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/10.1152/ajplung.00445.2010" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajplung.00445.2010</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
L804-L811
Issue
5
Volume
301
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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
Phosphatidylinositol 4,5-bisphosphate Stimulates Alveolar Epithelial Fluid Clearance In Male And Female Adult Rats
Publisher
An entity responsible for making the resource available
American Journal of Physiology-Lung Cellular and Molecular Physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-11
Subject
The topic of the resource
5-bisphosphate; absorption; acute lung injury; alpha; alveolar epithelial barrier; amiloride; beta; beta-adrenoceptor agonists; catecholamines; female advantage; in alveolar fluid clearance; lung liquid clearance; na+ channel enac; permeability; phosphatidylinositol-4; Physiology; pulmonary edema; Respiratory System; rna interference; sodium transport; sodium-channel; transport; water
Creator
An entity primarily responsible for making the resource
Kooijman E E; Kuzenko S R; Gong D H; Best M D; Folkesson H G
Description
An account of the resource
Kooijman EE, Kuzenko SR, Gong D, Best MD, Folkesson HG. Phosphatidylinositol 4,5-bisphosphate stimulates alveolar epithelial fluid clearance in male and female adult rats. Am J Physiol Lung Cell Mol Physiol 301: L804-L811, 2011. First published August 26, 2011; doi:10.1152/ajplung.00445.2010.-Cell membrane phospholipids, like phosphatidylinositol 4,5-bisphosphate [PI(4,5)P-2], can regulate epithelial Na channel (ENaC) activity. Gender differences in lung ENaC expression have also been demonstrated. However, the effects in vivo on alveolar fluid clearance are uncertain. Thus PI(4,5)P-2 effects on alveolar fluid clearance were studied in male and female rats. An isosmolar 5% albumin solution was intrapulmonary instilled; alveolar fluid clearance was studied for 1 h. Female rats had a 37 +/- 19% higher baseline alveolar fluid clearance than male rats. Bilateral ovariectomy attenuated this gender difference. Compared with controls, PI(4,5)P-2 instillation (300 mu M) increased alveolar fluid clearance by similar to 93% in both genders. Amiloride or the specific alpha ENaC small-interfering RNA inhibited baseline and PI(4,5)P-2-stimulated alveolar fluid clearance in both genders, indicating a dependence on amiloride-sensitive pathways. The fraction of amiloride inhibition was greater in PI(4,5)P-2-instilled rats (male: 64 +/- 10%; female: 70 +/- 11%) than in controls (male: 30 +/- 6%; female: 44 +/- 8%). PI(4,5)P-2 instillation lacked additional alveolar fluid clearance stimulation above that of terbutaline, nor did propranolol inhibit alveolar fluid clearance after PI(4,5)P-2 instillation, indicating that PI(4,5)P-2 stimulation was not secondary to endogenous beta-adrenoceptor activation. PI(4,5)P-2 amine instillation resulted in an intermediate alveolar fluid clearance stimulation, suggesting that, to reach maximal alveolar fluid clearance stimulation, PI(4,5)P-2 must reside in cell membranes. In summary, PI(4,5)P-2 instillation upregulated in vivo alveolar fluid clearance similar to short-term beta-adrenoceptor upregulation of alveolar fluid clearance. PI(4,5)P-2 stimulation was mediated partly by increased amiloride-sensitive Na transport. There exist important gender-related effects suggesting a female advantage that may have clinical implications for resolution of acute lung injury.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajplung.00445.2010" target="_blank" rel="noreferrer noopener">10.1152/ajplung.00445.2010</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2011
5-bisphosphate
Absorption
acute lung injury
alpha
alveolar epithelial barrier
American Journal of Physiology-Lung Cellular and Molecular Physiology
amiloride
Best M D
beta
beta-adrenoceptor agonists
catecholamines
female advantage
Folkesson H G
Gong D H
in alveolar fluid clearance
Journal Article or Conference Abstract Publication
Kooijman E E
Kuzenko S R
lung liquid clearance
na+ channel enac
Permeability
phosphatidylinositol-4
Physiology
pulmonary edema
Respiratory System
RNA Interference
sodium transport
sodium-channel
transport
Water
-
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/hep.23049" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep.23049</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
880-892
Issue
3
Volume
50
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
Fenofibrate Differentially Regulates Plasminogen Activator Inhibitor-1 Gene Expression via Adenosine Monophosphate-Activated Protein Kinase-Dependent Induction of Orphan Nuclear Receptor Small Heterodimer Partner
Publisher
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Hepatology
Date
A point or period of time associated with an event in the lifecycle of the resource
2009
2009-09
Subject
The topic of the resource
cells; binding; complex; fibrosis; Gastroenterology & Hepatology; promoter; beta; mechanisms; pai-1; shp; smad3
Creator
An entity primarily responsible for making the resource
Chanda D; Lee C H; Kim Y H; Noh J R; Kim D K; Park J H; Hwang J H; Lee M R; Jeong K H; Lee I K; Kweon G R; Shong M; Oh G T; Chiang J Y L; Choi H S
Description
An account of the resource
Plasminogen activator inhibitor type I (PAI-1) is a marker of the fibrinolytic system and serves as a possible predictor for hepatic metabolic syndromes. Fenofibrate, a peroxisome proliferator-activated receptor alpha (PPAR alpha) agonist, is a drug used for treatment of hyperlipidemia. Orphan nuclear receptor small heterodimer partner (SHP) plays a key role in transcriptional repression of crucial genes involved in various metabolic pathways. In this Study, we show that fenofibrate increased SHP gene expression in cultured liver cells and in the normal and diabetic mouse liver by activating the adenosine monophosphate-activated protein kinase (AMPK signaling pathway in a PPAR alpha-independent manner. Administration of transforming growth factor beta (TGF-beta) or a methionine-deficient and choline-deficient (MCD) diet to induce the progressive fibrosing steatohepatitis model in C57BL/6 mice was significantly reversed by fenofibrate via AMPK-mediated induction of SHP gene expression with a dramatic decrease in PAI-1 messenger RNA (mRNA) and protein expression along with other fibrotic marker genes. No reversal was observed in SHP null mice treated with fenofibrate. Treatment with another PPAR alpha agonist, WY14643, showed contrasting effects on these marker gene expressions in wild-type and SHP null mice, demonstrating the specificity of fenofibrate in activating AMPK signaling. Fenofibrate exhibited a differential inhibitory pattern on PAI-1 gene expression depending on the transcription factors inhibited by SHP. Conclusion: By demonstrating that a PPAR alpha-independent fenofibrate-AMPK-SHP regulatory cascade can play a key role in PAI-1 gene down-regulation and reversal of fibrosis, our study suggests that various AMPK activators regulating SHP might provide a novel pharmacologic option in ameliorating hepatic metabolic syndromes. (HEPATOLOGY 2009;50:880-892.)
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/hep.23049" target="_blank" rel="noreferrer noopener">10.1002/hep.23049</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2009
beta
Binding
Cells
Chanda D
Chiang J Y L
Choi H S
complex
Fibrosis
Gastroenterology & Hepatology
Hepatology
Hwang J H
Jeong K H
Journal Article or Conference Abstract Publication
Kim D K
Kim Y H
Kweon G R
Lee C H
Lee I K
Lee M R
mechanisms
Noh J R
Oh G T
PAI-1
Park J H
promoter
Shong M
SHP
smad3