| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2002: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2001: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2000: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1999: ¥1,000,000 (Direct Cost: ¥1,000,000)
|
|---|
| Research Abstract |
There exists prolactin-releasing peptide (PrRP), PACAP, ANP, BNP, CNP and their receptors and RAS both in rat and human ovaries. PrRP regulates ovarian functions. In the case of human beings, the study was done after gaining sufficient informed consents. PrRP appears to regulate cyclic nucleotides, cytosolic Ca^<2+>, intracellular voltage, apoptosis, and adhesion molecule. Furthermore, PrRP regulates not only ovarian steroidogenesis but also gonadotropin-induced steroidogenesis. As for DNA polymerase activities, PrRP controls DNA polymerase α activity, a replicating enzyme for DNA synthesis, indicating the involvement of PrRP in ovarian cellular proliferation. In addition, PrRP is closely involved in each or mutual actions of PACAP, ANP and angiotensin 2, endothelin, gonadotropin and growth hormone, and further it appears to regulate each receptor. In contrast, the involvement of PrRP, different from that of angiotensin 2 in neovascularization has not been shown well. PrRP with each receptor exist mainly in the granulosa cells, also luteinized cells, than in thecal and interstitial cells. PrRP levels in human body fluids are very low and non-specific to gynecological diseases except for endometriosis which shows a sporadic increase. PrRP seems not to be involved in ovarian atresia and oocyte. Furthermore, PrRP does not stimulate prolactin release in vivo in rats more than thyroid-stimulating hormone. The role of PrRP on ovarian ion channels, ERKs and apoptosis is questionable.
|
