Linked Life Data

21342756

Source:http://linkedlifedata.com/resource/pubmed/id/21342756

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5-6
pubmed:dateCreated
2011-4-6
pubmed:abstractText
PGE(2) affects growth of many cell types. Thus, we hypothesized that PGE(2) would stimulate growth of cardiac fibroblasts. To test our hypothesis we used neonatal rat ventricular fibroblasts (NVF). RT-PCR demonstrated the presence of all 4 PGE(2) receptor (EPs) mRNAs in NVF. Using flow cytometry, we found that PGE(2) decreased the percentage of cells in G0/G1 and increased the number of cells in S phase. PGE(2) also increased expression of cyclin D3, a known regulator of the cell cycle and this effect was mimicked by the EP1/EP3 agonist sulprostone. Next, we found that treatment of NVF with PGE(2) increased phosphorylation of p42/44 MAPK and Akt and that PGE(2)-stimulation of cyclin D3 was antagonized with both a MEK inhibitor and a PI3 kinase inhibitor. In conclusion, PGE(2) stimulates cardiac fibroblast proliferation via EP1 and/or EP3, p42/44 MAPK and Akt-regulation of cyclin D3. These results may be relevant to cardiac fibrosis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1532-2823
pubmed:author
pubmed:copyrightInfo
Copyright © 2011 Elsevier Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
84
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
147-52
pubmed:meshHeading
pubmed:articleTitle
Prostaglandin E2 increases cardiac fibroblast proliferation and increases cyclin D expression via EP1 receptor.
pubmed:affiliation
Hypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, MI 48202, USA. phardin1@hfhs.org
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural