Linked Life Data

15078866

Source:http://linkedlifedata.com/resource/pubmed/id/15078866

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
29
pubmed:dateCreated
2004-7-12
pubmed:abstractText
Certain uterine prostaglandins (PGs) are elevated at implantation sites and are needed to trigger the events of blastocyst implantation that include blastocyst-uterine attachment and stromal decidualization with vascular permeability changes. Several decades of investigations showed that treatment with PG synthesis inhibitors, prior to or during the time of implantation, resulted in either complete inhibition or a delay in implantation or reduction in the number of implantation sites with diminished decidual tissue. Consistent with these findings, we observed that whereas a selective PG endoperoxide synthase (Ptgs) 1 inhibitor SC-560 failed to inhibit implantation, a selective Ptgs2 inhibitor SC-236 showed significantly reduced number and size of implantation sites in progesterone-treated ovariectomized pregnant hamsters. It is known that Ptgs2 expression and Ptgs2-derived prostacyclin (PGI2) synthesis at implantation sites are needed for implantation in the mouse (a rodent that needs ovarian estrogen for implantation). However, it is unknown which Ptgs and PG synthases produce which PGs at implantation sites of the hamster (a rodent that does not need ovarian estrogen for implantation). Here we demonstrate that as blastocyst implantation proceeds, a reduction in Ptgs1 expression from uterine luminal epithelial cells and a gradual induction in Ptgs2 expression exclusively in luminal epithelial and adjacent decidual cells occurred at implantation sites of hamsters. Results also reveal that PGE2, but not PGI2, is the major PG at implantation sites where Ptgs2 and microsomal type PGE synthases but not PGI synthases are co-expressed. This elevated uterine PGE2 at implantation sites may serve to initiate or amplify physiological signals required for specific aspects of the implantation process in hamsters.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
16
pubmed:volume
279
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
30579-87
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:15078866-Animals, pubmed-meshheading:15078866-Binding Sites, pubmed-meshheading:15078866-Blastocyst, pubmed-meshheading:15078866-Cricetinae, pubmed-meshheading:15078866-Dinoprostone, pubmed-meshheading:15078866-Embryo Implantation, pubmed-meshheading:15078866-Female, pubmed-meshheading:15078866-Immunohistochemistry, pubmed-meshheading:15078866-Intramolecular Oxidoreductases, pubmed-meshheading:15078866-Microscopy, Fluorescence, pubmed-meshheading:15078866-Microsomes, pubmed-meshheading:15078866-Models, Biological, pubmed-meshheading:15078866-Prostaglandin-Endoperoxide Synthases, pubmed-meshheading:15078866-Protein Isoforms, pubmed-meshheading:15078866-Pyrazoles, pubmed-meshheading:15078866-RNA, pubmed-meshheading:15078866-RNA, Messenger, pubmed-meshheading:15078866-Sulfonamides, pubmed-meshheading:15078866-Uterus
pubmed:year
2004
pubmed:articleTitle
Prostaglandin E2 is a product of induced prostaglandin-endoperoxide synthase 2 and microsomal-type prostaglandin E synthase at the implantation site of the hamster.
pubmed:affiliation
Division of Reproductive and Developmental Biology, the Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee 37232-2678, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't