1
40
3
-
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/10.1042/cs20070160" target="_blank" rel="noreferrer noopener">http://doi.org/10.1042/cs20070160</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
357-364
Issue
7
Volume
113
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<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>
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
Ace2 Overexpression Inhibits Hypoxia-induced Collagen Production By Cardiac Fibroblasts
Publisher
An entity responsible for making the resource available
Clinical Science
Date
A point or period of time associated with an event in the lifecycle of the resource
2007
2007-10
Subject
The topic of the resource
angiotensin-converting enzyme 2 (ACE2); angiotensin-converting enzyme-2; collagen; cross-talk; expression; fibroblast; growth-factor-beta; heart failure; hypoxia; Myocardial infarction; myofibroblast differentiation; oxidative stress; pathways; rat; remodelling; Research & Experimental Medicine; signaling; transforming growth factor beta (TGF beta)
Creator
An entity primarily responsible for making the resource
Grobe J L; Der Sarkissian S; Stewart J M; Meszaros J G; Raizada M K; Katovich M J
Description
An account of the resource
Cardiac remodelling is a key risk factor for the development of heart failure in the chronic phase following myocardial infarction. Our previous studies have shown an anti-remodelling role of ACE2 (angiotensin-converting enzyme 2) in vivo during hypertension and that these protective effects are mediated through increased circulating levels of Ang-(1-7) [angiotensin-(1-7)]. In the present study, we have demonstrated that cardiac myocytes have modest ACE2 activity, whereas cardiac fibroblasts do not: exhibit any endogenous activity. As fibroblasts are the major cell type found in an infarct zone following a myocardial infarction, we examined the effects of ACE2 gene delivery to cultured cardiac fibroblasts after acute hypoxic exposure. Cardiac fibroblasts from 5-day-old Sprague-Dawley rat hearts were grown to confluence and transduced with a lentiviral vector containing murine ACE2 cDNA under transcriptional control by the EFI alpha (elongation factor I alpha) promoter (lenti-ACE2). Transduction of fibroblasts with lenti-ACE2 resulted in a viral dose-dependent increase in ACE2 activity. This was associated with a significant attenuation of both basal and hypoxia/re-oxygenation-induced collagen production by the fibroblasts. Cytokine production, specifically TGF beta (transforming growth factor beta), by these cells was also significantly attenuated by ACE2 expression. Collectively, these results indicate that: (i) endogenous ACE2 activity is observed in cardiac myocytes, but not in cardiac fibroblasts; (ii) ACE2 overexpression in the cardiac fibroblast attenuates collagen production; and (iii) this prevention is probably mediated by decreased expression of cytokines. We conclude that ACE2 expression, limited to cardiac fibroblasts, may represent a novel paradigm for in vivo therapy following acute ischaemia.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1042/cs20070160" target="_blank" rel="noreferrer noopener">10.1042/cs20070160</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2007
angiotensin-converting enzyme 2 (ACE2)
angiotensin-converting enzyme-2
Clinical Science
Collagen
cross-talk
Der Sarkissian S
expression
fibroblast
Grobe J L
growth-factor-beta
Heart failure
hypoxia
Journal Article or Conference Abstract Publication
Katovich M J
Meszaros J G
myocardial infarction
myofibroblast differentiation
Oxidative Stress
pathways
Raizada M K
rat
remodelling
Research & Experimental Medicine
Signaling
Stewart J M
transforming growth factor beta (TGF beta)
-
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.0054804" target="_blank" rel="noreferrer noopener">http://doi.org/10.1371/journal.pone.0054804</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
11-11
Issue
1
Volume
8
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<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>
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
Extracellular ATP and Toll-Like Receptor 2 Agonists Trigger in Human Monocytes an Activation Program That Favors T Helper 17
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
2013
2013-01
Subject
The topic of the resource
adaptive immunity; calcium ionophore; cd14(+) monocytes; cells; growth-factor-beta; host-defense; human dendritic cells; il-12 production; in-vivo; Science & Technology - Other Topics; serum-free conditions; th17
Creator
An entity primarily responsible for making the resource
Paustian C; Taylor P; Johnson T; Xu M; Ramirez N; Rosenthal K S; Shu S Y; Cohen P A; Czerniecki B J; Koski G K
Description
An account of the resource
