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.00142.2011" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00142.2011</a>
Pages
H757–765
Issue
3
Volume
301
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
PKCalpha mediates acetylcholine-induced activation of TRPV4-dependent calcium influx in endothelial cells.
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
2011
2011-09
Subject
The topic of the resource
Acetylcholine/*pharmacology; Animals; Calcium Signaling/*drug effects; Carbazoles/pharmacology; Cells; Cultured; Endothelial Cells/*drug effects/enzymology; Enzyme Activation; Inbred C57BL; Knockout; Male; Mesenteric Arteries/drug effects/enzymology; Mice; Mutation; Nitric Oxide Synthase Type III/metabolism; Phosphorylation; Protein Kinase C-alpha/genetics/*metabolism; Protein Kinase Inhibitors/pharmacology; Tetradecanoylphorbol Acetate/pharmacology; Time Factors; Transfection; TRPV Cation Channels/*agonists/deficiency/genetics/metabolism; Vasodilation/*drug effects; Vasodilator Agents/*pharmacology
Creator
An entity primarily responsible for making the resource
Adapala Ravi K; Talasila Phani K; Bratz Ian N; Zhang David X; Suzuki Makoto; Meszaros J Gary; Thodeti Charles K
Description
An account of the resource
Transient receptor potential vanilloid channel 4 (TRPV4) is a polymodally activated nonselective cationic channel implicated in the regulation of vasodilation and hypertension. We and others have recently shown that cyclic stretch and shear stress activate TRPV4-mediated calcium influx in endothelial cells (EC). In addition to the mechanical forces, acetylcholine (ACh) was shown to activate TRPV4-mediated calcium influx in endothelial cells, which is important for nitric oxide-dependent vasodilation. However, the molecular mechanism through which ACh activates TRPV4 is not known. Here, we show that ACh-induced calcium influx and endothelial nitric oxide synthase (eNOS) phosphorylation but not calcium release from intracellular stores is inhibited by a specific TRPV4 antagonist, AB-159908. Importantly, activation of store-operated calcium influx was not altered in the TRPV4 null EC, suggesting that
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00142.2011" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00142.2011</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
Acetylcholine/*pharmacology
Adapala Ravi K
American journal of physiology. Heart and circulatory physiology
Animals
Bratz Ian N
Calcium Signaling/*drug effects
Carbazoles/pharmacology
Cells
Cultured
Department of Integrative Medical Sciences
Endothelial Cells/*drug effects/enzymology
Enzyme Activation
Inbred C57BL
Knockout
Male
Mesenteric Arteries/drug effects/enzymology
Meszaros J Gary
Mice
Mutation
NEOMED College of Medicine
Nitric Oxide Synthase Type III/metabolism
Phosphorylation
Protein Kinase C-alpha/genetics/*metabolism
Protein Kinase Inhibitors/pharmacology
Suzuki Makoto
Talasila Phani K
Tetradecanoylphorbol Acetate/pharmacology
Thodeti Charles K
Time Factors
Transfection
TRPV Cation Channels/*agonists/deficiency/genetics/metabolism
Vasodilation/*drug effects
Vasodilator Agents/*pharmacology
Zhang David X
-
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.00082.2011" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00082.2011</a>
Pages
H1135–1142
Issue
3
Volume
301
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
Endothelin-mediated in vivo pressor responses following TRPV1 activation.
