Linked Life Data

8699421

Source:http://linkedlifedata.com/resource/pubmed/id/8699421

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1996-9-5
pubmed:abstractText
Increased prolactin concentrations are known to inhibit the ovarian proteolytic enzyme cascade associated with follicular rupture. It is not known whether there is also an effect of prolactin on endogenous proteinase inhibitors such as the tissue inhibitors of metalloproteinases (TIMPs). We sought to study the effect of prolactin on ovarian metalloproteinase inhibitors in cultured rat granulosa cells. Granulosa cells were cultured for 24 h with prolactin (0-1000 ng ml-1) in the absence or presence of LH. Metalloproteinase inhibitor activity in the conditioned culture media was measured by a colorimetric assay. Prolactin at 1000 ng ml-1 increased inhibitor activity by 2.86 +/- 0.63 times. Expression of mRNA encoding TIMP-1 measured by Northern analysis increased by 2.34 +/- 0.34 times with 100 ng prolactin ml-1 and by 2.43 +/- 0.42 times with 1000 ng prolactin ml-1 compared with control cultures (no LH, no prolactin). In the presence of LH, expression of mRNA encoding TIMP-1 and inhibitor activity increased by 2.60 +/- 0.6 and 4.60 +/- 0.54 times, respectively. However, no further change in mRNA expression or inhibitor activity was apparent with the addition of prolactin to LH-treated cultures. Prolactin had no effect on expression of mRNA encoding TIMP-3 in the absence or presence of LH, although LH stimulated a 1.7-fold increase in mRNA encoding TIMP-3 compared with controls. Addition of prolactin had no effect on media concentrations of oestradiol or progesterone. These data demonstrate that metalloproteinase inhibitor activity increases with increasing doses of prolactin; however, when LH was added, this effect was no longer seen. With an increase in metalloproteinase inhibitor activity, tissue metalloproteinase action could be decreased, providing a possible explanation for the local inhibition on pre- and peri-ovulatory pathways by hyperprolactinaemia.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0022-4251
pubmed:author
pubmed:issnType
Print
pubmed:volume
107
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
103-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Regulation of granulosa cell-derived ovarian metalloproteinase inhibitor(s) by prolactin.
pubmed:affiliation
Department of Obstetrics & Gynecology, University of Kentucky Medical Center, Lexington 40536-0084, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.