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/10.1002/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
An entity responsible for making the resource available
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
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/prp2.153" target="_blank" rel="noreferrer noopener">10.1002/prp2.153</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).
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.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>
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).
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/10.1371/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
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1371/journal.pone.0180106" target="_blank" rel="noreferrer noopener">10.1371/journal.pone.0180106</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).
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/10.1097/ALN.0b013e31820dee67" target="_blank" rel="noreferrer noopener">http://doi.org/10.1097/ALN.0b013e31820dee67</a>
Pages
1169–1179
Issue
5
Volume
114
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 transient receptor potential vanilloid receptor subtype-1 sensitivity via activation of transient receptor potential ankyrin receptor subtype-1 in sensory neurons.
Publisher
An entity responsible for making the resource available
Anesthesiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-05
Subject
The topic of the resource
Male; Mice; Capsaicin; Cells; Anesthetics; Animal Studies; Genes – Drug Effects; Carrier Proteins – Drug Effects; Carrier Proteins – Metabolism; Intravenous – Pharmacodynamics; Propofol – Pharmacodynamics; Sensory Receptor Cells – Drug Effects
Creator
An entity primarily responsible for making the resource
Zhang H; Wickley PJ; Sinha S; Bratz IN; Damron DS; Zhang Hongyu; Wickley Peter J; Sinha Sayantani; Bratz Ian N; Damron Derek S
Description
An account of the resource
Background: Cross talk between peripheral nociceptors belonging to the transient receptor potential vanilloid receptor subtype-1 (TRPV1) and ankyrin subtype-1 (TRPA1) family has been demonstrated recently. Moreover, the intravenous anesthetic propofol has directly activates TRPA1 receptors and indirectly restores sensitivity of TRPV1 receptors in dorsal root ganglion (DRG) sensory neurons. Our objective was to determine the extent to which TRPA1 activation is involved in mediating the propofol-induced restoration of TRPV1 sensitivity.Methods: Mouse DRG neurons were isolated by enzymatic dissociation and grown for 24 h. F-11 cells were transfected with complementary DNA for both TRPV1 and TRPA1 or TRPV1 only. The intracellular Ca concentration was measured in individual cells via fluorescence microscopy. After TRPV1 desensitization with capsaicin (100 nM), cells were treated with propofol (1, 5, and 10 μM) alone or with propofol in the presence of the TRPA1 antagonist, HC-030031 (0.5 μM), or the TRPA1 agonist, allyl isothiocyanate (AITC; 100 μM); capsaicin was then reapplied.Results: In DRG neurons that contain both TRPV1 and TRPA1, propofol and AITC restored TRPV1 sensitivity. However, in DRG neurons containing only TRPV1 receptors, exposure to propofol or AITC after desensitization did not restore capsaicin-induced TRPV1 sensitivity. Similarly, in F-11 cells transfected with both TRPV1 and TRPA1, propofol and AITC restored TRPV1 sensitivity. However, in F-11 cells transfected with TRPV1 only, neither propofol nor AITC was capable of restoring TRPV1 sensitivity.Conclusions: These data demonstrate that propofol restores TRPV1 sensitivity in primary DRG neurons and in cultured F-11 cells transfected with both the TRPV1 and TRPA1 receptors via a TRPA1-dependent process. Propofol's effects on sensory neurons may be clinically important and may contribute to peripheral sensitization to nociceptive stimuli in traumatized tissue.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1097/ALN.0b013e31820dee67" target="_blank" rel="noreferrer noopener">10.1097/ALN.0b013e31820dee67</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).
2011
Anesthesiology
Anesthetics
Animal Studies
Bratz Ian N
Bratz IN
Capsaicin
Carrier Proteins – Drug Effects
Carrier Proteins – Metabolism
Cells
Damron Derek S
Damron DS
Genes – Drug Effects
Intravenous – Pharmacodynamics
Male
Mice
Propofol – Pharmacodynamics
Sensory Receptor Cells – Drug Effects
Sinha S
Sinha Sayantani
Wickley Peter J
Wickley PJ
Zhang H
Zhang Hongyu