Strategically-paired Toll-like receptor (TLR) ligands induce a unique dendritic cell (DC) phenotype that polarizes Th1 responses. We therefore investigated pairing single TLR ligands with a non TLR-mediated danger signal to cooperatively induce distinct DC properties from cultured human monocytes. Adenosine triphosphate (ATP) and the TLR2 ligand lipoteichoic acid (LTA) selectively and synergistically induced expression of IL-23 and IL-1 beta from cultured monocytes as determined by ELISA assays. Flow cytometric analysis revealed that a sizable sub-population of treated cells acquired DC-like properties including activated surface phenotype with trans-well assays showing enhanced migration towards CCR7 ligands. Such activated cells also preferentially deviated, in an IL-23 and IL-1-dependent manner, CD4(pos) T lymphocyte responses toward the IL-22(hi), IL-17(hi)/IFN-gamma(lo) Th17 phenotype in standard in vitro allogeneic sensitization assays. Although pharmacological activation of either ionotropic or cAMP-dependent pathways acted in synergy with LTA to enhance IL-23, only inhibition of the cAMP-dependent pathway antagonized ATP-enhanced cytokine production. ATP plus atypical lipopolysaccharide from P. gingivalis (signaling through TLR2) was slightly superior to E. coli-derived LPS (TLR4 ligand) for inducing the high IL-23-secreting DC-like phenotype, but greatly inferior for inducing IL-12 p70 production when paired with IFN-gamma, a distinction reflected in activated DCs' ability to deviate lymphocytes toward Th1. Collectively, our data suggest TLR2 ligands encountered by innate immune cells in an environment with physiologically-relevant levels of extracellular ATP can induce a distinct activation state favoring IL-23- and IL-1 beta-dependent Th17 type response.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1371/journal.pone.0054804" target="_blank" rel="noreferrer noopener">10.1371/journal.pone.0054804</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2013
Adaptive Immunity
calcium ionophore
cd14(+) monocytes
Cells
Cohen P A
Czerniecki B J
growth-factor-beta
host-defense
human dendritic cells
il-12 production
in-vivo
Johnson T
Journal Article
Koski G K
Paustian C
PloS one
Ramirez N
Rosenthal K S
Science & Technology - Other Topics
serum-free conditions
Shu S Y
Taylor P
th17
Xu M
-
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/10.1073/pnas.0408704102" target="_blank" rel="noreferrer noopener">http://doi.org/10.1073/pnas.0408704102</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
437-442
Issue
2
Volume
102
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<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>
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
Inhibition of cardiac myofibroblast formation and collagen synthesis by activation and overexpression of adenylyl cyclase
Publisher
An entity responsible for making the resource available
Proceedings of the National Academy of Sciences of the United States of America
Date
A point or period of time associated with an event in the lifecycle of the resource
2005
2005-01
Subject
The topic of the resource
adrenomedullin; angiotensin-ii; cardiac fibroblast; cyclic AMP; extracellular-matrix; failure; fibrosis; gene-expression; growth-factor-beta; heart; lung fibroblasts; modulation; necrosis-factor-alpha; phenotypic; rat ventricular myocytes; Science & Technology - Other Topics; smooth muscle actin
Creator
An entity primarily responsible for making the resource
Swaney J S; Roth D M; Olson E R; Naugle J E; Meszaros J G; Insel P A
Description
An account of the resource
Transformation of fibroblasts to myofibroblasts, characterized by expression of alpha-smooth muscle actin (alpha-SMA) and production of extracellular matrix (ECM) components, is a key event in connective tissue remodeling. Approaches to inhibit this transformation are needed in tissues, such as the heart, where excessive ECM production by cardiac fibroblasts (CFs) causes fibrosis, myocardial stiffening, and cardiac dysfunction. We tested whether adenylyl cyclase (AC) activation (increased cAMP levels) modulates the transformation of adult rat CF to myofibroblasts, as assessed by immunofluorescent microscopy, immunoblotting, and collagen synthesis. A 24-h incubation of CF with TGF-beta or angiotensin II increased alpha-SMA expression, which was inhibited by the AC agonist forskolin and a cAMP analog that activates protein kinase A. Treatment with forskolin blunted serum-, TGF-beta-, and angiotensin II-stimulated collagen synthesis. CFs engineered to overexpress type 6 AC had enhanced forskolin-promoted cAMP formation, greater inhibition by forskolin of TGF-beta-stimulated alpha-SMA expression, and a decrease in the EC50 of forskolin to reduce serum-stimulated collagen synthesis. The AC stimulatory agonist adrenomedullin inhibited collagen synthesis in CF that overexpressed AC6 but not in controls. Thus, AC stimulation blunts collagen synthesis and, in parallel, the transformation of adult rat CF to myofibroblasts. AC overexpression enhances these effects, "uncovering" an inhibition by adrenomedullin. These findings implicate cAMP as an inhibitor of ECM formation by means of blockade of the transformation of CF to myofibroblasts and suggest that increasing AC expression, thereby enhancing cAMP generation through stimulation of receptors expressed on CF, could provide a means to attenuate and prevent cardiac fibrosis and its sequelae.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1073/pnas.0408704102" target="_blank" rel="noreferrer noopener">10.1073/pnas.0408704102</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2005
adrenomedullin
angiotensin-ii
cardiac fibroblast
cyclic AMP
extracellular-matrix
failure
Fibrosis
gene-expression
growth-factor-beta
heart
Insel P A
Journal Article
lung fibroblasts
Meszaros J G
modulation
Naugle J E
necrosis-factor-alpha
Olson E R
phenotypic
Proceedings of the National Academy of Sciences of the United States of America
rat ventricular myocytes
Roth D M
Science & Technology - Other Topics
smooth muscle actin
Swaney J S