Source:http://linkedlifedata.com/resource/pubmed/id/11554693
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
|
| pubmed:dateCreated |
2001-9-13
|
| pubmed:abstractText |
Impaired trophoblast invasion during the first trimester of pregnancy is linked to spontaneous abortion, and defective invasion in the second trimester to hypertension + proteinuria (pre-eclampsia). Hypertension developing during the third trimester of human pregnancy represents, in part, a corrective response in the mother to provide adequate placental perfusion for fetal growth when trophoblast has not to invaded and converted the myometrial porprtion of maternal spiral arteries into to low resistance-high capacitance conduits. Deportation of vesicles from hypoxemic trophoblast is thought to cause hypertension plus proteinuria, vascular damage and a systemic coagulopathy. Trophoblast invasion may be inhibited by local cytokines, such as TGF-betas but Thl-type cytokines associated with pre-eclapmsia and spontaneous abortions (e.g., IL-1, TNF-alpha, IFN-gamma) are not known to inhibit migration at in situ concentrations. Trophoblast invasion is also inhibited by the binding of surface integrins to fibronectin and fibrin, and fibrin production is stimulated by these Th1 cytokines via up-regulation of prothrombinases(s) such as fg12 which directly and via TNF-alpha-facilitated inflamation compromise trophoblast cell integrity. We, therefore, asked if fg12 expression and TNF-alpha are increased in first trimester human miscarriage and in third trimester pre-eclampsia.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Sep
|
| pubmed:issn |
1046-7408
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
46
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
196-210
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:11554693-Abortion, Spontaneous,
pubmed-meshheading:11554693-Animals,
pubmed-meshheading:11554693-Enzyme Activation,
pubmed-meshheading:11554693-Female,
pubmed-meshheading:11554693-Humans,
pubmed-meshheading:11554693-In Situ Hybridization,
pubmed-meshheading:11554693-Male,
pubmed-meshheading:11554693-Mice,
pubmed-meshheading:11554693-Mice, Inbred BALB C,
pubmed-meshheading:11554693-Mice, Inbred CBA,
pubmed-meshheading:11554693-Mice, Inbred DBA,
pubmed-meshheading:11554693-Placenta,
pubmed-meshheading:11554693-Pre-Eclampsia,
pubmed-meshheading:11554693-Pregnancy,
pubmed-meshheading:11554693-Pregnancy Trimester, First,
pubmed-meshheading:11554693-Pregnancy Trimester, Third,
pubmed-meshheading:11554693-RNA, Messenger,
pubmed-meshheading:11554693-Thromboplastin,
pubmed-meshheading:11554693-Tumor Necrosis Factor-alpha
|
| pubmed:year |
2001
|
| pubmed:articleTitle |
Activation of the novel prothrombinase, fg12, as a basis for the pregnancy complications spontaneous abortion and pre-eclampsia.
|
| pubmed:affiliation |
Toronto General Hospital Research Institute, University of Toronto, Ontario, Canada.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|