Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1998-7-17
pubmed:abstractText
Two subtypes of the endothelin (ET) receptor (ETA and ETB) were studied in cultured ovarian granulosa cells. Immature 21-day-old female Wistar-Imamichi rats were implanted with diethylstilbestrol (DES) pellets for 5 days and granulosa cells were collected by repeated puncturing. Viable cells (2.5 or 5 x 10(5)) were cultured with 50--400 ng/ml of ovine NIH follicle-stimulating hormone (FSH) in the presence or absence of [125I-Tyr13]ET-1 (50 pM) in 1 ml McCoy's 5a medium for 72 h. FSH gradually increased the [125I-Tyr13]ET-1 binding to granulosa cells, whereas FSH-untreated granulosa cells had no significant changes. The dose of 200 ng/ml of FSH was most effective for [125I-Tyr13]ET-1 binding for 48-h culture, thereafter revealing a plateau. After 48 h of culture with 200 ng/ml of FSH, granulosa cells were further incubated with [125I-Tyr13]ET-1 (10 pM-1 nM) and/or [125I]IRL1620, the selective ETB receptor agonist (10 pM-1 nM) for 2 h for equilibrium study, and then the dissociation constant and the maximal binding capacity between receptors and ligands were determined by saturation curve and Scatchard plot analysis. ETA + ETB, ETB, and ETA (sites/cells) showed a 4.4-, 2.6-, and 7.5-fold increase, respectively. As for steroidogenesis, ET-1 (100 nM) or ET-3 (100 nM) suppressed FSH-induced progesterone and 17 beta-estradiol production. These results indicate that FSH upregulates both ETA and ETB receptors in DES-treated immature rat granulosa cells, with no significant differences between ET-1 and ET-3, and that ET-1 or ET-3 suppresses FSH-induced steroidogenesis. ETs may affect the granulosa cell function through the ETA and ETB receptors, and the increase in amount of ET binding does not reflect ET effects on granulosa cell function. The ET receptor plays an important role in the development of the ovary.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Endothelins, http://linkedlifedata.com/resource/pubmed/chemical/Estradiol, http://linkedlifedata.com/resource/pubmed/chemical/Follicle Stimulating Hormone, http://linkedlifedata.com/resource/pubmed/chemical/IRL 1620, http://linkedlifedata.com/resource/pubmed/chemical/Indicators and Reagents, http://linkedlifedata.com/resource/pubmed/chemical/Iodine Radioisotopes, http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments, http://linkedlifedata.com/resource/pubmed/chemical/Progesterone, http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Endothelin A, http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Endothelin B, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Endothelin, http://linkedlifedata.com/resource/pubmed/chemical/Testosterone
pubmed:status
MEDLINE
pubmed:issn
0160-2446
pubmed:author
pubmed:issnType
Print
pubmed:volume
31 Suppl 1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
S225-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9595444-Animals, pubmed-meshheading:9595444-Cells, Cultured, pubmed-meshheading:9595444-Endothelins, pubmed-meshheading:9595444-Estradiol, pubmed-meshheading:9595444-Female, pubmed-meshheading:9595444-Follicle Stimulating Hormone, pubmed-meshheading:9595444-Granulosa Cells, pubmed-meshheading:9595444-Indicators and Reagents, pubmed-meshheading:9595444-Iodine Radioisotopes, pubmed-meshheading:9595444-Ovary, pubmed-meshheading:9595444-Peptide Fragments, pubmed-meshheading:9595444-Pregnancy, pubmed-meshheading:9595444-Progesterone, pubmed-meshheading:9595444-Rats, pubmed-meshheading:9595444-Rats, Wistar, pubmed-meshheading:9595444-Receptor, Endothelin A, pubmed-meshheading:9595444-Receptor, Endothelin B, pubmed-meshheading:9595444-Receptors, Endothelin, pubmed-meshheading:9595444-Testosterone
pubmed:year
1998
pubmed:articleTitle
Effects of follicle-stimulating hormone on endothelin receptors in cultured rat ovarian granulosa cells.
pubmed:affiliation
Department of Obstetrics and Gynecology, Institute of Clinical Medicine, University of Tsukuba, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't