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/10.1016/j.yjmcc.2012.10.016" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.yjmcc.2012.10.016</a>
Pages
45–52
Volume
54
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
TRPV4 channels mediate cardiac fibroblast differentiation by integrating mechanical and soluble signals.
Publisher
An entity responsible for making the resource available
Journal of molecular and cellular cardiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-01
Subject
The topic of the resource
*Calcium Signaling; *Cell Differentiation; *Mechanotransduction; Animals; Cellular; Extracellular Matrix/metabolism/physiology; Fibroblasts/*physiology; Gene Knockdown Techniques; Male; Monoterpenes/pharmacology; Myocardium/cytology; Myofibroblasts/metabolism; Rats; RNA; Small Interfering/genetics; Sprague-Dawley; Transforming Growth Factor beta1/physiology; TRPM Cation Channels/antagonists & inhibitors/metabolism; TRPV Cation Channels/genetics/*metabolism
Creator
An entity primarily responsible for making the resource
Adapala Ravi K; Thoppil Roslin J; Luther Daniel J; Paruchuri Sailaja; Meszaros J Gary; Chilian William M; Thodeti Charles K
Description
An account of the resource
The phenotypic switch underlying the differentiation of cardiac fibroblasts into hypersecretory myofibroblasts is critical for cardiac remodeling following myocardial infarction. Myofibroblasts facilitate wound repair in the myocardium by secreting and organizing extracellular matrix (ECM) during the wound healing process. However, the molecular mechanisms involved in myofibroblast differentiation are not well known. TGF-beta has been shown to promote differentiation and this, combined with the robust mechanical environment in the heart, lead us to hypothesize that the mechanotransduction and TGF-beta signaling pathways play active roles in the differentiation of cardiac fibroblasts to myofibroblasts. Here, we show that the mechanosensitve ion channel TRPV4 is required for TGF-beta1-induced differentiation of cardiac fibroblasts into myofibroblasts. We found that the TRPV4-specific antagonist AB159908 and siRNA knockdown of TRPV4 significantly inhibited TGFbeta1-induced differentiation as measured by incorporation of alpha-SMA into stress fibers. Further, we found that
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.yjmcc.2012.10.016" target="_blank" rel="noreferrer noopener">10.1016/j.yjmcc.2012.10.016</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).
*Calcium Signaling
*Cell Differentiation
*Mechanotransduction
2013
Adapala Ravi K
Animals
Cellular
Chilian William M
Department of Integrative Medical Sciences
Extracellular Matrix/metabolism/physiology
Fibroblasts/*physiology
Gene Knockdown Techniques
Journal of molecular and cellular cardiology
Luther Daniel J
Male
Meszaros J Gary
Monoterpenes/pharmacology
Myocardium/cytology
Myofibroblasts/metabolism
NEOMED College of Medicine
Paruchuri Sailaja
Rats
RNA
Small Interfering/genetics
Sprague-Dawley
Thodeti Charles K
Thoppil Roslin J
Transforming Growth Factor beta1/physiology
TRPM Cation Channels/antagonists & inhibitors/metabolism
TRPV Cation Channels/genetics/*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/10.1016/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
An entity responsible for making the resource available
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
An unambiguous reference to the resource within a given context
<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>
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).
*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/10.1096/fj.201601045R" target="_blank" rel="noreferrer noopener">http://doi.org/10.1096/fj.201601045R</a>
Pages
1556–1570
Issue
4
Volume
31
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
Mechanosensitive transient receptor potential vanilloid 4 regulates Dermatophagoides farinae-induced airway remodeling via 2 distinct pathways modulating matrix synthesis and degradation.
Publisher
An entity responsible for making the resource available
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-04
Subject
The topic of the resource
*Airway Remodeling; *fibronectin; *myofibroblasts; *PAI-1; *PI3K; *TGF-beta1; Adult; Animals; Asthma/etiology/genetics/*metabolism/pathology; Cells; Cultured; Dermatophagoides farinae/immunology; Extracellular Matrix/*metabolism/pathology; Fibroblasts/metabolism; Fibronectins/*metabolism; Humans; Inbred C57BL; Male; Mice; Phosphatidylinositol 3-Kinases/metabolism; Plasminogen Activator Inhibitor 1/metabolism; Transforming Growth Factor beta/metabolism; TRPV Cation Channels/genetics/*metabolism
Creator
An entity primarily responsible for making the resource
Gombedza Farai; Kondeti Vinay; Al-Azzam Nosayba; Koppes Stephanie; Duah Ernest; Patil Prachi; Hexter Madison; Phillips Daniel; Thodeti Charles K; Paruchuri Sailaja
Description
An account of the resource
Contributions of mechanical signals to airway remodeling during asthma are poorly understood. Transient receptor potential vanilloid 4 (TRPV4), a mechanosensitive ion channel, has been implicated in cardiac and pulmonary fibrosis; however, its role in asthma remains elusive. Employing a Dermatophagoides farinae-induced asthma model, we report here that TRPV4-knockout mice were protected from D. farinae-induced airway remodeling. Furthermore, lung fibroblasts that were isolated from TRPV4-knockout mice showed diminished differentiation potential compared with wild-type mice. Fibroblasts from asthmatic lung exhibited increased TRPV4 activity and enhanced differentiation potential compared with normal human lung fibroblasts. Of interest, TGF-beta1 treatment enhanced TRPV4 activation in a
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1096/fj.201601045R" target="_blank" rel="noreferrer noopener">10.1096/fj.201601045R</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).
*Airway Remodeling
*fibronectin
*myofibroblasts
*PAI-1
*PI3K
*TGF-beta1
2017
Adult
Al-Azzam Nosayba
Animals
Asthma/etiology/genetics/*metabolism/pathology
Cells
Cultured
Department of Integrative Medical Sciences
Dermatophagoides farinae/immunology
Duah Ernest
Extracellular Matrix/*metabolism/pathology
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
Fibroblasts/metabolism
Fibronectins/*metabolism
Gombedza Farai
Hexter Madison
Humans
Inbred C57BL
Kondeti Vinay
Koppes Stephanie
Male
Mice
NEOMED College of Medicine
Paruchuri Sailaja
Patil Prachi
Phillips Daniel
Phosphatidylinositol 3-Kinases/metabolism
Plasminogen Activator Inhibitor 1/metabolism
Thodeti Charles K
Transforming Growth Factor beta/metabolism
TRPV Cation Channels/genetics/*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/10.1371/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