1
40
6
-
Text
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URL Address
<a href="http://doi.org/10.1002/prp2.153" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/prp2.153</a>
Pages
e00153–e00153
Issue
4
Volume
3
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
Propofol restores TRPV1 sensitivity via a TRPA1-, nitric oxide synthase-dependent activation of PKCepsilon.
Publisher
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Pharmacology research & perspectives
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-08
Subject
The topic of the resource
PKCepsilon and NOS; propofol; TRPA1; TRPV1
Creator
An entity primarily responsible for making the resource
Sinharoy Pritam; Zhang Hongyu; Sinha Sayantani; Prudner Bethany C; Bratz Ian N; Damron Derek S
Description
An account of the resource
We previously demonstrated that the intravenous anesthetic, propofol, restores the sensitivity of transient receptor potential vanilloid channel subtype-1 (TRPV1) receptors via a protein kinase C epsilon (PKCepsilon)-dependent and transient receptor potential ankyrin channel subtype-1 (TRPA1)-dependent pathway in sensory neurons. The extent to which the two pathways are directly linked or operating in parallel has not been determined. Using a molecular approach, our objectives of the current study were to confirm that TRPA1 activation directly results in PKCepsilon activation and to elucidate the cellular mechanism by which this occurs. F-11 cells were transfected with complimentary DNA (cDNA) for TRPV1 only or both TRPV1 and TRPA1. Intracellular Ca(2+) concentration was measured in individual cells via fluorescence microscopy. An immunoblot analysis of the total and phosphorylated forms of PKCepsilon, nitric oxide synthase (nNOS), and TRPV1 was also performed. In F-11 cells containing both channels, PKCepsilon inhibition prevented the propofol- and allyl isothiocyanate (AITC)-induced restoration of TRPV1 sensitivity to agonist stimulation as well as increased phosphorylation of PKCepsilon and TRPV1. In cells containing TRPV1 only, neither agonist induced PKCepsilon or TRPV1 phosphorylation. Moreover, NOS inhibition blocked propofol-and AITC-induced restoration of TRPV1 sensitivity and PKCepsilon phosphorylation, and PKCepsilon inhibition prevented the nitric oxide donor, SNAP, from restoring TRPV1 sensitivity. Also, propofol-and AITC-induced phosphorylation of nNOS and nitric oxide (NO) production were blocked with the
Identifier
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<a href="http://doi.org/10.1002/prp2.153" target="_blank" rel="noreferrer noopener">10.1002/prp2.153</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).
2015
Bratz Ian N
Damron Derek S
Pharmacology research & perspectives
PKCepsilon and NOS
propofol
Prudner Bethany C
Sinha Sayantani
Sinharoy Pritam
TRPA1
TRPV1
Zhang Hongyu
-
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/10.1371/journal.pone.0180106" target="_blank" rel="noreferrer noopener">http://doi.org/10.1371/journal.pone.0180106</a>
Pages
e0180106–e0180106
Issue
6
Volume
12
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
TRPA1 and TRPV1 contribute to propofol-mediated antagonism of U46619-induced constriction in murine coronary arteries.
