Circulation research
contrast echocardiography
Coronary Circulation/*physiology
Coronary Vessels/*metabolism
Department of Integrative Medical Sciences
Department of Pharmaceutical Sciences
Enrick Molly
Fu Frances Kwan
Graham Jacqueline
Hakobyan Tatevik
Hou Huagang
Hydrogen peroxide
Inbred C57BL
ion channel
Janota Danielle
Khan Nadeem
Kmetz John
Knockout
Kolz Christopher
Kuppusamy Periannan
Kv1.5 Potassium Channel/*physiology
Lindner Jonathan R
Logan Suzanna
Luli Jordan
Mice
Muscle
Nagane Masaki
NEOMED College of Medicine
NEOMED College of Pharmacy
Ohanyan Vahagn
Oyewumi Moses O
Smooth
Transgenic
Transgenic mice
Vascular/*metabolism
vasodilation
Vasodilation/*physiology
voltage-gated potassium channels
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/10.1152/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>
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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).
*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/10.1152/ajpcell.00068.2016" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpcell.00068.2016</a>
Pages
C212–224
Issue
2
Volume
311
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
Leptin augments recruitment of IRF-1 and CREB to thrombospondin-1 gene promoter in vascular smooth muscle cells in vitro.
Publisher
An entity responsible for making the resource available
American journal of physiology. Cell physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-08
Subject
The topic of the resource
*cAMP response element-binding protein; *interferon regulatory factor-1; *leptin; *thrombospondin-1; *transcription; *vascular smooth muscle cells; Binding Sites/genetics; Cells; Chromatin Immunoprecipitation/methods; Cultured; Cyclic AMP Response Element-Binding Protein/*metabolism; Gene Expression Regulation/genetics; Genetic/genetics; Humans; Interferon Regulatory Factor-1/*metabolism; Leptin/*metabolism; Muscle; Mutagenesis; Myocytes; Promoter Regions; Response Elements/genetics; Site-Directed/methods; Smooth; Smooth Muscle/*metabolism; Thrombospondin 1/*genetics/*metabolism; Transcription; Transcriptional Activation/genetics; Transfection/methods; Up-Regulation/genetics; Vascular/*metabolism
Creator
An entity primarily responsible for making the resource
Sahu Soumyadip; Ganguly Rituparna; Raman Priya
Description
An account of the resource
We previously reported that high pathophysiological concentrations of leptin, the adipocyte-secreted peptide, upregulate the expression of a potent proatherogenic matricellular protein, thrombospondin-1 (TSP-1), in vascular smooth muscle cells. Moreover, this regulation was found to occur at the level of transcription; however, the underlying molecular mechanisms remain unknown. The goal of the present study was to investigate the specific transcriptional mechanisms that mediate upregulation of TSP-1 expression by leptin. Primary human aortic smooth muscle cell cultures were transiently transfected with different TSP-1 gene (THBS1) promoter-linked luciferase reporter constructs, and luciferase activity in response to leptin (100 ng/ml) was assessed. We identified a long THBS1 promoter (-1270/+750) fragment with specific leptin response elements that are required for increased TSP-1 transcription by leptin. Promoter analyses, protein/DNA array and gel shift assays demonstrated activation and association of transcription factors, interferon regulatory factor-1 (IRF-1) and cAMP response element-binding protein (CREB), to the distal fragment of the THBS1 promoter in response to leptin. Supershift, chromatin immunoprecipitation, and coimmunoprecipitation assays revealed formation of a single complex between IRF-1 and CREB in response to leptin; importantly, recruitment of this complex to the THBS1 promoter mediated leptin-induced TSP-1 transcription. Finally, binding sequence decoy oligomer and site-directed mutagenesis revealed that regulatory elements for both IRF-1 (-1019 to -1016) and CREB (-1198 to -1195), specific to the distal THBS1 promoter, were required for leptin-induced TSP-1 transcription. Taken together, these findings demonstrate that leptin promotes a cooperative association between IRF-1 and CREB on the THBS1 promoter driving TSP-1 transcription in vascular smooth muscle cells.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpcell.00068.2016" target="_blank" rel="noreferrer noopener">10.1152/ajpcell.00068.2016</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).
*cAMP response element-binding protein
*interferon regulatory factor-1
*leptin
*thrombospondin-1
*Transcription
*vascular smooth muscle cells
2016
American journal of physiology. Cell physiology
Binding Sites/genetics
Cells
Chromatin Immunoprecipitation/methods
Cultured
Cyclic AMP Response Element-Binding Protein/*metabolism
Department of Integrative Medical Sciences
Ganguly Rituparna
Gene Expression Regulation/genetics
Genetic/genetics
Humans
Interferon Regulatory Factor-1/*metabolism
Leptin/*metabolism
Muscle
Mutagenesis
Myocytes
NEOMED College of Medicine
Promoter Regions
Raman Priya
Response Elements/genetics
Sahu Soumyadip
Site-Directed/methods
Smooth
Smooth Muscle/*metabolism
Thrombospondin 1/*genetics/*metabolism
Transcription
Transcriptional Activation/genetics
Transfection/methods
Up-Regulation/genetics
Vascular/*metabolism