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Regulation of PKC Delta in the Pregnant Rat Corpus Luteum

其他書名	Involvement in the Induction of Relaxin Expression
出版	Northwestern University, 1999
URL	http://books.google.com.hk/books?id=fR8dAQAAMAAJ&hl=&source=gbs_api

註釋The purpose of the studies described in this dissertation was to analyze the hormonal regulation of protein kinase C (PKC) delta expression and activation in the pregnant rat corpus luteum. The hormonal regulation of relaxin mRNA expression and the role of PKC delta in this regulation was also analyzed. These analyses were initiated due to previous studies in our lab which revealed an increase in PKC delta protein and mRNA expression during the second half of pregnancy. The corpus luteum of the second half of pregnancy is responsive to placental signals, namely rat placental lactogens (rPL)-1 and -2 as well as estrogen (E2) aromatized from testosterone. The role of these hormones in regulation of PKC delta and relaxin expression were assessed in a luteinized granulosa cell culture system. I have found that PKC delta protein but not mRNA expression is regulated by E2. Signaling through the prolactin (PRL) receptor by physiological concentrations of rPL-1 was capable on increasing PKC delta mRNA and protein. E2 and rPL-1 cooperated to increase PKC delta mRNA and protein expression. Similarly, relaxin mRNA expression was induced by rPL-1 but not E2 alone and E2 enhanced rPL-1 induction of relaxin mRNA expression. Furthermore, PKC delta activity is present in corpora lutea of the second half of pregnancy. Signaling through the PRL receptor may be responsible for this activation. PKC delta kinase activity is necessary but not sufficient for rPL-1 induction of relaxin mRNA expression. The target of PKC delta downstream of the PRL receptor may be signal transducer and activator of transcription (Stat) 3. Stat 3 is phosphorylated on tyrosine 705 and serine 727, which are required for Stat 3-dependent transcription, and Stat 3 co-immunoprecipitates with PKC delta in pregnant rat corpora lutea and in response to rPL-1. Stat 3 phosphorylation and co-immunoprecipitation with PKC delta require PKC delta kinase activity. These studies demonstrate that PKC delta is poised to regulate luteal function in the second half of pregnancy when it is highly expressed and active. Regulation of relaxin expression is one target of PKC delta due to PRL receptor-dependent regulation of Stat 3 phosphorylation.