1
40
2
-
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/s00395-020-0775-5" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s00395-020-0775-5</a>
Pages
14-14
Issue
2
Volume
115
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<a href="http://ezproxy.neomed.idm.oclc.org/login?url=http://doi.org/10.1007/s00395-020-0775-5" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1007/s00395-020-0775-5</a>
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
Update Year & Number
March 2020 Update
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Integrative Medical Sciences
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 deletion protects heart from myocardial infarction-induced adverse remodeling via modulation of cardiac fibroblast differentiation.
Publisher
An entity responsible for making the resource available
Basic research in cardiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-01
Subject
The topic of the resource
Mechanotransduction; TRPV4; Myocardial infarction; Myocardial infarction; TGF-beta1; Rho/Rho kinase; Mechanotransduction; TGF-β1; Myocardial infarction; EXTRACELLULAR matrix; HEART failure; HEART fibrosis; HEART; Cardiac fibroblast; Cardiac fibrosis; Rho/Rho kinase; TRPV4; Cardiac fibroblast; Cardiac fibrosis; DELETION mutation
Creator
An entity primarily responsible for making the resource
Adapala Ravi K; Kanugula Anantha K; Paruchuri Sailaja; Chilian William M; Thodeti Charles K
Description
An account of the resource
Cardiac fibrosis caused by adverse cardiac remodeling following myocardial infarction can eventually lead to heart failure. Although the role of soluble factors such as TGF-beta is well studied in cardiac fibrosis following myocardial injury, the physiological role of mechanotransduction is not fully understood. Here, we investigated the molecular mechanism and functional role of TRPV4 mechanotransduction in cardiac fibrosis. TRPV4KO mice, 8 weeks following myocardial infarction (MI), exhibited preserved cardiac function compared to WT mice. Histological analysis demonstrated reduced cardiac fibrosis in TRPV4KO mice. We found that WT CF exhibited hypotonicity-induced calcium influx and extracellular matrix (ECM)-stiffness-dependent differentiation in response to
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s00395-020-0775-5" target="_blank" rel="noreferrer noopener">10.1007/s00395-020-0775-5</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).
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2020
Adapala Ravi K
Basic research in cardiology
cardiac fibroblast
Cardiac fibrosis
Chilian William M
DELETION mutation
Department of Integrative Medical Sciences
Extracellular Matrix
heart
Heart failure
HEART fibrosis
Kanugula Anantha K
Mechanotransduction
myocardial infarction
NEOMED College of Medicine
NEOMED Postdoc Publications
Paruchuri Sailaja
Rho/Rho kinase
TGF-beta1
TGF-β1
Thodeti Charles K
TRPV4
-
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/10.18632/oncotarget.8405" target="_blank" rel="noreferrer noopener">http://doi.org/10.18632/oncotarget.8405</a>
Pages
25849–25861
Issue
18
Volume
7
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 regulate tumor angiogenesis via modulation of Rho/Rho kinase pathway.
Publisher
An entity responsible for making the resource available
Oncotarget
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-05
Subject
The topic of the resource
Animals; Mice; TRPV4; endothelial cell; Cell Movement/physiology; Endothelial Cells/metabolism/pathology; mechanotransduction; rho-Associated Kinases/*metabolism; Rho/Rho kinase; TRPV Cation Channels/*metabolism; tumor angiogenesis; Carcinoma; Inbred C57BL; Knockout; Neovascularization; Lewis Lung/metabolism/*pathology; Pathologic/*metabolism/pathology
Creator
An entity primarily responsible for making the resource
Thoppil Roslin J; Cappelli Holly C; Adapala Ravi K; Kanugula Anantha K; Paruchuri Sailaja; Thodeti Charles K
Description
An account of the resource
Targeting angiogenesis is considered a promising therapy for cancer. Besides curtailing soluble factor mediated tumor angiogenesis, understanding the unexplored regulation of angiogenesis by mechanical cues may lead to the identification of novel therapeutic targets. We have recently shown that expression and activity of mechanosensitive ion channel transient receptor potential vanilloid 4 (TRPV4) is suppressed in tumor endothelial cells and restoring TRPV4 expression or activation induces vascular normalization and improves cancer therapy. However, the molecular mechanism(s) by which TRPV4 modulates angiogenesis are still in their infancy. To explore how TRPV4 regulates angiogenesis, we have employed TRPV4 null endothelial cells (TRPV4KO EC) and TRPV4KO mice. We found that absence of TRPV4 (TRPV4KO EC) resulted in a significant increase in proliferation, migration, and abnormal tube formation in vitro when compared to WT EC. Concomitantly, sprouting angiogenesis ex vivo and vascular growth in vivo was enhanced in TRPV4KO mice. Mechanistically, we observed that loss of TRPV4 leads to a significant increase in basal Rho activity in TRPV4KO EC that corresponded to their aberrant mechanosensitivity on varying stiffness ECM gels. Importantly, pharmacological inhibition of the Rho/Rho kinase pathway by Y-27632 normalized abnormal mechanosensitivity and angiogenesis exhibited by TRPV4KO EC in vitro. Finally, Y-27632 treatment increased pericyte coverage and in conjunction with Cisplatin, significantly reduced tumor growth in TRPV4KO mice. Taken together, these data suggest that TRPV4 regulates angiogenesis endogenously via modulation of EC mechanosensitivity through the Rho/Rho kinase pathway and can serve as a potential therapeutic target for cancer therapy.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.18632/oncotarget.8405" target="_blank" rel="noreferrer noopener">10.18632/oncotarget.8405</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).
2016
Adapala Ravi K
Animals
Cappelli Holly C
Carcinoma
Cell Movement/physiology
Department of Integrative Medical Sciences
endothelial cell
Endothelial Cells/metabolism/pathology
Inbred C57BL
Kanugula Anantha K
Knockout
Lewis Lung/metabolism/*pathology
Mechanotransduction
Mice
NEOMED College of Medicine
Neovascularization
Oncotarget
Paruchuri Sailaja
Pathologic/*metabolism/pathology
rho-Associated Kinases/*metabolism
Rho/Rho kinase
Thodeti Charles K
Thoppil Roslin J
TRPV Cation Channels/*metabolism
TRPV4
tumor angiogenesis