Publisher
An entity responsible for making the resource available
PloS one
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017
Subject
The topic of the resource
Male; Animals; Mice; TRPV Cation Channels/genetics/*metabolism; TRPA1 Cation Channel; Endothelial Cells/drug effects/metabolism; Nitric Oxide Synthase Type III/metabolism; Vasodilator Agents/*pharmacology; Coronary Vessels/*drug effects/metabolism; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits/metabolism; Microvessels/drug effects/metabolism; Propofol/*pharmacology; Transient Receptor Potential Channels/genetics/*metabolism; Vasoconstrictor Agents/antagonists & inhibitors/pharmacology; Vasodilation/drug effects/physiology; Cells; Cultured; Inbred C57BL; Knockout; 15-Hydroxy-11 alpha; 9 alpha-(epoxymethano)prosta-5; 13-dienoic Acid/*antagonists & inhibitors/pharmacology
Creator
An entity primarily responsible for making the resource
Sinharoy Pritam; Bratz Ian N; Sinha Sayantani; Showalter Loral E; Andrei Spencer R; Damron Derek S
Description
An account of the resource
BACKGROUND: Transient receptor potential (TRP) ion channels have emerged as key components contributing to vasoreactivity. Propofol, an anesthetic is associated with adverse side effects including hypotension and acute pain upon infusion. Our objective was to determine the extent to which TRPA1 and/or TRPV1 ion channels are involved in mediating propofol-induced vasorelaxation of mouse coronary arterioles in vitro and elucidate the potential cellular signal transduction pathway by which this occurs. METHODS: Hearts were excised from anesthetized mice and coronary arterioles were dissected from control C57Bl/6J, TRPA1-/-, TRPV1-/- and double-knockout mice (TRPAV-/-). Isolated microvessels were cannulated and secured in a temperature-controlled chamber and allowed to equilibrate for 1 hr. Vasoreactivity studies were performed in microvessels pre-constricted with U46619 to assess the dose-dependent relaxation effects of propofol on coronary microvascular tone. RESULTS: Propofol-induced relaxation was unaffected in vessels obtained from TRPV1-/- mice, markedly attenuated in pre-constricted vessels obtained from TRPA1-/- mice and abolished in vessels obtained from
Identifier
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<a href="http://doi.org/10.1371/journal.pone.0180106" target="_blank" rel="noreferrer noopener">10.1371/journal.pone.0180106</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).
13-dienoic Acid/*antagonists & inhibitors/pharmacology
15-Hydroxy-11 alpha
2017
9 alpha-(epoxymethano)prosta-5
Andrei Spencer R
Animals
Bratz Ian N
Cells
Coronary Vessels/*drug effects/metabolism
Cultured
Damron Derek S
Endothelial Cells/drug effects/metabolism
Inbred C57BL
Knockout
Large-Conductance Calcium-Activated Potassium Channel alpha Subunits/metabolism
Male
Mice
Microvessels/drug effects/metabolism
Nitric Oxide Synthase Type III/metabolism
PloS one
Propofol/*pharmacology
Showalter Loral E
Sinha Sayantani
Sinharoy Pritam
Transient Receptor Potential Channels/genetics/*metabolism
TRPA1 Cation Channel
TRPV Cation Channels/genetics/*metabolism
Vasoconstrictor Agents/antagonists & inhibitors/pharmacology
Vasodilation/drug effects/physiology
Vasodilator Agents/*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/10.1371/journal.pone.0122189" target="_blank" rel="noreferrer noopener">http://doi.org/10.1371/journal.pone.0122189</a>
Pages
e0122189–e0122189
Issue
4
Volume
10
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
Propofol causes vasodilation in vivo via TRPA1 ion channels: role of nitric oxide and BKCa channels.