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
2011
2011-09
Subject
The topic of the resource
*Blood Pressure/drug effects; *Vasoconstriction/drug effects; Adrenergic alpha-Agonists/administration & dosage; Analysis of Variance; Animal; Animals; Azepines/administration & dosage; Biphenyl Compounds/administration & dosage; Capsaicin/administration & dosage; Cells; Cultured; Diabetes Mellitus; Diabetic Angiopathies/genetics/*metabolism/physiopathology; Dipeptides/administration & dosage; Disease Models; Dose-Response Relationship; Drug; Endothelial Cells/metabolism; Endothelin A Receptor Antagonists; Endothelin A/metabolism; Endothelin B Receptor Antagonists; Endothelin B/metabolism; Endothelin-1/*metabolism; Enzyme-Linked Immunosorbent Assay; Femoral Artery/drug effects/*metabolism/physiopathology; Inbred C57BL; Indoles/administration & dosage; Infusions; Intravenous; Knockout; Male; Mice; Phenylephrine/administration & dosage; Receptor; TRPV Cation Channels/agonists/deficiency/genetics/*metabolism; Type 2/genetics/*metabolism/physiopathology; Vasoconstrictor Agents/administration & dosage
Creator
An entity primarily responsible for making the resource
Ohanyan Vahagn A; Guarini Giacinta; Thodeti Charles K; Talasila Phani K; Raman Priya; Haney Rebecca M; Meszaros J Gary; Damron Derek S; Bratz Ian N
Description
An account of the resource
Transient receptor potential vanilliod 1 (TRPV1) channels have recently been postulated to play a role in the vascular complications/consequences associated with diabetes despite the fact that the mechanisms through which TRPV1 regulates vascular function are not fully known. Accordingly, our goal was to define the mechanisms by which TRPV1 channels modulate vascular function and contribute to vascular dysfunction in diabetes. We subjected mice lacking TRPV1 [TRPV1((-/-))], db/db, and control C57BLKS/J mice to in vivo infusion of the TRPV1 agonist capsaicin or the alpha-adrenergic agonist phenylephrine (PE) to examine the integrated circulatory actions of TRPV1. Capsaicin (1, 10, 20, and 100 mug/kg) dose dependently increased MAP in control mice (5.7 +/- 1.6, 11.7 +/- 2.1, 25.4 +/- 3.4, and 51.6 +/- 3.9%), which was attenuated in db/db mice (3.4 +/- 2.1, 3.9 +/- 2.1, 7.0 +/- 3.3, and 17.9 +/- 6.2%). TRPV1((-/-)) mice exhibited no changes in MAP in response to capsaicin, suggesting the actions of this agonist are specific to TRPV1 activation. Immunoblot analysis revealed decreased aortic TRPV1 protein expression in db/db compared with control mice. Capsaicin-induced responses were recorded following inhibition of endothelin A and B receptors (ET(A) /ET(B)). Inhibition of ET(A) receptors abolished the capsaicin-mediated increases in MAP. Combined antagonism of ET(A) and ET(B) receptors did not further inhibit the capsaicin response. Cultured endothelial cell exposure to capsaicin increased endothelin production as shown by an endothelin ELISA assay, which was attenuated by inhibition of TRPV1 or endothelin-converting enzyme. TRPV1 channels contribute to the regulation of vascular reactivity and MAP via production of endothelin and subsequent activation of vascular ET(A) receptors. Impairment of TRPV1 channel function may contribute to vascular dysfunction in diabetes.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00082.2011" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00082.2011</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).
*Blood Pressure/drug effects
*Vasoconstriction/drug effects
2011
Adrenergic alpha-Agonists/administration & dosage
American journal of physiology. Heart and circulatory physiology
Analysis of Variance
Animal
Animals
Azepines/administration & dosage
Biphenyl Compounds/administration & dosage
Bratz Ian N
Capsaicin/administration & dosage
Cells
Cultured
Damron Derek S
Department of Integrative Medical Sciences
Diabetes Mellitus
Diabetic Angiopathies/genetics/*metabolism/physiopathology
Dipeptides/administration & dosage
Disease Models
Dose-Response Relationship
Drug
Endothelial Cells/metabolism
Endothelin A Receptor Antagonists
Endothelin A/metabolism
Endothelin B Receptor Antagonists
Endothelin B/metabolism
Endothelin-1/*metabolism
Enzyme-Linked Immunosorbent Assay
Femoral Artery/drug effects/*metabolism/physiopathology
Guarini Giacinta
Haney Rebecca M
Inbred C57BL
Indoles/administration & dosage
Infusions
Intravenous
Knockout
Male
Meszaros J Gary
Mice
NEOMED College of Medicine
Ohanyan Vahagn A
Phenylephrine/administration & dosage
Raman Priya
Receptor
Talasila Phani K
Thodeti Charles K
TRPV Cation Channels/agonists/deficiency/genetics/*metabolism
Type 2/genetics/*metabolism/physiopathology
Vasoconstrictor Agents/administration & dosage
-
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.bmcl.2012.06.096" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.bmcl.2012.06.096</a>
Pages
5675–5678
Issue
17
Volume
22
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
Identification of a novel serum and glucocorticoid regulated kinase-1 (SGK1) ligand from virtual screening.
