Linked Life Data

12135903

Source:http://linkedlifedata.com/resource/pubmed/id/12135903

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2002-7-23
pubmed:abstractText
The presence of cAMP-dependent protein kinase (PKA) in the plasma membrane compartment and its association with an A-kinase anchoring protein (AKAP150) is implicated in mediating cAMP regulatory events in the rat myometrium. The association of PKA with purified myometrial plasma membrane declined gradually between Day 16 and Day 21 of gestation, with a decrease of 53% +/- 11% of the catalytic subunit and of 61% +/- 7% of the regulatory subunit at Day 21 compared with Day 19. To determine the role of progesterone in this association, pregnancy was prolonged by administration of progesterone or shortened by administration of the antiprogestin RU486. Progesterone treatment maintained PKA association with plasma membrane at Day 21 at 123% +/- 23% (catalytic subunit) and 92% +/- 4% (regulatory subunit) of Day 19 levels. In contrast, protein phosphatase 1, protein phosphatase 2B, phospholipase Cbeta(3), and AKAP150 concentrations in the plasma membrane did not change over this interval or with progesterone treatment. Changes in PKA coimmunoprecipitated with membrane-associated AKAP150 paralleled those in total plasma membrane on Days 19 and 21 and on Day 21 following progesterone treatment. In contrast, plasma membrane PKA catalytic and regulatory subunits decreased by 20 h after RU486 injection on Day 15 of pregnancy to levels resembling those on Day 21. These data indicate that progesterone prevents the decline in PKA associated with myometrial plasma membrane and with AKAP150 in the pregnant rat. The decrease in membrane-bound PKA between Days 19 and 21 and after RU486 treatment precedes the onset of parturition in both experimental paradigms. The loss of plasma membrane PKA may be critical for the decrease in the inhibitory effect of cAMP on oxytocin-induced phosphatidylinositide turnover that occurs near the end of pregnancy and may contribute to enhanced myometrial contractile responsiveness near term.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0006-3363
pubmed:author
pubmed:issnType
Print
pubmed:volume
67
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
605-9
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:12135903-A Kinase Anchor Proteins, pubmed-meshheading:12135903-Adaptor Proteins, Signal Transducing, pubmed-meshheading:12135903-Animals, pubmed-meshheading:12135903-Blotting, Western, pubmed-meshheading:12135903-Carrier Proteins, pubmed-meshheading:12135903-Cell Membrane, pubmed-meshheading:12135903-Cyclic AMP-Dependent Protein Kinases, pubmed-meshheading:12135903-Female, pubmed-meshheading:12135903-Hormone Antagonists, pubmed-meshheading:12135903-Mifepristone, pubmed-meshheading:12135903-Myometrium, pubmed-meshheading:12135903-Precipitin Tests, pubmed-meshheading:12135903-Pregnancy, pubmed-meshheading:12135903-Pregnancy, Animal, pubmed-meshheading:12135903-Progesterone, pubmed-meshheading:12135903-Rats, pubmed-meshheading:12135903-Rats, Sprague-Dawley, pubmed-meshheading:12135903-Signal Transduction
pubmed:year
2002
pubmed:articleTitle
Progesterone prevents the pregnancy-related decline in protein kinase A association with rat myometrial plasma membrane and A-kinase anchoring protein.
pubmed:affiliation
Department of Biochemistry and Molecular Biology, University of Texas Medical School at Houston, Houston, TX 77030, USA. chun-ying.ku@uth.tmc.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.