Publisher
An entity responsible for making the resource available
PloS one
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
1905-07
Subject
The topic of the resource
Female; Male; Animals; Mice; Signal Transduction; TRPA1 Cation Channel; Arterial Pressure/drug effects; Vasodilator Agents/*pharmacology; Propofol/*pharmacology; Transient Receptor Potential Channels/genetics/*metabolism; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits/*physiology; Nitric Oxide/*physiology; TRPV Cation Channels/genetics/metabolism; Inbred C57BL; Knockout; Drug Evaluation; Preclinical
Creator
An entity primarily responsible for making the resource
Sinha Sayantani; Sinharoy Pritam; Bratz Ian N; Damron Derek S
Description
An account of the resource
BACKGROUND: Transient receptor potential (TRP) ion channels of the A1 (TRPA1) and V1 (TRPV1) subtypes are key regulators of vasomotor tone. Propofol is an intravenous anesthetic known to cause vasorelaxation. Our objectives were to examine the extent to which TRPA1 and/or TRPV1 ion channels mediate propofol-induced depressor responses in vivo and to delineate the signaling pathway(s) involved. METHODS: Mice were subjected to surgery under 1.5-2.5% sevoflurane gas with supplemental oxygen. After a stable baseline in mean arterial pressure (MAP) was achieved propofol (2.5, 5.0, 10.0 mg/kg/min) was administered to assess the hemodynamic actions of the intravenous anesthetic. The effect of nitric oxide synthase (NOS) inhibition with L-NAME and/or calcium-gated K+ channel (BKCa) inhibition with Penetrim A (Pen A), alone and in combination, on propofol-induced decreases in mean arterial pressure were assessed in control C57Bl/6J, TRPA1-/-, TRPV1-/- and double-knockout mice (TRPAV-/-). RESULTS: Propofol decreased MAP in control mice and this effect was markedly attenuated in
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1371/journal.pone.0122189" target="_blank" rel="noreferrer noopener">10.1371/journal.pone.0122189</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).
2015
Animals
Arterial Pressure/drug effects
Bratz Ian N
Damron Derek S
Drug Evaluation
Female
Inbred C57BL
Knockout
Large-Conductance Calcium-Activated Potassium Channel alpha Subunits/*physiology
Male
Mice
Nitric Oxide/*physiology
PloS one
Preclinical
Propofol/*pharmacology
Signal Transduction
Sinha Sayantani
Sinharoy Pritam
Transient Receptor Potential Channels/genetics/*metabolism
TRPA1 Cation Channel
TRPV Cation Channels/genetics/metabolism
Vasodilator Agents/*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/10.1016/j.freeradbiomed.2016.09.021" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.freeradbiomed.2016.09.021</a>
Pages
10–19
Volume
101
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
4-Hydroxynonenal dependent alteration of TRPV1-mediated coronary microvascular signaling.
Publisher
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Free radical biology & medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-12
Subject
The topic of the resource
*4-Hydroxynonenal; *Coronary regulation; *Lipid peroxidation; *Post-translational modification; *Protein Processing; *Reactive oxygen species; *Signal Transduction; *TRPV1; Action Potentials/drug effects; Aldehydes/antagonists & inhibitors/metabolism/*pharmacology; Animal; Animals; Blood Flow Velocity; Calcium Signaling/drug effects; Capsaicin/*pharmacology; Cardiovascular Agents/*pharmacology; Coronary Circulation/drug effects; Coronary Vessels/metabolism/physiopathology; Cysteine/genetics/metabolism; Diabetes Mellitus/drug therapy/*metabolism/physiopathology; Disease Models; Femoral Artery/metabolism/physiopathology; HEK293 Cells; Humans; Inbred C57BL; Lipid Peroxidation; Male; Mice; Patch-Clamp Techniques; Post-Translational; TRPV Cation Channels/genetics/*metabolism; Vasodilation/drug effects
Creator
An entity primarily responsible for making the resource
DelloStritto Daniel J; Sinharoy Pritam; Connell Patrick J; Fahmy Joseph N; Cappelli Holly C; Thodeti Charles K; Geldenhuys Werner J; Damron Derek S; Bratz Ian N
Description
An account of the resource
We demonstrated previously that TRPV1-dependent regulation of coronary blood flow (CBF) is disrupted in diabetes. Further, we have shown that endothelial TRPV1 is differentially regulated, ultimately leading to the inactivation of TRPV1, when exposed to a prolonged pathophysiological oxidative environment. This environment has been shown to increase lipid peroxidation byproducts including
Identifier
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<a href="http://doi.org/10.1016/j.freeradbiomed.2016.09.021" target="_blank" rel="noreferrer noopener">10.1016/j.freeradbiomed.2016.09.021</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).