Publisher
An entity responsible for making the resource available
Bioorganic & medicinal chemistry letters
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-09
Subject
The topic of the resource
Binding Sites; Drug Discovery; Humans; Immediate-Early Proteins/*antagonists & inhibitors/chemistry/metabolism; Ligands; Molecular Docking Simulation; Protein Kinase Inhibitors/*chemistry/*pharmacology; Protein-Serine-Threonine Kinases/*antagonists & inhibitors/chemistry/metabolism
Creator
An entity primarily responsible for making the resource
Geldenhuys Werner J; Talasila Phani K; Sadana Prabodh
Description
An account of the resource
The serum and glucocorticoid regulated kinase-1 (SGK1) is part of the serine/threonine kinase family and has therapeutic potential in several neurodegenerative diseases such as ischemic stroke and Parkinson's disease. Here we use structure-based virtual screening to identify a novel ligand which inhibits SGK1 activity. The data presented here can be used for future scaffold hopping and possible drug development efforts.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.bmcl.2012.06.096" target="_blank" rel="noreferrer noopener">10.1016/j.bmcl.2012.06.096</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).
2012
Binding Sites
Bioorganic & medicinal chemistry letters
Department of Pharmaceutical Sciences
Department of Pharmacy Practice
Drug Discovery
Geldenhuys Werner J
Humans
Immediate-Early Proteins/*antagonists & inhibitors/chemistry/metabolism
Ligands
Molecular Docking Simulation
NEOMED College of Graduate Studies
NEOMED College of Pharmacy
Protein Kinase Inhibitors/*chemistry/*pharmacology
Protein-Serine-Threonine Kinases/*antagonists & inhibitors/chemistry/metabolism
Sadana Prabodh
Talasila Phani K
-
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/s13346-012-0117-8" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s13346-012-0117-8</a>
Pages
309–317
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
Engineering triiodothyronine (T3) nanoparticle for use in ischemic brain stroke.
Publisher
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Drug delivery and translational research
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-08
Subject
The topic of the resource
Blood-brain barrier; Brain stroke; Nanoparticles; Neuroprotection; Thyroid hormone
Creator
An entity primarily responsible for making the resource
Mdzinarishvili Alexander; Sutariya Vijaykumar; Talasila Phani K; Geldenhuys Werner J; Sadana Prabodh
Description
An account of the resource
A potential means of pharmacological management of ischemic stroke is rapid intervention using potent neuroprotective agents. Thyroid hormone (T3) has been shown to protect against ischemic damage in middle cerebral artery occlusion (MCAO) model of ischemic brain stroke. While thyroid hormone is permeable across the blood-brain barrier, we hypothesized that efficacy of thyroid hormone in ischemic brain stroke can be enhanced by encapsulation in nanoparticulate delivery vehicles. We tested our hypothesis by generating poly-(lactide-co-glycolide)-polyethyleneglycol (PLGA-b-PEG) nanoparticles that are either coated with glutathione or are not coated. We have previously reported that glutathione coating of PLGA-PEG nanoparticles is an efficient means of brain targeted drug delivery. Encapsulation of T3 in PLGA-PEG delivery vehicle resulted in particles that were in the nano range and exhibited a zeta potential of -6.51 mV (uncoated) or -1.70 mV (coated). We observed that both glutathione-coated and uncoated nanoparticles are taken up in cells wherein they stimulated the expression of thyroid hormone response element driven reporter robustly. In MCAO model of ischemic stroke, significant benefit of administering T3 in nanoparticulate form was observed over injection of a T3 solution. A 34 % decrease in tissue infarction and a 59 % decrease in brain edema were seen upon administration of T3 solution in MCAO stroke model. Corresponding measurements for uncoated T3 nanoparticles were 51 % and 68 %, whereas for the glutathione coated were 58 % and 75 %. Our study demonstrates that using nanoparticle formulations can significantly improve the efficacy of neuroprotective drugs in ischemic brain stroke.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s13346-012-0117-8" target="_blank" rel="noreferrer noopener">10.1007/s13346-012-0117-8</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).
2013
Blood-brain barrier
Brain stroke
Department of Pharmaceutical Sciences
Department of Pharmacy Practice
Drug delivery and translational research
Geldenhuys Werner J
Mdzinarishvili Alexander
Nanoparticles
NEOMED College of Graduate Studies
NEOMED College of Pharmacy
Neuroprotection
Sadana Prabodh
Sutariya Vijaykumar
Talasila Phani K
Thyroid hormone