Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1995-10-13
pubmed:abstractText
A growing body of evidence suggests that growth hormone (GH) plays a role in regulating ovarian function by augmenting gonadotropin stimulation of granulosa cell differentiation and folliculogenesis. The majority of follicles in the mammalian ovary do not ovulate, but instead undergo a degenerative process (atresia) involving apoptotic cell death. The objective of the present study was to investigate the role of GH in regulating follicle apoptosis and to determine whether or not insulin-like growth factor-I (IGF-I) mediates GH action in this process. Preovulatory follicles obtained from eCG-primed rats were cultured for 24 h in serum-free conditions with or without hormone treatments. After culture, follicular apoptotic DNA fragmentation was analyzed by autoradiography of size-fractionated DNA labeled at 3' ends with [32P]dideoxy-ATP. Culture of preovulatory follicles resulted in a spontaneous onset of apoptotic DNA fragmentation that was suppressed by ovine GH (oGH) in a dose-dependent manner, reaching a maximum of 65% suppression. To rule out the effect of residual gonadotropin in the oGH preparation, follicles were also cultured with recombinant bovine growth hormone (rbGH). Like oGH, rbGH suppressed apoptotic DNA fragmentation. Our earlier study indicated that hCG and FSH treatment also suppress apoptosis in the present model system, but no additive effect of GH and either hCG or FSH on the suppression of apoptosis was observed. To determine whether the observed effect of GH action on follicle apoptosis is mediated by IGF-I, three types of studies were carried out.(ABSTRACT TRUNCATED AT 250 WORDS)
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0006-3363
pubmed:author
pubmed:issnType
Print
pubmed:volume
53
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
13-20
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:7545438-Animals, pubmed-meshheading:7545438-Apoptosis, pubmed-meshheading:7545438-Carrier Proteins, pubmed-meshheading:7545438-Cells, Cultured, pubmed-meshheading:7545438-Chorionic Gonadotropin, pubmed-meshheading:7545438-DNA, pubmed-meshheading:7545438-Drug Interactions, pubmed-meshheading:7545438-Estrogens, pubmed-meshheading:7545438-Female, pubmed-meshheading:7545438-Follicle Stimulating Hormone, pubmed-meshheading:7545438-Growth Hormone, pubmed-meshheading:7545438-Humans, pubmed-meshheading:7545438-Insulin-Like Growth Factor Binding Proteins, pubmed-meshheading:7545438-Insulin-Like Growth Factor I, pubmed-meshheading:7545438-Ovarian Follicle, pubmed-meshheading:7545438-Ovulation, pubmed-meshheading:7545438-Progesterone, pubmed-meshheading:7545438-RNA, Messenger, pubmed-meshheading:7545438-Rats, pubmed-meshheading:7545438-Rats, Sprague-Dawley
pubmed:year
1995
pubmed:articleTitle
Growth hormone suppression of apoptosis in preovulatory rat follicles and partial neutralization by insulin-like growth factor binding protein.
pubmed:affiliation
Department of Gynecology and Obstetrics Stanford University School of Medicine, California 94305-5317, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't