*4-Hydroxynonenal
*Coronary regulation
*Lipid peroxidation
*Post-translational modification
*Protein Processing
*Reactive oxygen species
*Signal Transduction
*TRPV1
2016
Action Potentials/drug effects
Aldehydes/antagonists & inhibitors/metabolism/*pharmacology
Animal
Animals
Blood Flow Velocity
Bratz Ian N
Calcium Signaling/drug effects
Cappelli Holly C
Capsaicin/*pharmacology
Cardiovascular Agents/*pharmacology
Connell Patrick J
Coronary Circulation/drug effects
Coronary Vessels/metabolism/physiopathology
Cysteine/genetics/metabolism
Damron Derek S
DelloStritto Daniel J
Department of Integrative Medical Sciences
Diabetes Mellitus/drug therapy/*metabolism/physiopathology
Disease Models
Fahmy Joseph N
Femoral Artery/metabolism/physiopathology
Free radical biology & medicine
Geldenhuys Werner J
HEK293 Cells
Humans
Inbred C57BL
Lipid Peroxidation
Male
Mice
NEOMED College of Medicine
Patch-Clamp Techniques
Post-Translational
Sinharoy Pritam
Thodeti Charles K
TRPV Cation Channels/genetics/*metabolism
Vasodilation/drug effects
-
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/10.1080/19336950.2016.1185579" target="_blank" rel="noreferrer noopener">http://doi.org/10.1080/19336950.2016.1185579</a>
Pages
395–409
Issue
5
Volume
10
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
TRPA1 is functionally co-expressed with TRPV1 in cardiac muscle: Co-localization at z-discs, costameres and intercalated discs.
Publisher
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Channels (Austin, Tex.)
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-09
Subject
The topic of the resource
Animals; Ca2+; Calcium/physiology; Cardiac/*physiology; cardiomyocytes; Inbred C57BL; Male; Mice; Myocytes; Transient Receptor Potential Channels/genetics/*physiology; TRPA1; TRPA1 Cation Channel; TRPV Cation Channels/genetics/*physiology; TRPV1; Z-disc
Creator
An entity primarily responsible for making the resource
Andrei Spencer R; Sinharoy Pritam; Bratz Ian N; Damron Derek S
Description
An account of the resource
Transient receptor potential channels of the ankyrin subtype-1 (TRPA1) and vanilloid subtype-1 (TRPV1) are structurally related, non-selective cation channels that show a high permeability to calcium. Previous studies indicate that TRP channels play a prominent role in the regulation of cardiovascular dynamics and homeostasis, but also contribute to the pathophysiology of many diseases and disorders within the cardiovascular system. However, no studies to date have identified the functional expression and/or intracellular localization of TRPA1 in primary adult mouse ventricular cardiomyocytes (CMs). Although TRPV1 has been implicated in the regulation of cardiac function, there is a paucity of information regarding functional expression and localization of TRPV1 in adult CMs. Our current studies demonstrate that TRPA1 and TRPV1 ion channels are co-expressed at the protein level in CMs and both channels are expressed throughout the endocardium, myocardium and epicardium. Moreover, immunocytochemical localization demonstrates that both channels predominantly colocalize at the Z-discs, costameres and intercalated discs. Furthermore, specific TRPA1 and TRPV1 agonists elicit dose-dependent, transient rises in intracellular free calcium concentration ([Ca(2+)]i) that are abolished in CMs obtained from TRPA1(-/-) and TRPV1(-/-) mice. Similarly, we observed a dose-dependent attenuation of the TRPA1 and TRPV1 agonist-induced increase in [Ca(2+)]i when WT CMs were pretreated with increasing concentrations of selective TRPA1 or TRPV1 channel antagonists. In summary, these findings demonstrate functional expression and the precise ultrastructural localization of TRPA1 and TRPV1 ion channels in freshly isolated mouse CMs. Crosstalk between TRPA1 and TRPV1 may be important in mediating cellular signaling events in cardiac muscle.
Identifier
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<a href="http://doi.org/10.1080/19336950.2016.1185579" target="_blank" rel="noreferrer noopener">10.1080/19336950.2016.1185579</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).
2016
Andrei Spencer R
Animals
Bratz Ian N
Ca2+
Calcium/physiology
Cardiac/*physiology
cardiomyocytes
Channels (Austin, Tex.)
Damron Derek S
Inbred C57BL
Male
Mice
Myocytes
Sinharoy Pritam
Transient Receptor Potential Channels/genetics/*physiology
TRPA1
TRPA1 Cation Channel
TRPV Cation Channels/genetics/*physiology
TRPV1
Z-disc
-
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/10.1080/19336950.2017.1365206" target="_blank" rel="noreferrer noopener">http://doi.org/10.1080/19336950.2017.1365206</a>
Pages
587–603
Issue
6
Volume
11
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
TRPA1 ion channel stimulation enhances cardiomyocyte contractile function via a CaMKII-dependent pathway.
Publisher
An entity responsible for making the resource available
Channels (Austin, Tex.)
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-11
Subject
The topic of the resource
[Ca2+]i; *Myocardial Contraction; Animals; Calcium-Calmodulin-Dependent Protein Kinase Type 2/*metabolism; CaMKII; Cardiac/*metabolism; cardiomyocytes; contractility; Inbred C57BL; Knockout; Mice; Myocytes; TRPA1; TRPA1 Cation Channel/deficiency/*metabolism
Creator
An entity primarily responsible for making the resource
Andrei Spencer R; Ghosh Monica; Sinharoy Pritam; Dey Souvik; Bratz Ian N; Damron Derek S
Description
An account of the resource
RATIONALE: Transient receptor potential channels of the ankyrin subtype-1 (TRPA1) are non-selective cation channels that show high permeability to calcium. Previous studies from our laboratory have demonstrated that TRPA1 ion channels are expressed in adult mouse ventricular cardiomyocytes (CMs) and are localized at the z-disk, costamere and intercalated disk. The functional significance of TRPA1 ion channels in the modulation of CM contractile function have not been explored. OBJECTIVE: To identify the extent to which TRPA1 ion channels are involved in modulating CM contractile function and elucidate the cellular mechanism of action. METHODS AND RESULTS: Freshly isolated CMs were obtained from murine heart and loaded with Fura-2 AM. Simultaneous measurement of intracellular free Ca(2+) concentration ([Ca(2+)]i) and contractility was performed in individual CMs paced at 0.3 Hz. Our findings demonstrate that TRPA1 stimulation with AITC results in a dose-dependent increase in peak [Ca(2+)]i and a concomitant increase in CM fractional shortening. Further analysis revealed a dose-dependent acceleration in time to peak [Ca(2+)]i and velocity of shortening as well as an acceleration in [Ca(2+)]i decay and velocity of relengthening. These effects of TRPA1 stimulation were not observed in CMs pre-treated with the TRPA1 antagonist, HC-030031 (10 micromol/L) nor in CMs obtained from TRPA1(-/-) mice. Moreover, we observed no significant increase in cAMP levels or PKA activity in response to TRPA1 stimulation and the PKA inhibitor peptide (PKI
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1080/19336950.2017.1365206" target="_blank" rel="noreferrer noopener">10.1080/19336950.2017.1365206</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).
[Ca2+]i
*Myocardial Contraction
2017
Andrei Spencer R
Animals
Bratz Ian N
Calcium-Calmodulin-Dependent Protein Kinase Type 2/*metabolism
CaMKII
Cardiac/*metabolism
cardiomyocytes
Channels (Austin, Tex.)
contractility
Damron Derek S
Dey Souvik
Ghosh Monica
Inbred C57BL
Knockout
Mice
Myocytes
Sinharoy Pritam
TRPA1
TRPA1 Cation Channel/deficiency/*metabolism